Helpful Links – Information Dump – clean up

The Hardt Lab – Salmonella Pathogenesis, Institute of Microbiology, ETH Zurich – http://www.micro.biol.ethz.ch/research/hardt.html (research Salmonella shedding from humans)

Salmonella Typhimurium diarrhea reveals basic principles of Enteropathogen Infection and disease-promoted DNA exchange: cell host & microbe – https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30119-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2Fs1931312817301191%3Fshowall%2Dtrue

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798295/

Precursors like acetyl acid for liver metabolism evidence that creatures have needed fermentation as part of their diet for long enough to have evolved dependencies on it. Natural sources of fermentation: ruminant gut contents and rotten fruits, etc. Adding certain bacteria can result in sterilization of products under conditions of poor storage. Most grain products come with mycotoxins and mildews and pathogens in them, ready to feed on the sugars and starches the moment they are exposed to enough moisture or warmth. The only cost effective way to add a real safety measure is to either eliminate the starches/sugars, or to add these special bacteria.

L. monocytes is submissive to other bacteria.  Hpp does not kill it but the presence of other bacteria prevent its proliferation

Karen’s interests for sharing: FDA referenced documents that state the relationship of dry kibble and pathogen risk but urge consumers not to use raw, elaboration on studies referenced in first mercola article, no dogs got sick when fed raw meat that was intentionally contaminated with salmonella strains,

FDA commits to disclose retailer information for some food recalls: Petfoodindustry.com https://www.petfoodindustry.com/articles/7516-fda-commits-to-disclose-retailer-info-for-some-food-recalls?utm_source=KnowledgeMarketing&utm_medium=email&utm_content=Pet%20eNews&utm_campaign=18_10_02_PetENews&eid=223857144&bid=2257026

Raw food trials with pets: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003575/#!po=0.431034

http://www.drmasiello.com/2015/04/my-comments-to-the-fda/

http://www.dogsnaturallymagazine.com/consumer-pleas-fda-warnings-ignored-by-all-major-retailers/

http://www.mercola.com/downloads/bonus/the-FDA-exposed/default.aspx

http://www.infowars.com/the-truth-about-the-fda/

http://www.forbes.com/forbes/2011/0214/opinions-steve-forbes-fact-comment-fda-may-kill-millions.html

https://www.google.com/amp/www.undergroundhealth.com/fda-approved-prescription-drugs-kill-hundreds-of-thousands-of-people-annually/amp/

http://www.fdareview.org/05_harm.php

http://mobile.wnd.com/2012/12/how-many-have-died-because-of-the-fda/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709812/

Book

In order to compete effectively with other microorganisms in the anaerobic, nutritionally sparse conditions of the gut, Salmonella needs to  be able to take up limited nutrients effectively and to adapt to rapidly changing conditions. Bile sales, fatty acids and glycerides all have detergent-like actions. The intestinal lumen is replete with proteases and lipases, and these must be prevented from gaining access to the vicinity of the cytoplasmic membrane where they will cause damage to the membrane structures. (pg 21)

In 1958 it was discovered that Salmonella’s ability to agglutinate certain species of erythrocytes and its association between fimbriae and erythrocytes included mannose-containing carbohydrates in lectin-based interactions (pg 35)

The major factor for intestinal penetration is encoded by genes that are clustered in a large area (40kb) on the chromosome designated Salmonella pathogenicity island 1 (SPI1) (pg 61) Studies using murine ligated ileal loops revealed that the genes located on SPI1 are necessary for invasion of M cells in the FAE (follicle associated epithelium) of Peyer’s Patches.

Symptoms associated with Salmonella were markedly decreased by treatment with nitrogen mustard, an agent that depletes the polymorphonuclear neutrophil (PMN)… which also inhibits fluid secretion induced by cholera toxin) (pg 62)

As the host mounts an inflammatory response at the site of mucosal invasion, Salmonella genes involved in defence against inflammation have to be expressed subsequently to bacterial entry into the epithelium. Coordinated expression of these virulence genes appears to be mediated by PhoPQ, a two-component regulatiory system that changes gene expression in response to changes in the external Mg2+ and Ca2+ concentrations. Ca2+ and Mg2+ cations stabilize the outer membrane by neutralizing the negative charge of phosphate groups and bridging adjuacent LPS molecules. The intracellular parasitophorous vacuole in which salmonella resides was shown to be low in Mg2+ and Ca2+. In such environments, PhoPQ activates pmrAB, two genes encoding a second two-component regulatory system. Activation of PmrAB increases the substitution of phosphates in both the core oligosaccharide and the lipid A part of the LPS with 4-amino-4-deoxy-L-arabinose, thereby compensating for the lack of Ca2+ and Mg2+ cations. These structural changes in LPS result in increased resistance to bacteriacidal/permeability increasing protein (BPIs), a cationic antibacterial protein that is released by human PMN during inflammation. Furthermore, in response to low Mg2+ and Ca2+ concentrations, PhoPQ activates a second pmrAB-independent pathway, which results in increased resistence to defensins released by recruited PMN and crypdins produced by Paneth cells located in the intestinal crypts. (pg 63)

Only 1% of the inoculum survives the low pH during the passage through the stomach. The surviving bacteria then reach the small intestine, which contains bacteriacidal compounds, such as bile salts. About 80% of the bacteria that survive the passage through the stomach are passed with the faeces within 6-10 hours post-infection, About 15% remain localized in the lumen of the caecum and large intestinge, and only 5% manage to penetrate the intestinal wall of the small intestine and reach the GALT (Gut associated lymphatic tissue).

An important factor that impedes colonization by salmonella serovars is the normal gut flora. Disruption in the indogenous flora by streptomycin treatment results in a 100,000 fold reduction in the 50% implantation dose. The phenomenon of the indogenous flora being able to prevent colonization by exogenous bacteria is known as bacterial interference. Some of these things are production of inhibitory substances, competition for tissue adhesion sites, and limiting resources.

Peyers patches serve as the main port of entry for Salmonella serovars.

Intestinal perforations at areas of Peyer’s patches are the most frequent cause of death during typhoid fever. (Pg 59)

Calves could be protected from lethal salmonella challenge when fed colostrum from salmonella infected cows although this protection could not be coorelated with serum antibodies to flagellar or somatic antigens (pg 76)

The predominant immunoglobin of mucosal immunity is IgA although IgG and/or IgM responses can also be observed. IgA has been shown to mediate protection against infection through anti-body dependent cellular cytotoxicity, potentiate bacteriacidal action by iron-sequestering compounds, serve as a possible opsonin for mucosal phagotyes, inhibit bacterial adherence, and neutralize toxin moieties. Secretory IgA therefore exhibits exceptional diversity in its ability to mediate protection at mucosal surfaces. (pg76)

Cytokines play a critical role in the protection mediated by the immune system. They regulate whether a predominately humoral or cell-mediated response will be mounted . Besides modulating the type and intensity of an immune response, these protein signals can also alter the response, these protein signals can also alter the activity of the effector cells. In mice, IFN-y was shown to activate macrophages resulting in increased killing capacity of the cells for a variety of microbials pathogens. Incubation of the macrophages with recombinant IFN-y enhanced their activity against s. typhimurium and mice administered exogenous IFN-y exhibited reduced disseminated infection by that organism. Similar protection against salmonella infection was observed in mice receiving tumour necrosis factor alpha (TNF-a) an inflammatory cytokine, or IL-12 (pg 77)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5644655/ “Little evidence also exists on the significance of raw meat feeding on the shedding of CampylobacterSalmonella, and enteropathogenic Yersinia in the feces of pets.”

Results (3): Enteric pathogens were detected in 28% of the RMBDs, originating from 12 producers… Salmonella was detected in only 2% of the samples…”

Discussion (4): Salmonella was rarely detected in our study and the occurrence (2% by PCR and <1% by culturing) was clearly lower than reported in Canada and USA.

Conclusions (5): These pathogens were not found by culturing, indicating a low contamination level in frozen commercial RMBDs produced in Finland. Salmonella and enteropathoenic Yersinia were detected only in dogs fed RMBDs: however, the infection source and transmission routes remained unclear.

https://pdfs.semanticscholar.org/1bd6/123a6ba70af32f68d0f496814d142db1add2.pdf Salmonella is considered to be a ‘universal pathogen’ as it is successfully isolated from all vertebrates and many insects.

Recent studies show that a mechanism making one serovar virulent for one animal species could make the same serovar less or completely avirulent in another animal host [6]. In addition, other factors like the dose of infection, the age during which the host is infected and their immune response contribute equally to a successful infection [7].

Hence, current research is mainly focused on understanding the acquired ability of Salmonella’s host preference by Salmonella.

Out of these 2,500 serovars nearly 1500 belong to the Salmonella subsp. enterica. Figure represents different Salmonella serovars with core genome and with unique genes marked in black [12].

The first group includes serovars which have a broad host range also called as unrestricted serovars as these infect nearly all animals. This group includes serovars like Salmonella Typhimurium and Salmonella Enteritidis.

Although the severity of disease increases in young hosts when compared to adults, this is because of their inability to counter the mature immune responses in older hosts [8].

The second group includes serovars which cause highly severe systemic infection in their preferred host and are usually excreted without any clinical symptoms when they accidentally infect hosts others then their most adapted or preferred. Serovars such as Dublin, Choleraesuis fall into this category, as these prove to only cause systemic infection in cattle and pigs respectively [13, 14]; however these upon infection into other hosts like rodents and humans are usually excreted making these hosts as ‘carriers’. Serovars of this group are referred to as the ‘Host-adapted Serovars’.

The third group comprises of serovars which are restricted very strictly with one very specific host only; these serovars are called ‘host–restricted serovars’. They exclusively cause systemic infection, which often proves to be fatal within their host. Serovars such as Typhi, Gallinarum, Abortusequi etc belong to this group.

Salmonella thrives on the Payer’s patches, which is abundant with specialized epithelial M cells, and are considered as the primary site for infection. Upon breaching the mucosal layer, it then translocate to lymphoidal follicles and mesenteric lymph nodes [17]. Salmonella has developed mechanisms to infect and proliferate both in phagocytic and non-phagocytic cells. These include the epithelial cells, macrophages, dendritic cells, enterocytes and neutrophils [18]. The entry of Salmonella within cells is either by phagocytosis, Salmonella mediated through Type Three Secretion System-1 (T3SS1) or T3SS1 independent [10]. The process involves secretion of virulence factors called effector proteins encoded by SPI-1, which bring about actin re-modulation, leading to ruffling and extension of the plasma membrane of the host and hence resulting in invasion of the bacterium [10, 19, 20]. Once inside the epithelial cells, Salmonella develops around it a niche called the Salmonella Containing Vacuole (SCV). These SCVs interact with the endocytic vesicles within the host, thereby accumulating various factors in the process [21]. These include Rho GTPase such as Rab5 and Rab7 and also lysosomal associated membrane protein LAMP-1 [22]. From the SCV, the bacterium secrets another set of effector proteins encoded by SPI-2 genes that are responsible for intracellular replication and survival [23, 24]. After 4-6hrs of invasion the replicating bacteria within the SCV results in formation of tubular network like filaments called the Salmonella induced filaments (Sifs), which helps in maintain the integrity of the SCV [23]. These Sif ’s tend to grow outwards to the plasma membrane accumulating various host constituents. The formation of these Sif ’s is facilitated by TTSS-2 effector protein called SifA [21, 23, 24]. These Sif ’s are highly enriched in cholesterol and LAMP-1. Internalization of Salmonella, also affects other cellular process such as apoptosis, cell division, cytokine production and antigen presentation [25].

Although the precise mechanisms leading to host specificity by Salmonella is not very well understood, however the pathogenicity of Salmonella serovars is influenced by selective pressure within a particular host and its surroundings [5, 8].

Serovars such as a Salmonella Typhimurium, Enteritidis, Pullorum, Gallinarium Dublin and Paratyphi C are a classic example which has undergone gene deletions [13]. As a result, these serovars have lost the ability to replicate in the intestinal lumen of their respective host, although these successfully cause systemic infections [26].

Mannose sensitive pathogenicity determinants like FimH adhesins play an important role in adhesion of Salmonella on its host cell surface [27].

Apart from genetic factors, other paradigms such as physiological state of host cell, availability of amino acids and the ability of one serovar over other to replicate, has a critical role to play in the virulence pattern of a serovar [17].

Regardless of various genetic and physiological parameters effecting host specificity, it is also observed that stress has a significant role to play in pathogenicity and virulence of Salmonella in various hosts leading to its consistent presence in the food chain and environment.

http://legacy.iica.int/Esp/regiones/sur/uruguay/Documentos%20de%20la%20Oficina/CursoBPPPA/Literatura/ScientificTechnicalFactorsSalmonellaRawPoultry.pdf A particular concern for the group was the use of criteria implying a zero tolerance for Salmonella and suggesting complete absence of the pathogen. The notion can be interpreted differently by various stakeholders and was considered inappropriate because there is neither an effective means of eliminating Salmonella from raw poultry nor any practical method for verifying its absence.

An example is the different criteria (and subsequent actions in the case of noncompliance) addressing the presence of Salmonella on raw chicken, all of which depend on the stage in the food chain, the sensitivity of the sampling plan and method, and the analytical method used.

