Temperature Most Salmonella serotypes can grow over the temperature range 7 – 48 ºC, but growth is slow at temperatures below 10 ºC. Reports suggesting that some serotypes can grow at temperatures as low as 4 ºC are not universally accepted. Nevertheless Salmonella is able to survive for extended periods in chilled and frozen foods. The majority of Salmonella serotypes are not particularly heat resistant and are usually killed by pasteurisation processes. D-values are typically 1 – 10 mins at 60 ºC and less than 1 min at 70 ºC, with typical z-values of 4 – 5 ºC. However, there are some important exceptions. Some rare serotypes such as S. Senftenberg are much more heat resistant (approximately 10 – 20 times) than others at high water activities, and some foods with high fat content or low water activity reduce the effectiveness of heat treatments that would normally destroy the cells. pH A few Salmonella serotypes can grow over a range of pH values from 3.7- 9.5 under otherwise ideal conditions, but the optimum is 6.5 – 7.5. Although Salmonella cannot grow under very acid conditions, the cells are able to survive for some time in acid environments. Water activity Salmonellae are not able to grow in dry environments and require water activity values of at least 0.94 to multiply in foods. The cells will die out at lower water activities values, but inactivation can be extremely slow in some products (measured in years), particularly those with very low moisture and high fat content, such as chocolate. Salmonella may also survive for some time on dry food production surfaces. Atmosphere All salmonellae can grow with or without oxygen (facultative anaerobes) and in atmospheres containing high levels of carbon dioxide (possibly up to 80 % in some conditions). Chemicals Salmonella is not especially resistant to sanitisers used in the food industry, but is able to form protective biofilms if cleaning is inadequate.

Salmonella has evolved to live in the gastrointestinal tracts of animals and so the primary sources of contamination are animals and their faeces. Many different animals can be infected with Salmonella, often without suffering from any obvious symptoms. Birds, rodents, reptiles, frogs, fish and snails can all carry the bacteria. This can result in contamination of soil and surface waters, leading to infection of food animals and contamination of fruits and vegetables, herbs, spices, seeds, nuts and shellfish. Food animals can also become infected via their feed or from other infected animals.

Ampicillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name "penicillin" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Ampicillin has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Ampicillin results from the inhibition of cell wall synthesis and is mediated through Ampicillin binding to penicillin binding proteins (PBPs). Ampicillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases.Mechanism of actionBy binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, Ampicillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Ampicillin interferes with an autolysin inhibitor.

An Outbreak of Yersinia enterocolitica O:8 Infections Associated with Pasteurized Mil

The resistance to Cm is known to be me-diated by the plasmid-located enzymes called chlo-ramphenicol acetyltransferases (CAT) (Cannon et al., 1990), or by the nonenzymatic chloramphenicol resistance gene cmlA (Dorman and Foster, 1982), that encodes an efflux pump.

The antibiotic used depends upon susceptibility patterns in the particular geographical region. Currently, the antibiotics of choice are fluoroquinolones or azithromycin, with an emerging role for rifaximin

Resistance to beta-lactam antibiotics has become a particular problem in recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common.[55] These beta-lactamase enzymes make many, if not all, of the penicillins and cephalosporins ineffective as therapy

In stool samples, microscopy will show gram-negative rods, with no particular cell arrangement. Then, either MacConkey agar or EMB agar (or both) are inoculated with the stool. On MacConkey agar, deep red colonies are produced, as the organism is lactose-positive, and fermentation of this sugar will cause the medium's pH to drop, leading to darkening of the medium. Growth on EMB agar produces black colonies with a greenish-black metallic sheen. This is diagnostic of E. coli. The organism is also lysine positive, and grows on TSI slant with a (A/A/g+/H2S-) profile. Also, IMViC is {+ + – -} for E. coli; as it is indole-positive (red ring) and methyl red-positive (bright red), but VP-negative (no change-colourless) and citrate-negative (no change-green colour).

Table 1

E. coli O157:H7 infection often causes severe, acute hemorrhagic diarrhea (although nonhemorrhagic diarrhea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in five to 10 days. It can also be asymptomatic.

Antibiotics that interfere with DNA synthesis, such as fluoroquinolones, have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins.

Marburg virus disease

Marburg virus

Host Cell Factors in Filovirus Entry: Novel Players, New Insights

Ebola virus entry requires the cholesterol transporter Niemann-Pick C1

Cellular Entry of Ebola Virus Involves Uptake by a Macropinocytosis-Like Mechanism and Subsequent Trafficking through Early and Late Endosomes

Tissue and cellular tropism, pathology and pathogenesis of Ebola and Marburg viruses

Ebola and Marburg haemorrhagic fever

Outbreaks Chronology: Marburg Hemorrhagic Fever

Filovirus Tropism: Cellular Molecules for Viral Entry

en TSTs wer

Such symptoms are followed by watery, mucoid diarrhea (78-96%); fever (43-47%); colicky abdominal pain (22-84%); bloody stools (< 10%); and white blood cells (WBCs) in the stool (25%).

Virulence Factors:

Mechanism of Action Sulfamethoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with paraaminobenzoic acid (PABA). Trimethoprim blocks the production of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting the required enzyme, dihydrofolate reductase. Thus, SEPTRA blocks two consecutive steps in the biosynthesis of nucleic acids and proteins essential to many bacteria. Mechanism of Resistance In vitro studies have shown that bacterial resistance develops more slowly with SEPTRA than with either trimethoprim or sulfamethoxazole alone. SEPTRA has have been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections as described in the INDICATIONS AND USAGE section.

Salmonella can also actively invade both phagocytic and non-phagocytic cells using a type III secretion system (T3SS), T3SS1.

nternalization into host cells

Flagella

Fimbriae

DNA gyrase has two subunits, which in turn have two subunits each, i.e. 2A and 2B subunits. The A and B subunits together bind to DNA, hydrolyze ATP, and introduce negative supertwists. The A subunit carries out nicking of DNA, B subunit introduces negative supercoils, and then A subunit reseals the strands. Fluoroquinolones bind to the A subunit and interfere with its strand cutting and resealing function.

were recalled due to evidence of Salmonella contamination.[9]

Mechanism Of Action The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination. Mechanism Of Resistance The mechanism of action of fluoroquinolones, including ciprofloxacin, is different from that of penicillins, cephalosporins, aminoglycosides, macrolides, and tetracyclines; therefore, microorganisms resistant to these classes of drugs may be susceptible to ciprofloxacin. Resistance to fluoroquinolones occurs primarily by either mutations in the DNA gyrases, decreased outer membrane permeability, or drug efflux. In vitro resistance to ciprofloxacin develops slowly by multiple step mutations. Resistance to ciprofloxacin due to spontaneous mutations occurs at a general frequency of between < 10-9 to 1x10-6 .

Mechanism Of Action

Although Tir is essential for the strong bacterial attachment to host cells, and is a key molecule involved in the attaching and effacing lesion observed during infection, it has since been discovered to suppress innate immune signaling pathways

extracellular pathogens such as members of the Attaching and Effacing (A/E) pathogen group that include enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli O157:H7 (EHEC), and Citrobacter rodentium, inhibit innate immune responses while maintaining intimate contact with the host plasma membrane

Campylobacter jejuni is known to possess a LuxS/ autoinducer-2 (AI-2) mediated system that have been partially characterized over the last decade

A second cardinal virulence factor of E. coli O157:H7 is Shiga toxin, which causes bloody diarrhea and hemolytic uremic syndrome (HUS), a sequelae of EHEC infection. E. coli O157:H7 produces Stx-2, an A-B toxin comprised of a single A subunit noncovalently associated with a pentamer of B subunits. The B subunits bind specifically to globotrioacyl ceramide on host cell cytosolic membranes and facilitates A-subunit uptake by endocytosis. Stx is an N-glycosidase that targets the 28S rRNA, which it depurinates at a specific adenine residue, causing protein synthesis to cease and infected cells to die from apoptosis

Lipid A is the toxic component of LPS, also known as endotoxin, which is a heat-stable toxin

outer facing leaflet of lipopolysaccharide (LPS)

Locus of Enterocyte Effacement (LEE), which is contained on a pathogenicity island that encodes all of the gene products needed for attaching and effacing the colonic epithelium

Sorbitol non-fermenting colonies should be assayed for Shiga toxin using EIA or PCR

cefixime tellurite-sorbitol MacConkey agar (CT-SMAC), or CHROMagar O157

four distinct systems for acid tolerance. There are four corresponding acid resistance (AR) gene systems. The mechanism of AR1 is unknown. AR2, AR3, and AR4 each depend upon amino acid decarboxylation and consequent consumption of protons, whcih results in pH homeostasis. Expression of the AR systems is induced by acid environment, anaerobiosis, entry into stationary phase. Collectively, one or more of these systems is likely to be "on" when EHEC is exposed to acid, as would be expected to occur upon consumption by a potential host and subsequent passage through the stomach

EHEC virulence factors include the ability to adhere tightly to plant materials, acid tolerance, attachment and effacement of intestinal epithelium, and production of endotoxin and Shiga toxin. The regulator of "hyper-adherence", TdcR, and OmpA, an outer membrane protein that is expressed during hyper-adherence are implicated in binding of EHEC to alfalfa sprouts and seed coats. Loss of these virulence factors results in decreased adherence.