Increasingly, risk-based concepts are being adopted for both domestic policy and international trade, despite sometimes being poorly understood and not always applied consistently or with transparency.

A recent risk assessment of Salmonella contamination in Belgian chicken meat preparations revealed that levels greater than 1 CFU/g were most likely to be associated with human salmonellosis (185).

Legislation has been introduced that makes testing compulsory and specifies deadlines for establishing the required targets in chicken breeders, layers, and broilers and in turkeys (56, 57)

Serovar-specific control measures. In some parts of the world, strategies have been adopted to target specific Salmonella serovars associated with both poultry and human salmonellosis. Salmonella Enteritidis caused a pandemic of human illness from infected layer and broiler flocks beginning in the 1980s (3). Particular strains of Salmonella TABLE 1. Prevalence of Salmonella-positive broiler flocks in the EU, 2005 and 2006 (61) Member state No. of flocks sampleda % flocks positive for Salmonella Austria 365 7.7 Belgium 373 15.3 Cyprus 248 10.9 Czech Republic 334 22.5 Denmark 295 3.1 Estonia 131 2.2 Finland 360 0.3 France 381 8.9 Germany 377 17.2 Greece 245 27.3 Hungary 359 65.7 Ireland 351 27.9 Italy 313 30.4 Latvia 121 9.1 Lithuania 156 5.1 Poland 357 57.7 Portugal 367 42.8 Slovakia 230 8.3 Slovenia 326 3.1 Spain 388 42.3 Sweden 291 0.0 The Netherlands 362 10.2 United Kingdom 382 10.7 a The number of samples taken was statistically determined. Pooled fecal samples were obtained from boot swabs, and five swabs per flock were tested. J. Food Prot., Vol. 73, No. 8 SALMONELLA ON RAW POULTRY 1569 Enteritidis with an apparent predilection for the reproductive tract of the laying hen were responsible for contamination of egg contents, resulting in vertical transmission

For Salmonella Enteritidis and Salmonella Typhimurium in particular there is a clear linkage between human illness and poultry consumption. Conversely, although all Salmonella serovars are considered to be potentially pathogenic to humans, some of those found in poultry are rarely if ever associated with human illness. A classical example is Salmonella serovar II 1,4,12,[27]:b:[e,n,x], also known as Salmonella Sofia, which is often isolated from chicken in Australia but rarely from human salmonellosis cases there (146).

Predominant poultry serovars differ among countries and can change over time within a single country or region (76), and successful control of one serovar may allow another to predominate. For example, epidemiological evidence suggests that Salmonella Enteritidis may have filled the ecological niche occupied previously by the antigenically related Salmonella Gallinarum, which was eradicated in most of the major poultry producing countries by the 1970s (148).

Feed can be a latent source of Salmonella for food animals because it is made from a wide range of potentially contaminated ingredients (44, 151). When present in dry feed, Salmonella can survive for more than 1 year, and even low numbers may be significant because for some strains ,1 cell per g is sufficient to colonize young chicks (157).

The heat sensitivity of nonsporulating bacteria, including Salmonella, is influenced by the temperature and time and the prevailing water activity of the feed. The heating process aims to eliminate Salmonella during pelleting, expansion, or extrusion and minimize any adverse effect on the nutritional quality of the feed (42, 50, 104, 119, 126). However, there is a significant risk of recontamination during postpelleting stages of the milling operation and during storage and transport of feed. Because of this risk, various chemical treatments have been considered, e.g., addition of certain short-chain fatty acids, such as formic and propionic acids. These acids have many of the attributes that are desirable in a feed treatment (92, 113, 151, 189, 195).

Instead of depending on extensive product testing, a better alternative is to apply good manufacturing practices (GMPs) and hazard analysis critical control point (HACCP) principles to the manufacturing process.

Effective implementation of the HACCP system requires measures to prevent recontamination of the feed after heat treatment. As with raw ingredients, these measures involve adequate storage conditions (including rigorous dust control), appropriate control of transport vehicles, regular cleaning and disinfection of the vehicles, and protection of the load up to and including the point of delivery.

when used with water-immersion chilling systems, reduces the organic load in the chill water (168), making any added chlorine more effective. However, the removal of bacteria from carcasses in the spray washing process is not enhanced by using chlorine and/or hot water (137), probably because organisms that become firmly attached to the tissues are protected from the effects of these agents and are not easily removed (118, 138).

Chilling of poultry carcasses to about 4uC or lower ensures that any Salmonella present will be unable to multiply…or exposure to cold air either by passing carcasses through an air blast system or holding them in a chill room. The continuous immersion system has a washing effect that reduces microbial contamination by up to 1 log unit (131).

The U.S. system (170) also includes a zero-tolerance policy for visible fecal contamination on carcasses entering the chilling process (181) and the need for a HACCP plan to ensure that avoidance of fecal contamination is a critical control point (182). Otherwise, the determination of critical control points is a matter for the individual company, and their number and location are likely to differ among establishments (180).

No feasible sampling plan can guarantee the absence of Salmonella, but sampling on a regular basis will reveal changes in infection or contamination so that corrective action can be taken, as required. The sampling strategy should be defined according to the public health risk involved, the anticipated prevalence of the target organism, the desired level of confidence in the results obtained, and the general principles of statistical control, which will indicate the degree of confidence offered by negative results. Other factors to consider are the stage in the food chain at which samples should be taken, the type of sample in each case, how many samples to take at any one time, how often material is collected, and what quantity of the material to collect. Standardized methods of analysis should always be used; methods advocated for international adoption are provided by organizations such as the International Organization for Standardization (ISO) and the World Organization for Animal Health (OIE). There also is the question of who should carry out the sampling, although regulations may specify that sampling must be done, at least in part, by a competent authority (71). An effective control strategy requires detailed consideration of the nature of the food chain and the points at which sampling will provide the most meaningful information. No single sampling site is ever sufficient. Testing for Salmonella at any stage should always have a clear objective that is related to control of the organism, allowing appropriate action to be taken on the basis of the results obtained. Other factors include the likelihood of infection or contamination at a particular stage and whether there are practices or interventions that might minimize the risk. Resources can then be allocated appropriately and costeffectively in relation to the risk involved. However, feasible levels of sampling are not usually sufficient to determine fully the effectiveness of a specific control measure.

In monitoring the mill environment, Jones and Richardson (104) noted that TABLE 2. Sampling for Salmonella at different stages of the supply chain Stage in supply chain What to sample When to sample Feed manufacture Bulk ingredients Before use Mill environment and equipment Finished feed Grandparent or parent flocks Litter Sampling should be more intensive for grandparent stock; sample before and just after moving to production house Dead birds Dust Feces Surfaces and equipment After cleaning and disinfection Hatchery Internal surface of hatching cabinet After hatching Chick box liners Eggshells Meconium Dead-in-shell chicks Culled chicks Surfaces and equipment After cleaning and disinfection Broiler flocks Litter Before slaughter Dust Feces Surfaces and equipment After cleaning and disinfection Slaughter and processing Neck skin or carcass rinse After carcass chilling Plant environment and equipment After cleaning and disinfection Portioning and deboning Meat surface and skin As required Plant environment and equipment After cleaning and disinfection Wholesale (fresh and frozen) Meat surface and skin As required Retail Meat surface and skin As required J. Food Prot., Vol. 73, No. 8 SALMONELLA ON RAW POULTRY 1575 dust was consistently contaminated with Salmonella throughout the mill and especially near pellet coolers, which draw in large amounts of air. Thus, sampling of dust and the mill environment is much more effective than monitoring the end product, and the sampling should be done as part of a HACCP program (63, 197).

Sampling at retail. Testing products at the retail stage rather than during processing is more relevant to the exposure of consumers to Salmonella via raw poultry meat. The results obtained can be of greater value in assessing the human health risk, which is required in risk assessments, and in verifying the effectiveness of Salmonella control measures for different types of product. This information will provide a scientific basis for any new criteria that are deemed necessary. The sampling strategy should be based on statistical methods and related to the sources of Salmonella exposure for the majority of the population, i.e., it should be largely focused on retail products that are on display in major towns and cities and in the principal retail outlets from which most poultry meat is sold. All the main forms in which poultry products are marketed should be sampled, e.g., whole carcasses, portions, meat preparations, and fresh and frozen products, and it will be important to distinguish between domestic and imported products

The adoption of quantitative risk assessment practices in microbiological food safety underscores the reality that zero risk is unattainable for all raw foods, a reality in everyday events and everyday life. The choice of zero tolerance, implying the complete absence of a hazard, may be regarded as the expression of a regulatory preference for the precautionary principle and has little to do with food safety and human health (80, 176). In the United States, the Committee on the Review of the Use of Scientific Criteria and Performance Standards for Safe Foods formed under the National Research Council (135) noted that the term ‘‘zero tolerance’’ is commonly used but generally poorly defined or understood. Use of this language in expressing objectives is troublesome because the terminology has different meanings for different audiences, as highlighted by the definition the Committee offered for its own purposes: ‘‘lay audience perception of the absence of a hazard that cannot be scientifically assured, but is operationally defined as the absence of a hazard in a specified amount of food as determined by a specific method.’’ To some people, zero tolerance implies a notional concept of zero risk associated with the food or zero prevalence of a pathogen in the food commodity. Such a misunderstanding could easily arise from the pending EU requirement for the absence of Salmonella in 25 g of fresh (raw) poultry meat (56) because no details are given on how this requirement would be interpreted. In the absence of any means of eliminating the pathogen from a raw food product, the ‘‘zero’’ concept is misleading to those consumers who may interpret such regulations as implying no risk; these consumers would have unrealistic expectations of the effectiveness of regulatory action. If a hazard exists, there is some probability it will cause an adverse effect, no matter how small (85). Zero tolerance may also imply that both minor and major deviations from a policy will be treated with the same severity. This is obviously not a sensible approach to identifying and resolving problems. Internationally, there is no consistency in interpreting the concept and what action should result from any deviations. The purpose of a zero tolerance policy should be to provide an alert, leading to a review of control policies and procedures while permitting distribution of the final product to the marketplace in situations where withdrawal would not give a risk reduction proportional to cost and other practical considerations. Little is to be gained when dealing with food safety management practices based on microbiological criteria for end product testing alone (accept or reject) because even when a process is completely under control some, albeit small, probability exists for exceeding the established parameters (191, 203). Without knowledge of the degree of variability in a process or product or of where the uncertainties of a food process lie, the likelihood of exceeding the limits is unknown. Several other challenges exist to applying a zero tolerance policy for Salmonella in poultry meat: defining the accuracy, sampling intensity, sampling material, and method sensitivity. At which point is the assessment to be made, preharvest or postharvest, who bears the repercussions for enforcement, and who has and what is the enforcement capacity? Ultimately, regulatory choices in establishing control policies must be verified through scientific evidence for their effectiveness for reducing risk so that social costs can be made transparent (80).

The term ‘‘zero tolerance’’ for specific pathogens such as Salmonella in food products is interpreted differently by scientists and other stakeholders in different countries and therefore has been confusing, misleading, and misapplied. All countries signing the international WTO agreements are entitled to establish sovereign levels of protection. However, with regard to sanitary measures that include MCs, the most appropriate and legally defensible approach is to define such criteria by limits of detection according to the analytical method imposed and confidence limits of sampling and testing. Using terms such as ‘‘zero tolerance’’ or ‘‘absence of a microbe’’ in relation to raw poultry should be avoided unless these terms are defined and explained by international agreement. New metrics, such as POs that are linked to human health outcomes based on risk assessment, should be used throughout the food chain and will define the resultant public health risk.

In addition to principal authors listed above, members of the Salmonella on Raw Poultry Writing Committee include Raphael Andreatti Filho, Sao Paulo State University, Sao Paulo, Brazil; Roy Biggs, Tegel Foods Ltd., Auckland, New Zealand; Jeff Buhr, U.S. Department of Agriculture, Agricultural Research Service, Athens, GA, USA; Sarah Cahill, Food and Agriculture Organization of the United Nations, Rome, Italy; John Cason, U.S. Department of Agriculture, Agricultural Research Service, Athens, GA, USA; Thongchai Chalermchaikit, Chulalongkorn Univeristy, Bangkok, Thailand; Hector Hidalgo, University of Chile, Santiago, Chile; Charles Hofacre, University of Georgia, Athens, GA, USA; Henk Hupkes, Meyn Food Processing Technology, B.V., Oostzaan, The Netherlands; Mogens Madsen, Dianova, Aarhus, Denmark; Roel Mulder, Spelderholt Poultry Consulting and Research, Burg, The Netherlands; Lars Plym Forshell, National Food Administration, Uppsala, Sweden; Martha Pulido Landinez, Universidad National de Colombia, Bogota´, Colombia; Jason Richardson, The Coca-Cola Co., Atlanta, GA, USA; Douglas Smith, North Carolina State University, Raleigh, NC, USA; Yvonne Vizzier Thaxton, Mississippi State University, Mississippi State, MS, USA; Hajime Toyofuku, National Institute of Public Health, Japan; Pirkko Tuominen, Finnish Food Safety Authority, Helsinki, Finland; Mieke Uyttendaele, Ghent University, Ghent, Belgium; Sian Ming Shi, Shanghai Jiaotong University, Shanghai, China; and Marcel Zwietering, Wageningen University, Wageningen, The Netherlands.

Infective Dose of Foodborne Pathogens in Volunteers: A Review (Mahendra Kothary) mkothary@cfsan.fda.gov – Division of Virulence Assessment (HFS327) Center for Food Safety and Applied Nutrition, US FDA

“The human infective dose varies depending on the serovar of the organism. Results from the volunteer studies indicated that the infective dose for various serovars was 105 – 1010 organisms. The attack rate depended on the serovar of the organism and ranged from about 16-50%. However, data from outbreaks suggest that infection dose may be as high as 107 – 109 organisms. Various authors of these studies suggested that the high fat and protein content of the food vehicle involved in the outbreaks may have played an important role in protecting the organism from gastric acidity.

http://www.veterinaryworld.org/Vol.6/Oct-2013/1.pdf Salmonella enterica, the most pathogenic species of the genus Salmonella

The differences observed between serovars in their host preference and clinical manifestations are referred to as “serovar-host specificity” or “serovar-host adaptation”. The genus Salmonella, highly adaptive to vertebrate hosts, has many pathogenic serovars showing host specificity

WAITING ON NATE TO HELP ME MAKE THIS SO I CAN COPY AND PASTE IT… MEANWHILE I BROUGHT IT

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869595/pdf/11117946.pdf The current view of salmonella taxonomy assigns the members of this genus to two species: S. enterica and S. bongori. S. enterica itself is divided into six subspecies, enterica, salamae, arizonae, diarizonae, indica, and houtenae, also known as subspecies I, II, IIIa, IIIb, IV, and VI, respectively [1] .

The pathogenicity of most of the distinct serotypes remains undefined, and even within the most common serotypes, many questions remain to be answered regarding the interactions between the organism and the infected host.

Salmonellosis manifests itself in three major forms: enteritis, septicaemia, and abortion, each of which may be present singly or in combination, depending on both the serotype and the host involved. Although currently over 2300 serovars of Salmonella are recognized, only about 50 serotypes are isolated in any significant numbers as human or animal pathogens [2, 3] and they all belong to subspecies enterica

Only a small number of serotypes typically cause severe systemic disease in man or animals, characterized by septicaemia, fever and}or abortion, and such serotypes are often associated with one or few host species [4–6].

Host-adapted serotypes (Table 1) typically cause systemic disease in a limited number of related species. For example, Typhi, Gallinarum and Abortusovis are almost exclusively associated with systemic disease in humans [7], fowl [8] and ovines [5] respectively

In the past, special attention has been dedicated to nutritional requirements and distinct biochemical characters of Salmonella serotypes. In particular, Salmonella strains had been divided in ‘ ammonium weak’ and ‘ ammonium strong’ strains on the basis of their ability to assimilate nitrogen from ammonia in a defined media that contained simple carbon compounds such as citrate (Simmons citrate agar) or other sugars as sole source of carbon and energy [15]

Serotypes noted as ‘ ammonium weak’ were all host-adapted (Dublin, Rostock, and Choleraesuis) or host-restricted (Paratyphi A, Abortusovis, Typhisuis, Typhi, and Sendai) [15]. . It is important to note that a negative result of this test might be due also to the failure of the organism to grow in absence of other substances that were not provided with such minimal media.

Fierer and colleagues have examined the biochemical features of several Dublin strains and found them all unable to grow in Simmons citrate agar [17]. In the presence of supplemental nicotinic acid, however, all strains were able to utilize citrate. Similarly, we found Abortusovis strains able to utilize citrate in a minimal defined medium only when cystine and nicotinic acid were supplemented (Uzzau and colleagues, unpublished results). Detailed analysis of the nutritional requirement of Salmonella spp. has led to the observation that whereas ubiquitous Typhimurium and Enteritidis were able to grow in relatively simple defined media, certain amino acids and vitamins must be supplied for most strains of Typhi, Typhisuis, Abortusovis, Gallinarum, Paratyphi A, and Dublin [18, 19]. Auxotrophy therefore, seems to be a characteristic of HR and HA serotypes (Table 2).

The taxonomic classification of salmonella has been continually revised over the years. Beyond the level of subspecies, serotyping is used for differentiation, and serotypes have been described within S. enterica subspecies enterica on the basis of somatic (O), flagellar (H), and capsular (Vi) antigens [1]. Within subspecies enterica, some serotypes are polyphyletic; identical serotypes occur among isolates of distantly related clones that also differ in pathogenic potential and host range. This can be attributed to horizontal genetic transfer and recombination of antigen genes between lineages, an event that has been proposed to happen with relatively high frequency [22]. However, overall the subspecies remain clonal [23].

Epithelial cell adhesion and invasion may not be uncoupled in Typhi, since all Typhi invasion mutants isolated in recent studies [47, 52] were also adhesion-defective, whereas mutants obtained from UR serotypes like Typhimurium and Enteritidis were found to adhere to cell monolayers but invaded significantly less [53–55].

Other salmonellae which are primarily or exclusively restricted in host range to humans are Paratyphi A and C and Sendai, all of which cause enteric fever. Some strains of Paratyphi B cause human enteric fever, whereas others, designated as Java, produce gastroenteritis in both humans and animals. Miami, which is serologically related to Sendai, is largely limited to humans but causes gastroenteritis rather than enteric fever in animals [24].

Gallinarum as host-restricted since all reported cases of systemic disease are from avian hosts [8].

Typhisuis This serotype does not naturally infect animals other than the pig and, for this reason, is considered host restricted to swine

Choleraesuis This serotype is defined as host-adapted on the basis that 99% of incidents are associated with pigs. However, it does naturally infect other host species, including man, in which the disease can be severe. Human infections were well known for severity with 10–40% case mortality and the majority of isolates were from non-intestinal sites (i.e. blood-stream, bones, joints)

Dublin is host-adapted to bovine and affects both young and adult cattle causing enteritis and}or systemic disease. In humans Dublin infection generally occurs in patients with underlying chronic diseases, and arises from contact with animals or via the food chain.

Immediately following the invasion of the organisms beyond the intestinal mucosa, more than 90% of the organisms are destroyed at, or close to, the site of inoculation, primarily by resident phagocytic cells. Surviving organisms disseminate, and bacterial growth occurs in the cells of the reticuloendothelial system. The crucial phase occurs when bacterial multiplication is either controlled or continues in an uncontrolled fashion. Polymorphonuclear leukocytes (PMN) are the first phagocytic cells to be attracted towards infected tissues by means of salmonella-induced cytokines secretion [147, 148]. PMNs have been recognized for many years as having a function in the inflammatory response, and recently PMNs have also been implicated in the modulation of the other immune cells [149]. Salmonella has adapted to grow inside macrophages where it is relatively sheltered from PMN [150]. Macrophages play a dual role in the salmonella infection process. Once activated, they can kill salmonella, but macrophages are also the site of bacterial multiplication. Infected macrophages are therefore responsible for the dissemination of the Serotypes of S. enterica 239 infection via the lymphatic ducts to other organs [151]

When Salmonella serotypes colonize in the intestinal mucosa of mammals, before progression to a systemic infection in the body, they face to an effective barrier of macrophages that line the lymphatic sinuses of lymph nodes. The granuloma formations caused by the accumulation in inflamed tissue of polynuclear granulocytes in mammals, also exist in avian hosts where it is the heterophiles that are involved, and are morphologically similar to inflammatory lesions in reptiles [160]. Therefore, one of the first steps in the salmonella development towards being a systemic, facultative intracellular pathogen may have been to enter the macrophage in order to escape from the aggressive environment. It is tempting to speculate that it is the ability of HA and HR serotypes to escape cellular defences that has led to the development of host specificity. That pathogens have adopted different tactics to escape immune systems is well known. Immune evasion of virus and helminth parasites related to cytokine activities is beginning to be explored [161], and also bacteria can be supposed to contain and produce a large number of diverse molecules, which can selectively induce the synthesis of cytokines, as LPS does [162]. Unfortunately, little evidence has been accumulated to date with respect to salmonella.

Salmonella serotypes capable of disseminate in a particular host may utilize alveolar macrophages and pulmonary intravascular macrophages (PIM) for translocation [195]. Calves, sheep, goats, and pigs, but not man or small rodents, possess PIM densities and clearance capacity in the lung parenchyma similar to that of human and murine Kupffer cells in the liver [196]. Pigs rooting behaviour and the ovine and bovine grazing allow salmonella in the environment an easy access to the nasal cavity and thus to the lungs. Salmonella serotypes (i.e. Dublin, Abortusovis, Choleraesuis, and Typhimurium) able to produce systemic infection in these animals might have developed specific mechanisms to take advantage of both the intestinal and the pulmonary route of entry and dissemination. It is worth noting that salmonella infection of these hosts is often characterized by pneumonia and that bovine-adapted Dublin may cause pneumonia as a major sign of infection in sheep

In vitro studies have demonstrated that host-specific pathogenesis of Salmonella serotypes may depend on the selective recognition of complement receptor (CR) types on the macrophages membrane [206]. Typhi and Typhimurium induced their own uptake by micropinocytosis in both human and murine macrophages, but only Typhi was capable of growth in human macrophages. Conversely, Typhimurium survived in murine macrophages whereas Typhi did not. The molecular basis of such restriction has been hypothesized based on the fact that intracellular survival and replication is only made possible by recognition, in the presence of serum opsonin, of the CR type 1 (CR1) but not of CR type 3 (CR3). Strikingly, Typhi and Typhimurium recognized, respectively, CR1 and CR3 on human macrophages, whereas they recognized, respectively, CR3 and CR1 on murine macrophages. Baker and Morona have recently observed that phorbol myristate acetate (PMA) differentiated U937 (PMA-U937, human) cells restricted the net growth of Typhi but not Typhimurium phoP mutants, suggesting that the phoP}Q locus may control expression of genes involved in host specificity, particularly affecting differential effects on Typhi and Typhimurium LPS [206].

At least 11 serotypes are known to carry virulence plasmids, which share common and unique sequences [230]. Typhi does not carry virulence plasmids and not all isolates of those serotypes associated with the plasmids do. The role of the virulence plasmid in pathogenesis has been mainly studied using the mouse model of salmonellosis

https://www.fda.gov/food/guidanceregulation/guidancedocumentsregulatoryinformation/salmonella/ucm295271.htm In this document, we use the phrase “adequately reduce” to mean reducing the presence of Salmonella spp. to an extent sufficient to prevent illness. The extent of reduction sufficient to prevent illness is usually determined by the estimated extent to which Salmonella spp. may be present in the food combined with a safety factor to account for uncertainty in that estimate. For example, if it is estimated that there would be no more than 1000 (i.e., 3 logs) Salmonella organisms per gram of food, and a safety factor of 100 (i.e., 2 logs) is employed, a process adequate to reduce Salmonella spp. would be a process capable of reducing Salmonella spp. by 5 logs per gram of food.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145416 Serotype Typhi, for example, is known to exist only in humans, serotype Choleraesuis has a primary reservoir in pigs, and serotype Dublin in cattle 

Serotype IV 48:g,z51:− causes sporadic illness from contact with the environment of a marine iguana, the serotype’s only known host

Counts for serotypes I,4,[5],12:i:− and Typhimurium (including Typhimurium var. 5-) were combined (and labeled Typhimurium+) because not all state laboratories could make the distinction. 

CVs for 37 serotypes examined by state, month, age group, and sex are shown in S1 Table. The serotypes with the most evenly distributed rates across all states and regions were Typhimurium+ (CV 30%), Infantis (CV 40%), and Heidelberg (CV 33%). At the other end of the spectrum, serotypes Mississippi (CV 256%), Rubislaw (CV 197%), and Give (CV 195%) were heavily concentrated in the Gulf Coast states. Other serotypes that showed geographic concentration included Norwich (CV 161%), being reported mostly from the lower Midwest into the South, and Javiana (CV 135%), also most frequently reported from the South.

Serotypes with the largest CVs by month were Norwich (CV 87%), Javiana (CV 83%), Mississippi (CV 69%), and Newport (CV 68%). All were highly concentrated in months that are generally warmer in the US, averaging 45% of reported isolates of these four serotypes (range, 41% to 47%) in summer (June-Aug) and 8% (range, 7% to 11%) in winter (Dec-Feb). Conversely, serotypes Senftenberg, Mbandaka, Anatum, and Derby had low CVs by month (18%, 21%, 24%, and 24% respectively), indicating that isolations occurred fairly evenly throughout the year, with an average of 30% (range, 28% to 31%) of isolates reported in summer and 22% (range, 20% to 26%) in winter.

The variation in incidence rate by age was highest in serotypes Rubislaw (CV 265%), Mississippi (CV 160%), Poona (CV 151%), and Schwarzengrund (CV 150%)—all found mostly in young children. Enteritidis (CV 24%), Berta (CV 40%), and Braenderup (CV 41%) were the serotypes most equally distributed by age. The rate was highest among young children for 34 of the 37 common serotypes; the exceptions were Senftenberg (highest rates among adults aged 70 years and older), Paratyphi A (highest rates among 20- to 34-year-olds), and Tennessee (highest rate among adults aged ≥74 years).

Serotypes with higher variation in incidence by age group (ie, skewed toward particular ages) were more common among males (Spearman’s correlation p <0.01) and had higher incidence variation by state (p <0.01). There was no correlation between variation by age and season (p = 0.13), sex and season (p = 0.74), or sex and region (p = 0.36). Serotypes whose incidence increased the most in the second half of the 16-year study period had higher incidence variation by season (Spearman’s correlation p <0.01) and by state (p = .02). Changes in incidence did not correlate with variation by age or sex.

http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-40.5.317?code=FOPR-site (this document lists a couple of serovars and their direct affiliations with dogs, but they are interspersed and not, therefore, copied here). The magnitude of this reservoir may be considerable; a survey conducted by Galton et at. (4) revealed 27.6% of 8,157 rectal swabs, collected from dogs, were positive for Salmonella. Dogs, on occasion, have been observed to eat carrion and garbage and to practice coprophagy. Therefore, the mechanism for transmission of Salmonella to dogs, and re-infection among dogs, may be present continually.

Dried dog foods were incriminated as the source of Salmonella infections among colonies of laboratory animals as early as 1952. (5)

Bacteriological examination of a portion, approximately 44 g, of commercial dried dog food, obtained January 24, 1976, from a supply at the home of the index case, yielded isolates of S. enteriditis serotypes lnfantis and Minnesota.

Sampling and testing plans for Salmonella, as employed by the Food and Drug Administration (FDA), have been described (9). It would be prudent for the dried dog food industry to consider adopting the FDA sampling recommendation for foods in Category I.

It is abundantly clear that dogs, infected with Salmonella, can provide a link in disease transmission to humans (7). Therefore, manufacturers of dried dog food should be interested in adopting more stringent laboratory testing to provide evidence that their products present a low consumer risk.

As many as nine serotypes were detected in a single sample. These products were allegedly produced by an expansion extrusion process. It is reasonable to SALMONELLAE IN DOG FOOD 321 consider this a critical control point in production of dried dog food; time, temperature, and moisture parameters lend themselves to continual monitoring for quality control. Methods to eliminate the hazard of post-processing contamination, if it exists, might well be investigated. The possibility that dried dog foods may provide a vehicle to introduce Salmonella into the home is not sufficiently recognized by consumers. This investigation has brought forth the following questions: (a) Is it realistic to expect manufacturers to produce Salmonella-free dried dog food? (b) Should the answer to the first question be negative, what degree of hazard does dried dog food present to pets and to their owners? (c) Should pet owners be cautioned about the handling, storage, and potential for abuse of dried dog foods?

The Hardt Lab – Salmonella Pathogenesis, Institute of Microbiology, ETH Zurich – http://www.micro.biol.ethz.ch/research/hardt.html (research Salmonella shedding from humans)

Salmonella Typhimurium diarrhea reveals basic principles of Enteropathogen Infection and disease-promoted DNA exchange: cell host & microbe – https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30119-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2Fs1931312817301191%3Fshowall%2Dtrue

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798295/

Unrelated: http://www.danielvitalis.com/rewild-yourself-podcast/why-im-not-a-vegan-daniel-vitalis-94

Precursors like acetyl acid for liver metabolism evidence that creatures have needed fermentation as part of their diet for long enough to have evolved dependencies on it. Natural sources of fermentation: ruminant gut contents and rotten fruits, etc. Adding certain bacteria can result in sterilization of products under conditions of poor storage. Most grain products come with mycotoxins and mildews and pathogens in them, ready to feed on the sugars and starches the moment they are exposed to enough moisture or warmth. The only cost effective way to add a real safety measure is to either eliminate the starches/sugars, or to add these special bacteria.

L. monocytes is submissive to other bacteria.  Hpp does not kill it but the presence of other bacteria prevent its proliferation

Karen’s interests for sharing: FDA referenced documents that state the relationship of dry kibble and pathogen risk but urge consumers not to use raw, elaboration on studies referenced in first mercola article, no dogs got sick when fed raw meat that was intentionally contaminated with salmonella strains,

FDA commits to disclose retailer information for some food recalls: Petfoodindustry.com https://www.petfoodindustry.com/articles/7516-fda-commits-to-disclose-retailer-info-for-some-food-recalls?utm_source=KnowledgeMarketing&utm_medium=email&utm_content=Pet%20eNews&utm_campaign=18_10_02_PetENews&eid=223857144&bid=2257026

Raw food trials with pets: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003575/#!po=0.431034

http://www.drmasiello.com/2015/04/my-comments-to-the-fda/

http://politicalblindspot.com/former-monsanto-vice-president-running-fda

http://www.dogsnaturallymagazine.com/consumer-pleas-fda-warnings-ignored-by-all-major-retailers/

http://www.mercola.com/downloads/bonus/the-FDA-exposed/default.aspx

http://www.forbes.com/forbes/2011/0214/opinions-steve-forbes-fact-comment-fda-may-kill-millions.html

https://www.google.com/amp/www.undergroundhealth.com/fda-approved-prescription-drugs-kill-hundreds-of-thousands-of-people-annually/amp/

http://www.fdareview.org/05_harm.php

http://mobile.wnd.com/2012/12/how-many-have-died-because-of-the-fda/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709812/

Dulcitol Fermentation Test

ONPG Test for B-galactosidase)

Malonate broth for identification of enteric bacteria

Gelatin hydrolysis test

Sorbitol fermentation test

Growth in KCN

Toward pectin fermentation by Saccharomyces cerevisiae: expression of the first…

Gamma-glytamyl transferase (GGT)

Abnormalities in liver enzyme levels during Salmonella enteritidis enterocolitis

MUG (bata-glucoronidase)test for rapid ID of e.coli

Enzyme characteristics of b-d-glacatosidase and b-d-glucorondiase positive bacteria

Salicin fermentation test

Diagnostic and public health dilemma of lactose-fermenting salmonella enterica

Lysis timing and bacteriophage fitness

Phage lysis: three steps three choices, one outcome

Bacteriophages lytic for Salmonella rapidly reduce Salmonella contamination on gl

Improved lysis efficiency and immunogneticity of Salmonella ghosts mediated by co-…

Beneficial effect of salmonella typhimurium infection and of immunoglobulins from…

Beneficial effects of live and dead salmonella based vector strain on the course…

Salmonella bacteria used to stop viruses

HACCP Validation resource

Compendium of analytical laboratory methods for food and feed safety

Detection of salmonella spp by a loop-mediated isothermal amplification (LAMP)

PmrAB a Two-component regulatory system of pseudomonas aeruginosa that modulates…

Biofilm Formation and Detachment in Gram-Negative Pathogens is Modulated by Select Bile Acids – Laura M Sanchez, Andrw T. Cheng, and Roger G. Linington

CDC Outbreak Variances by Location and Serovar

  1. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145416 Serotype Typhi, for example, is known to exist only in humans, serotype Choleraesuis has a primary reservoir in pigs, and serotype Dublin in cattle 
  2. Serotype IV 48:g,z51:− causes sporadic illness from contact with the environment of a marine iguana, the serotype’s only known host
  3. Counts for serotypes I,4,[5],12:i:− and Typhimurium (including Typhimurium var. 5-) were combined (and labeled Typhimurium+) because not all state laboratories could make the distinction. 
  4. CVs for 37 serotypes examined by state, month, age group, and sex are shown in S1 Table. The serotypes with the most evenly distributed rates across all states and regions were Typhimurium+ (CV 30%), Infantis (CV 40%), and Heidelberg (CV 33%). At the other end of the spectrum, serotypes Mississippi (CV 256%), Rubislaw (CV 197%), and Give (CV 195%) were heavily concentrated in the Gulf Coast states. Other serotypes that showed geographic concentration included Norwich (CV 161%), being reported mostly from the lower Midwest into the South, and Javiana (CV 135%), also most frequently reported from the South.
  5. Serotypes with the largest CVs by month were Norwich (CV 87%), Javiana (CV 83%), Mississippi (CV 69%), and Newport (CV 68%). All were highly concentrated in months that are generally warmer in the US, averaging 45% of reported isolates of these four serotypes (range, 41% to 47%) in summer (June-Aug) and 8% (range, 7% to 11%) in winter (Dec-Feb). Conversely, serotypes Senftenberg, Mbandaka, Anatum, and Derby had low CVs by month (18%, 21%, 24%, and 24% respectively), indicating that isolations occurred fairly evenly throughout the year, with an average of 30% (range, 28% to 31%) of isolates reported in summer and 22% (range, 20% to 26%) in winter.
  6. The variation in incidence rate by age was highest in serotypes Rubislaw (CV 265%), Mississippi (CV 160%), Poona (CV 151%), and Schwarzengrund (CV 150%)—all found mostly in young children. Enteritidis (CV 24%), Berta (CV 40%), and Braenderup (CV 41%) were the serotypes most equally distributed by age. The rate was highest among young children for 34 of the 37 common serotypes; the exceptions were Senftenberg (highest rates among adults aged 70 years and older), Paratyphi A (highest rates among 20- to 34-year-olds), and Tennessee (highest rate among adults aged ≥74 years).
  7. Serotypes with higher variation in incidence by age group (ie, skewed toward particular ages) were more common among males (Spearman’s correlation p <0.01) and had higher incidence variation by state (p <0.01). There was no correlation between variation by age and season (p = 0.13), sex and season (p = 0.74), or sex and region (p = 0.36). Serotypes whose incidence increased the most in the second half of the 16-year study period had higher incidence variation by season (Spearman’s correlation p <0.01) and by state (p = .02). Changes in incidence did not correlate with variation by age or sex.
  8.  
  9. http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-40.5.317?code=FOPR-site (this document lists a couple of serovars and their direct affiliations with dogs, but they are interspersed and not, therefore, copied here). The magnitude of this reservoir may be considerable; a survey conducted by Galton et at. (4) revealed 27.6% of 8,157 rectal swabs, collected from dogs, were positive for Salmonella. Dogs, on occasion, have been observed to eat carrion and garbage and to practice coprophagy. Therefore, the mechanism for transmission of Salmonella to dogs, and re-infection among dogs, may be present continually.
  10. Dried dog foods were incriminated as the source of Salmonella infections among colonies of laboratory animals as early as 1952. (5)
  11. Bacteriological examination of a portion, approximately 44 g, of commercial dried dog food, obtained January 24, 1976, from a supply at the home of the index case, yielded isolates of S. enteriditis serotypes lnfantis and Minnesota.
  12. Sampling and testing plans for Salmonella, as employed by the Food and Drug Administration (FDA), have been described (9). It would be prudent for the dried dog food industry to consider adopting the FDA sampling recommendation for foods in Category I.
  13. It is abundantly clear that dogs, infected with Salmonella, can provide a link in disease transmission to humans (7). Therefore, manufacturers of dried dog food should be interested in adopting more stringent laboratory testing to provide evidence that their products present a low consumer risk.
  14. As many as nine serotypes were detected in a single sample. These products were allegedly produced by an expansion extrusion process. It is reasonable to SALMONELLAE IN DOG FOOD 321 consider this a critical control point in production of dried dog food; time, temperature, and moisture parameters lend themselves to continual monitoring for quality control. Methods to eliminate the hazard of post-processing contamination, if it exists, might well be investigated. The possibility that dried dog foods may provide a vehicle to introduce Salmonella into the home is not sufficiently recognized by consumers. This investigation has brought forth the following questions: (a) Is it realistic to expect manufacturers to produce Salmonella-free dried dog food? (b) Should the answer to the first question be negative, what degree of hazard does dried dog food present to pets and to their owners? (c) Should pet owners be cautioned about the handling, storage, and potential for abuse of dried dog foods?

Recommending against commercially available raw (rather than co-op and grocery) decreases FDA credibility because FDA is tasked with monitoring safety of these products yet they publicly state that they are unsafe to use

Raw food trials with pets: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003575/#!po=0.431034

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5644655/ “Little evidence also exists on the significance of raw meat feeding on the shedding of CampylobacterSalmonella, and enteropathogenic Yersinia in the feces of pets.”

Results (3): Enteric pathogens were detected in 28% of the RMBDs, originating from 12 producers… Salmonella was detected in only 2% of the samples…”

Discussion (4): Salmonella was rarely detected in our study and the occurrence (2% by PCR and <1% by culturing) was clearly lower than reported in Canada and USA.

Conclusions (5): These pathogens were not found by culturing, indicating a low contamination level in frozen commercial RMBDs produced in Finland. Salmonella and enteropathoenic Yersinia were detected only in dogs fed RMBDs: however, the infection source and transmission routes remained unclear.

The Hardt Lab – Salmonella Pathogenesis, Institute of Microbiology, ETH Zurich – http://www.micro.biol.ethz.ch/research/hardt.html (research Salmonella shedding from humans)

Salmonella Serovars and Effects of Anatomy

Salmonella enterica: survival, colonization, and virulence differences among serovars: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310208/

Only 1% of the inoculum survives the low pH during the passage through the stomach. The surviving bacteria then reach the small intestine, which contains bacteriacidal compounds, such as bile salts. About 80% of the bacteria that survive the passage through the stomach are passed with the faeces within 6-10 hours post-infection, About 15% remain localized in the lumen of the caecum and large intestines, and only 5% manage to penetrate the intestinal wall of the small intestine and reach the GALT (Gut associated lymphatic tissue).

An important factor that impedes colonization by salmonella serovars is the normal gut flora. Disruption in the endogenous flora by streptomycin treatment results in a 100,000 fold reduction in the 50% implantation dose. The phenomenon of the endogenous flora being able to prevent colonization by exogenous bacteria is known as bacterial interference. Some of these things are production of inhibitory substances, competition for tissue adhesion sites, and limiting resources.

Peyers patches serve as the main port of entry for Salmonella serovars.

Intestinal perforations at areas of Peyer’s patches are the most frequent cause of death during typhoid fever. (Pg 59)

As the host mounts an inflammatory response at the site of mucosal invasion, Salmonella genes involved in defense against inflammation have to be expressed subsequently to bacterial entry into the epithelium. Coordinated expression of these virulence genes appears to be mediated by PhoPQ, a two-component regulatory system that changes gene expression in response to changes in the external Mg2+ and Ca2+ concentrations. Ca2+ and Mg2+ cations stabilize the outer membrane by neutralizing the negative charge of phosphate groups and bridging adjacent LPS molecules. The intracellular parasitophorous vacuole in which salmonella resides was shown to be low in Mg2+ and Ca2+. In such environments, PhoPQ activates pmrAB, two genes encoding a second two-component regulatory system. Activation of PmrAB increases the substitution of phosphates in both the core oligosaccharide and the lipid A part of the LPS with 4-amino-4-deoxy-L-arabinose, thereby compensating for the lack of Ca2+ and Mg2+ cations. These structural changes in LPS result in increased resistance to bacteriacidal/permeability increasing protein (BPIs), a cationic antibacterial protein that is released by human PMN during inflammation. Furthermore, in response to low Mg2+ and Ca2+ concentrations, PhoPQ activates a second pmrAB-independent pathway, which results in increased resistance to defensins released by recruited PMN and crypdins produced by Paneth cells located in the intestinal crypts. (pg 63)

The major factor for intestinal penetration is encoded by genes that are clustered in a large area (40kb) on the chromosome designated Salmonella pathogenicity island 1 (SPI1) (pg 61) Studies using murine ligated ileal loops revealed that the genes located on SPI1 are necessary for invasion of M cells in the FAE (follicle associated epithelium) of Peyer’s Patches.

Symptoms associated with Salmonella were markedly decreased by treatment with nitrogen mustard, an agent that depletes the polymorphonuclear neutrophil (PMN)… which also inhibits fluid secretion induced by cholera toxin) (pg 62)

In 1958 it was discovered that Salmonella’s ability to agglutinate certain species of erythrocytes and its association between fimbriae and erythrocytes included mannose-containing carbohydrates in lectin-based interactions (pg 35)

Salmonella Typhimurium diarrhea reveals basic principles of Enteropathogen Infection and disease-promoted DNA exchange: cell host & microbe – https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30119-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2Fs1931312817301191%3Fshowall%2Dtrue

Cytokines play a critical role in the protection mediated by the immune system. They regulate whether a predominately humoral or cell-mediated response will be mounted . Besides modulating the type and intensity of an immune response, these protein signals can also alter the response, these protein signals can also alter the activity of the effector cells. In mice, IFN-y was shown to activate macrophages resulting in increased killing capacity of the cells for a variety of microbials pathogens. Incubation of the macrophages with recombinant IFN-y enhanced their activity against s. typhimurium and mice administered exogenous IFN-y exhibited reduced disseminated infection by that organism. Similar protection against salmonella infection was observed in mice receiving tumour necrosis factor alpha (TNF-a) an inflammatory cytokine, or IL-12 (pg 77)

Calves could be protected from lethal salmonella challenge when fed colostrum from salmonella infected cows although this protection could not be correlated with serum antibodies to flagellar or somatic antigens (pg 76)

The predominant immunoglobin of mucosal immunity is IgA although IgG and/or IgM responses can also be observed. IgA has been shown to mediate protection against infection through anti-body dependent cellular cytotoxicity, potentiate bacteriacidal action by iron-sequestering compounds, serve as a possible opsonin for mucosal phagotyes, inhibit bacterial adherence, and neutralize toxin moieties. Secretory IgA therefore exhibits exceptional diversity in its ability to mediate protection at mucosal surfaces. (pg76)

In order to compete effectively with other microorganisms in the anaerobic, nutritionally sparse conditions of the gut, Salmonella needs to  be able to take up limited nutrients effectively and to adapt to rapidly changing conditions. Bile sales, fatty acids and glycerides all have detergent-like actions. The intestinal lumen is replete with proteases and lipases, and these must be prevented from gaining access to the vicinity of the cytoplasmic membrane where they will cause damage to the membrane structures. (pg 21)

Bile formation and detachment in gram-negative pathogens is modulated by select bile acids – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798295/

Methods of Testing of Pathogens

  1. The FDA CVM cultures raw pet food samples in an enrichment broth which selects and enhances the growth of pathogens like Salmonella, while selectively killing microorganisms that would naturally compete with the pathogen and prevent its propagation.  The broth is then incubated for anywhere from 16 hours to 5 days, at up to 115.2⁰F (this is a very wide range for a scientific analysis).  Scientists are unable to differentiate live cells from dead cells.  Therefore, it’s likely that samples with large amounts of dead cells would still result in a “false positive” for pathogens. (44) FDA guidance advises, “you are cautioned that significant deviations between actual microbiological data in specific products and the predictions do occur.” (45) “Time and Temperature abuse at one step alone might not result in an unsafe product. However…abuse that occurs at successive processing steps (including storage steps) might be sufficient to result in unsafe levels of pathogenic bacteria or toxins.” The document also states that pathogens are only likely to grow in raw food products where “(pathogenic) growth is not prevented by a condition of the food” (such as fermentation, ozone, essential oils, naturally occurring competitive bacteria, freezing/refrigeration, etc). FDA acknowledges that “the preventative measures that can be applied for pathogenic bacteria growth and toxin formation due to time and temperature abuse include 1) refrigeration of the product and controlling refrigeration temperatures 2) proper icing of the product 3) controlling the amount of time that the product is exposed to temperatures that would permit pathogenic bacteria growth or toxin production 4) rapid cooling of the product.” Ultimately, they acknowledge that under normal handling conditions, raw foods are not likely to accumulate pathogens. They also admit that “pathogenic bacteria also could be introduced during processing, even after cooking. However, in most cases it is not reasonable to assume that they will fully prevent the introduction of pathogenic bacteria.” (45)(46) This indicates that they are fully aware that even cooked kibble and sterilized products can harbor high levels of pathogens.

Dulcitol Fermentation Test – http://www.vumicro.com/vumie/help/VUMICRO/Dulcitol_Fermentation_Test.htm

ONPG Test (for ?-galactosidase): Principle, procedure and results: https://microbeonline.com/onpg-test-%CE%B2-galactosidase-principle-procedure-results/

Malonate Broth for the identification of enteric bacteria – https://catalog.hardydiagnostics.com/cp_prod/content/hugo/malonatebroth.htm

Gelatin Hydrolysis Test: Principle, Procedure and expected results – https://microbeonline.com/gelatin-hydrolysis-test-principle-procedure-expected-results/

Sorbitol Fermentation Test – http://www.vumicro.com/vumie/help/VUMICRO/Sorbitol_Fermentation_Test.htm

Growth in KCN – http://www.vumicro.com/vumie/help/VUMICRO/KCN_Growth_Test.htm

Toward pectin fermentation by Saccharomyces cerevisiae: expression of the first two steps of a bacterial pathway for D-galacturonate metabolism – PubMed – NCBI – https://www.ncbi.nlm.nih.gov/pubmed/23079077

Gamma-Glutamyl Transferase (GGT) – Understand the Test & Your Results – https://labtestsonline.org/tests/gamma-glutamyl-transferase-ggt

Abnormalities in liver enzyme levels during Salmonella enteritidis enterocolitis. PubMed – NCBI – https://www.ncbi.nlm.nih.gov/pubmed/15449987

MUG (beta-Glucoronidase) test for rapid identification of e.coli – https://microbeonline.com/mug-test-b-glucuronidase-test-for-rapid-identification-of-e-coli/

Enzyme Characteristics of ?-d-Galactosidase- and ?-Glucoronidase – Positive Bacteria and Their Interference in Rapid Methods for Detection of Waterborne Coliforms and Escherichia coli – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106360/

Salicin Fermentation Test – http://www.vumicro.com/vumie/help/VUMICRO/Salicin_Fermentation_Test.htm

Mucate Broth – http://www.himedialabs.com/TD/M1226.pdf

The galacturonate TRAP Transporter GaaPQM of Agrobacterium tumefaciens and its involvement in virulence gene expression – https://aem.asm.org/content/early/2015/12/03/AEM.02891-15 

Malonate Inhibition of Oxidation in the Krebs Tricarboxylic Acid Cycle – http://www.jbc.org/content/178/1/241.full.pdf

Utilization of d-tartaric acid by Salmonella paratyphi B and Salmonella java: comparison of anaerobic plate test, lead acetate test and turbitidy test – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129498/

Diagnostic and Public Health Dilemma of Lactose-Fermenting Salmonella enterica Serotype Typhimurium in Cattle in the Northeastern United States – https://www.ncbi.nlm.nih.gov/pubmed/10699026

Lysis Timing and Bacteriophage Fitness – https://www.ncbi.nlm.nih.gov/pubmed/16219778

Phage lysis: three steps, three choices, one outcome – PubMed – NCBI – https://www.ncbi.nlm.nih.gov/pubmed/24585055

Bacteriophages lytic for Salmonella rapidly reduce Salmonella contamination on glass and stainless steel surfaces – https://www.ncbi.nlm.nih.gov/pubmed/24228226

Improved lysis efficiency and immunogenicity of Salmonella ghosts mediated by co-expression of phage – https://www.nature.com/articles/srep45139

Beneficial effect of Salmonella typhimurium infection and of immmunoglobulins from S. typhimurium-infected mice on the autoimmune disease of (NZB x NZW) F1 Mice – https://www.ncbi.nlm.nih.gov/pubmed/8625513

Beneficial effects of live and dead Salmonella-based vector strain on the course of colitis in mice – https://www.ncbi.nlm.nih.gov/pubmed/8625513

Salmonella bacteria used to stop viruses – https://newatlas.com/salmonella-bacteria-used-to-stop-viruses/17827/

HACCP Validation Resources – https://www.fsis.usda.gov/wps/portal/fsis/topics/regulatory-compliance/haccp/resources-and-information/haccp-validation/haccp-validation-resources

Methods to Reduce/ Eliminate Pathogens from Fresh and Fresh-Cut Produce – https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1541-4337.2003.tb00033.x

Department of Agriculture Pathogen Reduction: HACCP Systems Final Rule, Part II – https://www.fsis.usda.gov/wps/wcm/connect/e113b15a-837c-46af-8303-73f7c11fb666/93-016F.pdf?MOD=AJPERES

Compendium of analytical laboratory methods for food and feed safety

Detection of salmonella spp by a loop-mediated isothermal amplification (LAMP)

PmrAB a Two-component regulatory system of pseudomonas aeruginosa that modulates…

Biofilm Formation and Detachment in Gram-Negative Pathogens is Modulated by Select Bile Acids – Laura M Sanchez, Andrw T. Cheng, and Roger G. Lining

Specialists on “Salmonella on Raw Poultry Writing Committee”

In addition to principal authors listed above, members of the Salmonella on Raw Poultry Writing Committee include

Raphael Andreatti Filho, Sao Paulo State University,

Sao Paulo, Brazil;

Roy Biggs, Tegel Foods Ltd., Auckland, New Zealand;

Jeff Buhr, U.S. Department of Agriculture, Agricultural Research Service, Athens, GA, USA;

Sarah Cahill, Food and Agriculture Organization of the United Nations, Rome, Italy;

John Cason, U.S. Department of Agriculture, Agricultural Research Service, Athens, GA, USA;

Thongchai Chalermchaikit, Chulalongkorn Univeristy, Bangkok, Thailand;

Hector Hidalgo, University of Chile, Santiago, Chile;

Charles Hofacre, University of Georgia, Athens, GA, USA;

Henk Hupkes, Meyn Food Processing Technology, B.V., Oostzaan, The Netherlands; Mogens Madsen, Dianova, Aarhus, Denmark;

Roel Mulder, Spelderholt Poultry Consulting and Research, Burg, The Netherlands;

Lars Plym Forshell, National Food Administration, Uppsala, Sweden;

Martha Pulido Landinez, Universidad National de Colombia, Bogota´, Colombia; Jason Richardson, The Coca-Cola Co., Atlanta, GA, USA;

Douglas Smith, North Carolina State University, Raleigh, NC, USA;

Yvonne Vizzier Thaxton, Mississippi State University, Mississippi State, MS, USA;

Hajime Toyofuku, National Institute of Public Health, Japan;

Pirkko Tuominen, Finnish Food Safety Authority, Helsinki, Finland;

Mieke Uyttendaele, Ghent University, Ghent, Belgium;

Sian Ming Shi, Shanghai Jiaotong University, Shanghai, China; and

Marcel Zwietering, Wageningen University, Wageningen, The Netherlands.

Regulatory Contacts

SenateRepresentativeDist.CountiesPty.Occupation   TelephoneE-mail
Acree, Cindy 40ArapahoeRBusiness Woman/Legislator   Cap: 303-866-2944
SenatorsElbertE-mail: cindy.acree.house@state.co.us  cindy.acree.house@state.co.us  
Member of Health and Human Services; Member of Local Government; Member of Joint Health and Human Services; Member of Joint Local Government
Apuan, Dennis 17El PasoDLegislator   Cap: 303-866-3069
E-mail: repdennisapuan@gmail.comrepdennisapuan@gmail.com 
Member of Health and Human Services; Member of Local Government; Member of Joint Health and Human Services; Member of Joint Local Government
Bacon, Bob 14LarimerDLegislator / Teacher (Retired)   Cap: 303-866-4841
(Wife: Bev)E-mail: bob.bacon.senate@state.co.usbob.bacon.senate@state.co.us 
Member of Appropriations; Chair of Education; Vice-Chair of State, Veterans & Military Affairs; Member of Joint State Veterans & Military Affairs Committee; Vice-Chair of Joint Education; Chair of Capital Development
Balmer, David G39ArapahoeR    Cap: 303-866-2935
(Wife: Karen)E-mail: david.balmer.house@state.co.usdavid.balmer.house@state.co.us 
Assistant Minority Leader; Member of Joint Business Affairs & Labor; Member of Business Affairs and Labor; Member of Legislative Council
Baumgardner, Randy 57GarfieldRRancher   Cap: 303-866-2949
(Wife: Lori)GrandE-mail: randy.baumgardner.house@state.co.usrandy.baumgardner.house@state.co.us 
 Jackson 
 Moffat 
 Rio Blanco 
 Routt 
Member of Transportation & Energy; Member of Joint Transportation; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Agriculture and Natural Resources
Benefield, Debbie 29JeffersonDLegislator   Cap: 303-866-2950
E-mail: debbie@debbiebenefield.orgdebbie@debbiebenefield.org 
Member of Education; Vice-Chair of Finance; Chair of House Services; Member of Joint Finance; Member of Joint Education
Boyd, Betty 21JeffersonDFormer Nonprofit Manager   Cap: 303-866-4857
(Husband: Douglas)E-mail: betty.boyd.senate@state.co.usbetty.boyd.senate@state.co.us 
President Pro Tempore; Chair of Health and Human Services; Member of State, Veterans & Military Affairs; Vice-Chair of Joint Health and Human Services; Member of Joint State Veterans & Military Affairs Committee; Member of Legislative Council
Bradford, Laura 55MesaRBusiness Owner   Cap: 303-866-2583
E-mail: laurabradford55@gmail.comlaurabradford55@gmail.com 
Member of Local Government; Member of Joint Business Affairs & Labor; Member of Joint Local Government; Member of Business Affairs and Labor
Brophy, Greg 1CheyenneRFarmer   Cap: 303-866-6360
(Wife: Angela)ElbertE-mail: greg@gregbrophy.netgreg@gregbrophy.net 
 Kiowa 
 Kit Carson 
 Lincoln 
 Logan 
 Morgan 
 Phillips 
 Prowers 
 Sedgwick 
 Washington 
 Yuma 
Assistant Minority Leader; Member of Finance; Member of Joint Finance; Member of Legal Services; Member of Agriculture and Natural Resources; Member of Joint Agriculture and Natural Resources
Cadman, Bill 10El PasoRBusiness Owner / Marketing   Cap: 303-866-2737
(Wife: Lisa)E-mail: bill.cadman.senate@state.co.usbill.cadman.senate@state.co.us 
Minority Caucus Chair; Member of Local Government and Energy; Member of State, Veterans & Military Affairs; Member of Joint Local Government; Member of Joint State Veterans & Military Affairs Committee; Member of Legislative Council
Carroll, Morgan 29ArapahoeDAttorney/Small Business Owner   Cap: 303-866-4879
E-mail: morgan.carroll.senate@state.co.usmorgan.carroll.senate@state.co.us 
Member of Health and Human Services; Chair of Judiciary; Member of Joint Health and Human Services; Vice-Chair of Joint Judiciary; Member of Legal Services; Member of Legislative Audit
Casso, Edward 32AdamsDLegislator   Cap: 303-866-2964
E-mail: edward.casso.house@state.co.usedward.casso.house@state.co.us 
Member of State, Veterans, & Military Affairs; Member of Joint Business Affairs & Labor; Member of Joint State Veterans & Military Affairs Committee; Member of Business Affairs and Labor
Court, Lois 6ArapahoeDCommunity College Instructor/Legislator   Cap: 303-866-2967
(Husband: Patrick Reynolds)DenverE-mail: loiscourt@msn.comloiscourt@msn.com 
Member of State, Veterans, & Military Affairs; Member of House Services; Member of Joint Judiciary; Member of Joint State Veterans & Military Affairs Committee; Member of Judiciary
Curry, Kathleen E61EagleULegislator   Cap: 303-866-2945
(Husband: Gregory Peterson)GarfieldE-mail: repcurry@gmail.comrepcurry@gmail.com 
 Gunnison 
 Hinsdale 
 Pitkin 
Member of Agriculture, Livestock, & Natural Resources
DelGrosso, Brian 51LarimerRSmall Business Owner   Cap: 303-866-2947
(Wife: Amber)E-mail: brian@briandelgrosso.combrian@briandelgrosso.com 
Member of Finance; Member of State, Veterans, & Military Affairs; Member of Joint Finance; Member of Joint State Veterans & Military Affairs Committee
Ferrandino, Mark 2DenverDLegislator   Cap: 303-866-2911
(Husband: Greg Wertsch)E-mail: mferrandino@yahoo.commferrandino@yahoo.com 
Vice-Chair of Appropriations; Chair of Joint Budget Committee; Member of Legislative Council
Fischer, Randy 53LarimerDConsulting Engineer   Cap: 303-866-2917
(Wife: Kathryn)E-mail: randyfischer@frii.comrandyfischer@frii.com 
Deputy Majority Whip; Member of Transportation & Energy; Member of Joint Transportation; Chair of Agriculture, Livestock, & Natural Resources; Member of Appropriations; Chair of Joint Agriculture and Natural Resources
Foster, Joyce 35ArapahoeDColorado State Senator   Cap: 303-866-4875
(Husband: Steven)DenverE-mail: joyce.foster.senate@state.co.usjoyce.foster.senate@state.co.us 
Member of Business, Labor and Technology; Vice-Chair of Local Government and Energy; Member of Joint Business Affairs & Labor; Member of Joint Local Government
Frangas, K.Jerry 4DenverDLegislator   Cap: 303-866-2954
(Wife: Gregoria)E-mail: kjerryfrangas@earthlink.netkjerryfrangas@earthlink.net 
Member of Finance; Vice-Chair of Transportation & Energy; Member of Joint Finance; Member of Joint Transportation
Gagliardi, Sara 27JeffersonDLPN   Cap: 303-866-2962
(Husband: Jack)E-mail: sara.gagliardi.house@state.co.ussara.gagliardi.house@state.co.us 
Vice-Chair of Health and Human Services; Member of Joint Business Affairs & Labor; Member of Joint Health and Human Services; Vice-Chair of Business Affairs and Labor
Gardner, Bob 21El PasoRAttorney   Cap: 303-866-2191
FremontE-mail: bob.gardner.house@state.co.usbob.gardner.house@state.co.us
Member of Joint Judiciary; Member of Legal Services; Member of Judiciary; Member of Appropriations 
Gardner, Cory 63AdamsRFarm Equipment Dealership/Attorney   Cap: 303-866-2906
(Wife: Jaime)CheyenneE-mail: gardner@plains.netgardner@plains.net 
 Crowley 
 Kiowa 
 Kit Carson 
 Lincoln 
 Morgan 
 Washington 
 Yuma 
Minority Whip; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Agriculture and Natural Resources
Gerou, Cheri 25JeffersonRArchitect   Cap: 303-866-2582
(Husband: Phil)E-mail: cheri.gerou@gmail.comcheri.gerou@gmail.com 
Member of Finance; Member of Health and Human Services; Member of Joint Finance; Member of Joint Health and Human Services; Member of Joint Budget Committee
Gibbs, Dan 16BoulderDWildland Fire Fighter   Cap: 303-866-4873
Clear CreekE-mail: dan.gibbs.senate@state.co.usdan.gibbs.senate@state.co.us 
Gilpin 
Grand 
Jefferson 
Summit 
Chair of Transportation; Vice-Chair of Joint Transportation; Member of Agriculture and Natural Resources; Member of Joint Agriculture and Natural Resources; Member of Legislative Council
Giron, Angela 3PuebloDLegislator   Cap: 303-866-4878
(Husband: Steve)E-mail: angela.giron.senate@state.co.usangela.giron.senate@state.co.us 
Guzman, Lucia 34DenverDExecutive Director of the Agency for Human Rights City and County of Denver   Cap: 303-866-4862
E-mail: lucia.guzman.senate@state.co.us
Harvey, Ted 30DouglasR    Cap: 303-866-4881
(Wife: Janie)E-mail: ted.harvey.senate@state.co.us
Member of Appropriations; Member of Business, Labor and Technology; Member of Joint Business Affairs & Labor; Member of Agriculture and Natural Resources; Member of Joint Agriculture and Natural Resources
Heath, Rollie 18BoulderDState Senator   Cap: 303-866-4872
(Wife: Josie)E-mail: rollie.heath.senate@state.co.us
Member of Appropriations; Member of Education; Chair of State, Veterans & Military Affairs; Vice-Chair of Joint State Veterans & Military Affairs Committee; Member of Joint Education
Hodge, Mary 25AdamsDProperty Management   Cap: 303-866-4855
(Husband: Richard)E-mail: mary.hodge.senate@state.co.us
Member of Appropriations; Member of Local Government and Energy; Member of Joint Local Government; Member of Joint Budget Committee; Member of Legislative Council
Hudak, Evie 19JeffersonDEducator   Cap: 303-866-4840
(Husband: Edward)E-mail: senatorhudak@gmail.com
Vice-Chair of Education; Member of Finance; Member of Judiciary; Member of Joint Finance; Member of Joint Judiciary; Member of Joint Education
Hullinghorst, Dickey Lee10BoulderDRetired Gov. Affairs   Cap: 303-866-2915
(Husband: Bob)E-mail: dl.hullinghorst.house@state.co.us
Member of State, Veterans, & Military Affairs; Member of Joint State Veterans & Military Affairs Committee; Member of Agriculture, Livestock, & Natural Resources; Member of Appropriations; Member of Joint Budget Committee; Member of Joint Agriculture and Natural Resources
Johnston, Michael 33AdamsDSchool Principal   Cap: 303-866-4864
(Wife: Courtney)DenverE-mail: mike.johnston.senate@state.co.us
Member of Business, Labor and Technology; Member of Education; Vice-Chair of Finance; Member of Joint Business Affairs & Labor; Member of Joint Finance; Member of Joint Education
Judd, Joel 5DenverDLawyer   Cap: 303-866-2925
E-mail: repjoeljudd@joeljudd.com
Chair of Finance; Chair of Joint Finance; Member of Appropriations
Kagan, Daniel 3ArapahoeDAttorney   Cap: 303-866-2921
(Wife: Faye)DenverE-mail: repkagan@gmail.com
Member of Finance; Member of Joint Finance; Member of Joint Judiciary; Member of Legal Services; Member of Judiciary
Kefalas, John 52LarimerDLegislator   Cap: 303-866-4569
(Wife: Elizabeth Helmers)E-mail: john.kefalas.house@state.co.us
Member of Finance; Member of Health and Human Services; Member of Joint Finance; Member of Joint Health and Human Services; Member of Appropriations
Keller, Maryanne “Moe”20JeffersonDTeacher of the Deaf (retired)   Cap: 303-866-2585
(Husband: Stephen)E-mail: moe.keller.senate@state.co.us
Member of Appropriations; Vice-Chair of Joint Budget Committee
Kerr, Andrew “Andy”26JeffersonDEducator   Cap: 303-866-2923
(Wife: Tammy)E-mail: andy.kerr.house@state.co.us
Assistant Majority Leader; Member of Joint Business Affairs & Labor; Member of Business Affairs and Labor; Member of Legislative Council
Kerr, James E “Jim”28JeffersonRLegislator   Cap: 303-866-2939
(Wife: Patsy)E-mail: james.kerr.house@state.co.us
Member of Health and Human Services; Member of Joint Health and Human Services; Member of Appropriations; Member of Legislative Audit
Kester, Ken 2BacaRBusinessman / Legislator   Cap: 303-866-4877
BentE-mail: electkenkester@hotmail.com
Crowley 
Custer 
Fremont 
Huerfano 
Las Animas 
Otero 
Pueblo 
Member of Local Government and Energy; Member of Joint Local Government; Member of Agriculture and Natural Resources; Member of Joint Agriculture and Natural Resources
King, Keith 12El PasoRAdministrator – Colorado Springs Early Colleges   Cap: 303-866-4880
(Wife: Sandra)E-mail: keith@keithking.org
Member of Appropriations; Member of Education; Member of Finance; Member of Judiciary; Member of Joint Finance; Member of Joint Judiciary; Member of Joint Education
King, Steve 54DeltaRViolent Crime Investigator   Cap: 303-866-3068
(Wife: Daun Marie)MesaE-mail: steve.king.house@state.co.us
Member of Transportation & Energy; Member of Joint Judiciary; Member of Joint Transportation; Member of Judiciary
Kopp, Mike 22JeffersonRManagement   Cap: 303-866-4859
(Wife: Kimberly)E-mail: mike.kopp.senate@state.co.us
Minority Leader; Member of Appropriations; Member of Transportation; Member of Joint Transportation; Member of Executive Committee of the Legislative Council; Member of Legislative Council
Labuda, Jeanne 1ArapahoeDAttorney   Cap: 303-866-2966
(Husband: Michael Taber)DenverE-mail: replabuda@yahoo.com
 Jefferson 
Member of Finance; Vice-Chair of State, Veterans, & Military Affairs; Member of Joint Finance; Member of Joint State Veterans & Military Affairs Committee; Chair of Legal Services
Lambert, Kent D14El PasoRColonel USAF (Ret)   Cap: 303-866-2937
(Wife: Gretchen A.)E-mail: rep.kent.lambert@comcast.net
Member of Appropriations
Levy, Claire 13BoulderDAttorney   Cap: 303-866-2578
(Husband: David Driscoll)Clear CreekE-mail: claire.levy.house@state.co.us
 Gilpin 
Chair of Joint Judiciary; Member of Legal Services; Chair of Judiciary
Liston, Larry G16El PasoRFinancial Consultant   Cap: 303-866-2965
(Wife: Mary Ann)E-mail: larry.liston.house@state.co.us
Member of Local Government; Member of Joint Business Affairs & Labor; Member of Joint Local Government; Member of Business Affairs and Labor
Looper, Marsha 19El PasoRSmall Business Owner & Rancher   Cap: 303-866-2946
(Husband: Lynn)E-mail: marshalooper@gmail.com
Member of Transportation & Energy; Member of Joint Transportation; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Agriculture and Natural Resources
Lundberg, Kevin 15LarimerR    Cap: 303-866-4853
(Wife: Sandy)E-mail: kevin@kevinlundberg.com
Member of Health and Human Services; Member of Judiciary; Member of Local Government and Energy; Member of Joint Health and Human Services; Member of Joint Judiciary; Member of Joint Local Government
Massey, Tom 60ChaffeeRRealtor/Broker   Cap: 303-866-2747
(Wife: Becky)CusterE-mail: tom.massey.house@state.co.us
 Fremont 
 Park 
 Pueblo 
 Saguache 
Member of Education; Member of Local Government; Member of House Services; Member of Joint Local Government; Member of Joint Education
May, Mike 44DouglasRHumble Innkeeper   Cap: 303-866-5523
(Wife: Traci)E-mail: mike.may.house@state.co.us
Minority Leader; Member of Executive Committee of the Legislative Council; Member of Legislative Council
McCann, Elizabeth “Beth”8DenverDLegislator   Cap: 303-866-2959
(Husband: Christopher Linsmayer)E-mail: beth.mccann.house@state.co.us
Member of State, Veterans, & Military Affairs; Member of Joint Judiciary; Member of Joint State Veterans & Military Affairs Committee; Vice-Chair of Judiciary
McFadyen, Liane “Buffie”47FremontDMother/Self Employed   Cap: 303-866-2905
PuebloE-mail: mcfadyen2002@hotmail.com
Speaker Pro Tempore; Chair of Transportation & Energy; Chair of Joint Transportation
McKinley, Wes 64BacaDCowboy   Cap: 303-866-2398
(Wife: Janice)BentE-mail: wes.mckinley.house@state.co.us
 Huerfano 
 Las Animas 
 Otero 
 Prowers 
Member of Local Government; Member of Joint Local Government; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Agriculture and Natural Resources
McNulty, Frank 43DouglasRAttorney Cap: 303-866-2936
Member of Education; Member of Transportation & Energy; Member of Joint Transportation; Member of Joint Education; Member of Legislative Audit; Member of Legislative Council
Merrifield, Michael18El PasoDRetired Teacher   Cap: 303-866-2932
E-mail: michael.merrifield.house@state.co.us
Chair of Education; Member of Transportation & Energy; Member of Joint Transportation; Chair of Joint Education
Middleton, Karen 42ArapahoeD    Cap: 303-866-3911
(Husband: Larry Beer)E-mail: repmiddleton@gmail.com
Majority Caucus Chair; Member of Education; Member of Joint Business Affairs & Labor; Member of Business Affairs and Labor; Member of Joint Education
Miklosi, Joe 9DenverDNon profit Management   Cap: 303-866-2910
(Wife: Jennifer)ArapahoeE-mail: joe@joemiklosi.com
Member of State, Veterans, & Military Affairs; Member of Joint Judiciary; Member of Joint State Veterans & Military Affairs Committee; Member of Judiciary; Member of Legislative Audit
Mitchell, Shawn 23AdamsRAttorney   Cap: 303-866-4876
(Wife: Yvette)BroomfieldE-mail: shawnmitch@aol.com
 Weld 
Member of Business, Labor and Technology; Member of Health and Human Services; Member of Joint Business Affairs & Labor; Member of Joint Health and Human Services; Member of Legal Services; Member of Legislative Audit
Morse, John P.11El PasoDExecutive   Cap: 303-866-6364
E-mail: john.morse.senate@state.co.us
Majority Leader; Vice-Chair of Senate Services; Vice-Chair of Legal Services; Member of Executive Committee of the Legislative Council; Member of Legislative Council
Murray, Carole 45DouglasRRetired   Cap: 303-866-2948
TellerE-mail: murrayhouse45@gmail.com
Member of Education; Member of State, Veterans, & Military Affairs; Member of Joint State Veterans & Military Affairs Committee; Member of Joint Education
Newell, Linda 26ArapahoeDBusiness Consultant   Cap: 303-866-4846
JeffersonE-mail: linda.newell.senate@gmail.com
Vice-Chair of Health and Human Services; Member of Judiciary; Member of Local Government and Energy; Member of Joint Health and Human Services; Member of Joint Judiciary; Member of Joint Local Government
Nikkel, B.J. 49LarimerRLegislator   Cap: 303-866-2907
(Husband: Philip)WeldE-mail: rep.nikkel@gmail.com
Member of State, Veterans, & Military Affairs; Member of Joint Judiciary; Member of Joint State Veterans & Military Affairs Committee; Member of Judiciary
Pace, Sal 46PuebloDProfessor   Cap: 303-866-2968
(Wife: Marlene Valdez Pace)E-mail: sal.pace.house@state.co.us
Assist. Majority Caucus Chair; Member of Joint Judiciary; Vice-Chair of Agriculture, Livestock, & Natural Resources; Member of Judiciary; Member of Appropriations; Member of Joint Agriculture and Natural Resources
Peniston, Cherylin 35AdamsDRetired Teacher   Cap: 303-866-2843
(Husband: W.J.)E-mail: cherylin.peniston.house@state.co.us
Member of Education; Chair of Local Government; Chair of Joint Local Government; Member of Joint Education
Penry, Joshua 7GarfieldRBusiness Development   Cap: 303-866-3077
(Wife: Jamie)MesaE-mail: joshpenry@gmail.com
Pommer, Jack 11BoulderDTV/ Video Producer   Cap: 303-866-2780
(Wife: Jane)E-mail: jack.pommer.house@state.co.us
Chair of Appropriations
Primavera, Dianne 33AdamsD    Cap: 303-866-4667
BoulderE-mail: dianne.primavera.house@state.co.us
Broomfield 
Weld 
Member of Health and Human Services; Member of Transportation & Energy; Member of Joint Health and Human Services; Member of Joint Transportation; Member of Legislative Audit
Priola, Kevin 30AdamsRSmall Business Owner   Cap: 303-866-2912
(Wife: Michelle)E-mail: kpriola@gmail.com
Member of Local Government; Member of Joint Business Affairs & Labor; Member of Joint Local Government; Member of Business Affairs and Labor
Renfroe, Scott W.13WeldRConcrete Contractor   Cap: 303-866-4451
(Wife: Pamela)E-mail: senatorrenfroe@gmail.com
Member of Judiciary; Member of Transportation; Member of Joint Judiciary; Member of Joint Transportation; Member of Capital Development
Rice, Joe 38ArapahoeDConsultant/Army Reserve Officer   Cap: 303-866-2953
(Wife: Kendall)JeffersonE-mail: joe.rice.house@state.co.us
Chair of Joint Business Affairs & Labor; Chair of Business Affairs and Labor
Riesberg, Jim 50WeldDConsulting Gerontologist/   Cap: 303-866-2929
(Wife: Sharron)Small Business OwnerE-mail: jim.riesberg.house@state.co.us
Chair of Health and Human Services; Chair of Joint Health and Human Services; Member of Appropriations; Vice-Chair of Capital Development
Roberts, Ellen 59ArchuletaRAttorney   Cap: 303-866-2914
(Husband: Rick)La PlataE-mail: ellen.roberts.house@state.co.us
 Montezuma 
 San Juan 
Member of Finance; Member of Health and Human Services; Member of Joint Finance; Member of Joint Health and Human Services; Member of Legal Services
Romer, Chris 32DenverDPresident KIPP Schools   Cap: 303-656-9532
(Wife: Laurie)JeffersonE-mail: chris.romer.senate@state.co.us
Vice-Chair of Appropriations
Ryden, Su 36ArapahoeDLegislator   Cap: 303-866-2942
(Husband: E. Jerome)E-mail: su.ryden.house@state.co.us
Member of Joint Judiciary; Member of Agriculture, Livestock, & Natural Resources; Member of Judiciary; Member of Joint Agriculture and Natural Resources
Scanlan, Christine 56EagleD.   Cap: 303-866-2952
(Husband: Timothy)LakeE-mail: christine.scanlan.house@state.co.us
 Summit 
Majority Whip; Member of Education; Member of Joint Education; Member of Legislative Council
Schafer, Sue 24JeffersonDEducator/   Cap: 303-866-5522
Small Business OwnerE-mail: sue.schafer.house@state.co.us
Member of Education; Member of Local Government; Member of Joint Local Government; Member of Joint Education
Scheffel, Mark 4DouglasRAttorney   Cap: 303-866-4869
(Wife: Cheri)El PasoE-mail: mark.scheffel.senate@state.co.us
 Lake 
 Park 
 Teller 
Member of Business, Labor and Technology; Member of Education; Member of Finance; Member of Joint Business Affairs & Labor; Member of Joint Finance; Member of Joint Education; Member of Legislative Council
Schultheis, David C. “Dave”9El PasoRReal Estate Investor (Retired)   Cap: 303-866-4835
(Wife: Sandra)E-mail: senatorschultheis@gmail.com
Member of Health and Human Services; Member of State, Veterans & Military Affairs; Member of Joint Health and Human Services; Member of Joint State Veterans & Military Affairs Committee; Chair of Legislative Audit
Schwartz, Gail 5AlamosaDMarket Analyst   Cap: 303-866-4871
(Husband: Alan)ChaffeeE-mail: gail.schwartz.senate@gmail.com
 Conejos 
 Costilla 
 Delta 
 Gunnison 
 Hinsdale 
 Mineral 
 Pitkin 
 Rio Grande 
 Saguache 
Chair of Local Government and Energy; Vice-Chair of Joint Local Government; Member of Legal Services; Vice-Chair of Agriculture and Natural Resources; Member of Capital Development; Member of Joint Agriculture and Natural Resources
Shaffer, Brandon C.17BoulderDLawyer   Cap: 303-866-5291
(Wife: Jessicca)E-mail: brandon@brandonshaffer.com
President of the Senate; Chair of Senate Services; Vice-Chair of Executive Committee of the Legislative Council; Vice-Chair of Legislative Council
Solano, Judy 31AdamsDTeacher/Retired   Cap: 303-866-2918
(Husband: Manuel)E-mail: judy.solano.house@state.co.us
Vice-Chair of Education; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Education; Member of Joint Agriculture and Natural Resources
Sonnenberg, Jerry 65LoganRFarmer/Rancher   Cap: 303-866-3706
(Wife: Vonnie)PhillipsE-mail: jerry@repsonnenberg.com
 Sedgwick 
 Weld 
Member of Agriculture, Livestock, & Natural Resources; Member of Appropriations; Member of Capital Development; Member of Joint Agriculture and Natural Resources
Soper, John F34AdamsDRetired Electrician   Cap: 303-866-2931
(Wife: Juanita)E-mail: john.soper.house@state.co.us
Vice-Chair of Local Government; Member of Joint Business Affairs & Labor; Member of Joint Local Government; Member of Business Affairs and Labor
Spence, Nancy 27ArapahoeRLegislator   Cap: 303-866-4883
(Husband: Peter)E-mail: nancyspence@qwest.net
Member of Education; Member of Transportation; Member of Joint Transportation; Member of Joint Education; Member of Legislative Council
Steadman, Pat 31AdamsDLegislator   Cap: 303-866-4861
(Partner: Dave Misner)DenverE-mail: pat.steadman.senate@state.co.us
Member of Education; Member of Finance; Vice-Chair of Judiciary; Member of Joint Finance; Member of Joint Judiciary; Member of Joint Education
Stephens, Amy 20El PasoRConsultant   Cap: 303-866-2924
(Husband: Ron)E-mail: amy.stephens.house@state.co.us
Minority Caucus Chair; Member of Joint Business Affairs & Labor; Member of Business Affairs and Labor; Member of Legislative Council
Summers, Ken 22JeffersonRLegislator/Non-profit Executive   Cap: 303-866-2927
(Wife: Debbie)E-mail: ken.summers.house@state.co.us
Member of Education; Member of Finance; Member of Joint Finance; Member of Joint Education
Swalm, Spencer 37ArapahoeREmployee Benefit Broker   Cap: 303-866-5510
(Wife: Marleen)E-mail: spencer.swalm.house@state.co.us
Member of Finance; Member of Health and Human Services; Member of Joint Finance; Member of Joint Health and Human Services
Tipton, Scott R58DeltaRSelf-Employed   Cap: 303-866-2955
(Wife: Jean)DoloresE-mail: cohd58@yahoo.com
 Montezuma 
 Montrose 
 Ouray 
 San Miguel 
Member of Education; Member of Agriculture, Livestock, & Natural Resources; Member of Joint Education; Member of Joint Agriculture and Natural Resources
Tochtrop, Lois 24AdamsDRegistered Nurse   Cap: 303-866-4863
(Husband: Paul)E-mail: lotochtrop@aol.com
Assistant Majority Leader; Chair of Business, Labor and Technology; Member of Transportation; Vice-Chair of Joint Business Affairs & Labor; Member of Joint Transportation; Vice-Chair of Legislative Audit
Todd, Nancy 41ArapahoeDRetired Educator   Cap: 303-866-2919
(Husband: Terry)DenverE-mail: nancy.todd.house@state.co.us
Member of Education; Chair of State, Veterans, & Military Affairs; Chair of Joint State Veterans & Military Affairs Committee; Member of Joint Education
Tyler, Max 23JeffersonD    Cap: 303-866-2951
(Wife: Susan)E-mail: max@maxtyler.us
Member of Health and Human Services; Member of Transportation & Energy; Member of Joint Health and Human Services; Member of Joint Transportation
Vaad, Glenn 48WeldRRetired   Cap: 303-866-2943
(Wife: Mollie)E-mail: glenn.vaad.house@state.co.us
Member of Transportation & Energy; Member of House Services; Member of Joint Transportation; Member of Appropriations
Vigil, Edward 62AlamosaD    Cap: 303-866-2916
(Wife: Evelyn)ConejosE-mail: edvigil1@gmail.com
 Costilla 
 Huerfano 
 Mineral 
 Pueblo 
 Rio Grande 
 Saguache 
Member of Local Government; Member of Joint Local Government; Member of Agriculture, Livestock, & Natural Resources; Member of Capital Development; Member of Joint Agriculture and Natural Resources
Waller, Mark 15El PasoRAttorney   Cap: 303-866-5525
(Wife: Jennifer)E-mail: mark.waller.house@state.co.us
Member of State, Veterans, & Military Affairs; Member of Joint Judiciary; Member of Joint State Veterans & Military Affairs Committee; Member of Judiciary
Weissmann, Paul 12BoulderDBartender/ Restaurant Manager   Cap: 303-866-2348
(Wife: Brenda)E-mail: reppaul@aol.com
Majority Leader; Member of Executive Committee of the Legislative Council; Member of Legislative Council
White, Al 8EagleRBusiness Owner   Cap: 303-866-2586
(Wife: Jean)GarfieldE-mail: al.white.senate@state.co.us
 Jackson 
 Moffat 
 Rio Blanco 
 Routt 
Member of Appropriations; Member of Joint Budget Committee
Whitehead, Bruce 6ArchuletaDWater Engineer   Cap: 303-866-4884
(Wife: Becca)DoloresE-mail: bruce.whitehead.senate@state.co.us
 La Plata 
 Montezuma 
 Montrose 
 Ouray 
 San Juan 
 San Miguel 
Member of Transportation; Member of Joint Transportation; Chair of Agriculture and Natural Resources; Member of Joint Agriculture and Natural Resources
Williams, Suzanne 28ArapahoeDSpecial Education Educator/State Senator   Cap: 303-866-3432
(Husband: Ed)E-mail: suzanne.williams.senate@state.co.us
Majority Caucus Chair; Vice-Chair of Business, Labor and Technology; Vice-Chair of Transportation; Member of Joint Business Affairs & Labor; Member of Joint Transportation

Science about Pathogens

Only 1% of the inoculum survives the low pH during the passage through the stomach. The surviving bacteria then reach the small intestine, which contains bacteriacidal compounds, such as bile salts. About 80% of the bacteria that survive the passage through the stomach are passed with the faeces within 6-10 hours post-infection, About 15% remain localized in the lumen of the caecum and large intestines, and only 5% manage to penetrate the intestinal wall of the small intestine and reach the GALT (Gut associated lymphatic tissue).

An important factor that impedes colonization by salmonella serovars is the normal gut flora. Disruption in the endogenous flora by streptomycin treatment results in a 100,000 fold reduction in the 50% implantation dose. The phenomenon of the endogenous flora being able to prevent colonization by exogenous bacteria is known as bacterial interference. Some of these things are production of inhibitory substances, competition for tissue adhesion sites, and limiting resources.

Peyers patches serve as the main port of entry for Salmonella serovars.

Intestinal perforations at areas of Peyer’s patches are the most frequent cause of death during typhoid fever. (Pg 59)

As the host mounts an inflammatory response at the site of mucosal invasion, Salmonella genes involved in defense against inflammation have to be expressed subsequently to bacterial entry into the epithelium. Coordinated expression of these virulence genes appears to be mediated by PhoPQ, a two-component regulatory system that changes gene expression in response to changes in the external Mg2+ and Ca2+ concentrations. Ca2+ and Mg2+ cations stabilize the outer membrane by neutralizing the negative charge of phosphate groups and bridging adjacent LPS molecules. The intracellular parasitophorous vacuole in which salmonella resides was shown to be low in Mg2+ and Ca2+. In such environments, PhoPQ activates pmrAB, two genes encoding a second two-component regulatory system. Activation of PmrAB increases the substitution of phosphates in both the core oligosaccharide and the lipid A part of the LPS with 4-amino-4-deoxy-L-arabinose, thereby compensating for the lack of Ca2+ and Mg2+ cations. These structural changes in LPS result in increased resistance to bacteriacidal/permeability increasing protein (BPIs), a cationic antibacterial protein that is released by human PMN during inflammation. Furthermore, in response to low Mg2+ and Ca2+ concentrations, PhoPQ activates a second pmrAB-independent pathway, which results in increased resistance to defensins released by recruited PMN and crypdins produced by Paneth cells located in the intestinal crypts. (pg 63)

The major factor for intestinal penetration is encoded by genes that are clustered in a large area (40kb) on the chromosome designated Salmonella pathogenicity island 1 (SPI1) (pg 61) Studies using murine ligated ileal loops revealed that the genes located on SPI1 are necessary for invasion of M cells in the FAE (follicle associated epithelium) of Peyer’s Patches.

Symptoms associated with Salmonella were markedly decreased by treatment with nitrogen mustard, an agent that depletes the polymorphonuclear neutrophil (PMN)… which also inhibits fluid secretion induced by cholera toxin) (pg 62)

In 1958 it was discovered that Salmonella’s ability to agglutinate certain species of erythrocytes and its association between fimbriae and erythrocytes included mannose-containing carbohydrates in lectin-based interactions (pg 35)

FDA’s intent to disclose retailer information for some food recalls:

FDA commits to disclose retailer information for some food recalls: Petfoodindustry.com

In some cases information about retailers selling potentially harmful product may be key to protecting consumers.

Statement from FDA Commissioner Scott Gottlieb, M.D.:

Americans depend on the U.S. Food and Drug Administration to help ensure that the foods they buy and consume are safe. When we learn that potentially dangerous food products may be available in the U.S. marketplace, we must move quickly and efficiently to remove these food products from the market.

Our teams routinely work with food producers on voluntary recalls, and when necessary and where applicable, mandate recalls in order to keep people from getting sick or being harmed. We recognize that an important part of the recall process is also arming consumers with actionable information that they can use to avoid potentially contaminated food products. We’re committed to providing consumers with more information to take these actions. This is an area where we see more opportunity to improve the FDA’s role in protecting public health. To promote these goals, we’re advancing an important new policy.

When a food recall is initiated, the FDA typically works with companies to publicize labeling information, product descriptions, lot numbers, as well as photographs and geographic or retail-related distribution information. The aim is to enable consumers to identify whether they have the recalled product and take appropriate actions. That often includes discarding the product or returning it to the place of purchase.

The agency has not traditionally released lists of specific retailers where recalled foods may have been purchased. This is because certain supply chain information is confidential between the supplier and retailer. Moreover, in most cases, information publicized by the recalling company is sufficient to allow consumers to identify and avoid recalled product. But there are some cases where additional information about the retailers selling potentially harmful product may be key to protecting consumers such as when the food is not easily identified as being subject to a recall from its retail packaging and the food is likely to be available for consumption. It is particularly important in situations where the product has already been linked to foodborne illness. In these situations, providing retailer information can help consumers more quickly and accurately recognize recalled product and take action to avoid the product or seek assistance if they’ve already been exposed.

We recognize the importance of providing consumers with actionable information related to recalled food products. That’s why today the FDA issued new draft guidance that describes situations when disclosing retail information for products undergoing recalls is appropriate. The draft guidance outlines the circumstances when the FDA intends to make public the retail locations that may have sold or distributed a recalled human or animal food. These circumstances will particularly apply in situations associated with the most serious recalls, where consumption of the food has a reasonable probability of causing serious adverse health consequences or death to humans or animals.

Based on this new policy, moving forward the FDA intends to publicize retail consignee lists for food recalls when the food is not easily identified as being subject to a recall from its retail packaging, or lack thereof, and if the food is likely to be available for consumption. Some examples of this may include foods sold directly to consumers with no universal product code or UPC, or bar code. This might include deli cheese, nuts, rawhide chews, or pet treats sold in bulk and fresh fruits and vegetables sold individually.

The new draft guidance also states that the FDA may disclose retail consignee lists in certain recall situations, including when a recalled food is related to a foodborne illness outbreak and where the information is most useful to consumers. For example, the FDA might release retailer information for a packaged food that was distributed in a particular geographic region or through a particular online retailer if providing that information could help consumers protect their health and wellbeing from a recalled food potentially purchased at one of these establishments.

In recent months, we’ve already begun taking actions that align with this approach.

For example, this summer the agency released detailed retail distribution information by state during a recall of pre-cut melon associated with an outbreak of Salmonella infections so consumers could better identify where the recalled food may have been purchased. The draft guidance released today, provides greater transparency on our intention to regularly use this approach in these and other scenarios.

We believe that providing retailer information for certain recalls will also improve the efficiency of recalls by helping the public to identify and focus on the foods that are recalled. It’s important to note that in sharing this information, the FDA may also not be able to fully verify the accuracy or completeness of the information it receives from recalling companies or distributors, and information may change over time.

Identifying retail locations can be complex. It can involve obtaining information from multiple parts of the supply chain, including the recalling company and intermediate distributors. But we also know this information can be very important to consumers. Knowing where a recalled product was sold during the most dangerous food recalls can be the difference between a consumer going to the hospital or not. While we can’t prevent every illness, we can make sure we provide information to consumers to prevent more people from becoming sick from a recalled or hazardous food product.

Availability of this new draft guidance is the second in a series of policy steps we’re taking as part of a broader action plan to further improve our oversight of food safety and the recall process. Earlier this year, I committed the agency to further improve our recall processes because I believe that consumers should have actionable information for protecting themselves from recalled FDA-regulated products.

As part of these commitments, we took an important step in January when we released a draft guidance on public warnings for consumers. It outlined situations where the FDA and firms would publicize public warnings to help carry out a recall. All of these actions are a part of our overall efforts to ensure more comprehensive and timely information reaches consumers. The agency has since been communicating sooner and more often on food safety issues that pose serious threats to the health of consumers. For example, the FDA issued a public warning earlier this year on imported crab meat from Venezuela as soon as we knew there were Vibrioillnesses in several states associated with that product.

Assisting food producers in having effective recall practices in place, as well as taking immediate action to address unsafe products, are high priorities of mine. Our recall authorities – and how we deploy them – are a cornerstone of our vital consumer protection mission. I take these obligations very seriously.

We’re committed to doing our part in ensuring that recalls by firms are initiated, overseen, and completed promptly and effectively to best protect consumers; and that consumers have useful and timely information about recalled products. We’ll use all of our tools to carry through on this commitment.

We continue to assess how best to execute our authorities during food-related emergencies and build on our commitments to consumers. The new draft guidance issued today represents yet another meaningful step to improve our recall processes. We’ll continue to seek out opportunities for improved processes, education and awareness. And we constantly strive to learn from every recall, and every issue, so that we can help to prevent future outbreaks and limit their impact when they do occur.

I remain committed to investing in the FDA’s food program, building on our successes, and to applying the FDA’s food safety expertise to protect American families and keep our Nation safe.

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

https://www.petfoodindustry.com/articles/7516-fda-commits-to-disclose-retailer-info-for-some-food-recalls?utm_source=KnowledgeMarketing&utm_medium=email&utm_content=Pet%20eNews&utm_campaign=18_10_02_PetENews&eid=223857144&bid=2257026