E. coli O157:H7 readily colonizes the mammalian large intestine, including humans

Tissue tropism of EHEC at the rectal-anal junction and its stable colonization at this anatomical location ensures its persistence and shedding in feces

Treatment of EHEC typically involves rehydration without administration of antibiotics and hospitalization in severe cases, especially HUS.

E. coli pathotypes that cause diarrhea are transmitted via contaminated food or water, or through contact with infected animals or people

motile by means of peritrichous flagella

facultative anaerobe

Gram negative rod

To initiate infection the organism must penetrate the gastrointestinal mucus, which it does by using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and once adhered can then induce diarrhoea by toxin release.

Characterization of nalidixic acid and ciprofloxacin resistance mechanisms in isolates from Bangladesh.The 38 isolates from Bangladesh were categorized into the following 5 ciprofloxacin susceptibility groups: a susceptible group, with MICs of ≤0.03 μg/ml; a group with reduced susceptibility, with MICs of 0.12 to 0.5 μg/ml; and resistant groups, with MICs of 4 μg/ml, 8 μg/ml, and 16 μg/ml (Table 3). The isolates with reduced susceptibility to ciprofloxacin were resistant to nalidixic acid (MICs of 128 to 256 μg/ml), and the trait of resistance was associated with a mutation in gyrase subunit A (S83F, S83Y, or D87N) and enhanced activity of the efflux pump for nalidixic acid. The isolates with a ciprofloxacin MIC of 4 μg/ml were highly resistant to nalidixic acid (MICs of ≥256 μg/ml), and the resistance was associated with a mutation (S83Y) in gyrase A, the presence of qnrS, and enhanced activity of the efflux pumps for ciprofloxacin and nalidixic acid. The isolates with ciprofloxacin MICs of 8 and 16 μg/ml also displayed high nalidixic acid resistance (MICs of >256 μg/ml), carried two mutations (S83F and D87G) in gyrase A and one mutation (E92K) in topoisomerase IV, and showed enhanced efflux pump activity for nalidixic acid. The isolates with a ciprofloxacin MIC of 16 μg/ml also showed enhanced efflux pump activity for ciprofloxacin.

ability of this pathogen to survive in different environments is further investigated to provide rational measures to prevent or decrease associated disease risks.

The disease is spread worldwide although it is less common in tropical areas

Cephalosporins disrupt the synthesis of the peptidoglycan layer of bacterial cell walls, which causes the walls to break down and eventually the bacteria die.

work by binding to the bacterial 30S ribosomal subunit (some work by binding to the 50s subunit), inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth

The combination antibiotic TMP-SMZ inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid.

regimen includes doxycycline in combination with an aminoglycoside.

The main habitat where Salmonella is found is in the intestines of animals and humans (figure 4). Typical vectors of Salmonella enterica include chicken including their eggs, swine, dairy and beef cattle, and sometimes even insects, rodents, and other farm animals.

Salmonella spp., Listeria monocytogenes, Campylobacter jejuni, Vibrio parahaemolyticus, Vibrio vulnificus, and Yersinia enterocolitica.

E. coli (EHEC) typically cause acute bloody diarrhea, which may lead to hemolytic-uremic syndrome. Symptoms are abdominal cramps and diarrhea that may be grossly bloody. Fever is not prominent.

Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Infections Linked to I.M. Healthy Brand SoyNut Butter (Final Update)

Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Infections Linked to I.M. Healthy Brand SoyNut Butter (Final Update)

Bovine manure can harbor viable EHEC for more than seven weeks (Wang et al., 1996), and the long-term environmental persistence of EHEC poses an increased risk for transmission of EHEC through the fecal-oral route through wash-off to nearby farms or in contaminated grass consumed by other cattle.

humans acquire EHEC by consuming contaminated bovine-derived products such as meat, milk, and dairy products (Armstrong et al., 1996) or contaminated water, unpasteurized apple drinks, and vegetables (Cody et al., 1999; Hilborn et al., 1999; Olsen et al., 2002). Direct contact with ruminants at petting zoos or through interactions with infected people within families, daycare centers, and healthcare institutes represent another source of EHEC transmission

EHEC colonizes in the colon and causes electrolyte imbalances

Antibiotics promote Shiga toxin production by enhancing the replication and expression of stx genes that are encoded within a chromosomally integrated lambdoid prophage genome. Stx induction also promotes phage-mediated lysis of the EHEC cell envelope, allowing for the release and dissemination of Shiga toxin into the environment

patients treated with antibiotics for EHEC enteritis had a higher risk of developing HUS

Currently no treatment is available for EHEC infections (Goldwater and Bettelheim, 2012). The use of conventional antibiotics exacerbates Shiga toxin-mediated cytotoxicity

life-threatening complication hemolytic uremic syndrome (HUS)

abdominal cramps and bloody diarrhea

Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products

bloody diarrhea and hemolytic uremic syndrome (HUS)

Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products

antimicrobials trigger an SOS response in EHEC that promotes the release of the potent Shiga toxin that is responsible for much of the morbidity and mortality associated with EHEC infection

Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a human pathogen responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) worldwide

Cattle are a major reservoir

In anepidemiology study conducted by the Centers for Disease Controland Prevention, patients treated with antibiotics for EHEC enteri-tis had a higher risk of developing HUS

Currently no treatment is available for EHEC infections

75% of EHEC outbreaks are linked to the consumption of contaminatedbovine-derived products

Campylobacter species also produce the bacterial toxin cytolethal distending toxin (CDT), which produces a cell block at the G2 stage preceding mitosis. CDT inhibits cellular and humoral immunity via destruction of immune response cells and necrosis of epithelial-type cells and fibroblasts involved in the repair of lesions.

Cytotoxin production has been reported in Campylobacter strains from patients with bloody diarrhea

Infection with the organism produces diffuse, bloody, edematous, and exudative enteritis

C jejuni appears to invade and destroy epithelial cells. C jejuni are attracted to mucus and fucose in bile, and the flagella may be important in both chemotaxis and adherence to epithelial cells or mucus. Adherence may also involve lipopolysaccharides or other outer membrane components. Such adherence would promote gut colonization. PEB 1 is a superficial antigen that appears to be a major adhesin and is conserved among C jejuni strains.

Chickens may account for 50-70% of human Campylobacter infections.

Macrolide resistance in Campylobacter is mainly associated with target modification and active efflux [55–59]. Modification of the ribosomal target, leading to macrolide resistance in Campylobacter, can occur either by enzyme-mediated methylation or by point mutation in the 23S rRNA and/or ribosomal proteins L4 and L22

In addition to the mutations in GyrA, the multidrug efflux pump, CmeABC, also contributes to FQ resistance by reducing the accumulation of the agents in Campylobacter cells

In Campylobacter, the resistance to FQs is mainly mediated by point mutations in the quinolone resistance-determining region (QRDR) of DNA gyrase A (GyrA)

Generally, the prevalence of erythromycin resistance among Campylobacter strains (including both C. jejuni and Campylobacter coli) isolated from humans, broilers and cattle in the USA and Canada has been reported at 10% or lowe

19–47% of Campylobacter strains isolated from humans were resistant to ciprofloxacin [

Alternative drugs include tetracyclines and gentamicin, which are used in cases of systemic infection with Campylobacter [5]. However, Campylobacter is increasingly resistant to the clinically important antibiotics and this rising resistance is a concern for public health.

RESISTANCE OF CONCERN

Cefoperazone is added to inhibit many gram-positive and gram-negative organisms, both aerobic and anaerobic. Vancomycin inhibits gram-positive microorganisms. Amphotericin B is incorporated to inhibit the growth of yeast.

Campy CVA is recommended. The use of cefoperazone-containing media, as opposed to cephalothin-containing media, is recommended for the primary isolation of Campylobacter from fecal samples

C. jejuni continues to be the most common enteric pathogen isolated form patients with diarrhea

Plasmid O157 (pO157)

Background: Salmonella enterica subsp. enterica serovar Poona (antigenic formula 1,13,22:z:1,6:[z44],[z59]) is a serovar of the O:13 (G) serogroup.  This serovar has been isolated from found animal and produce sources.

In Campylobacter, a recurring theme is synergy between antibiotic efflux and a second mechanism.

There were 216 gastroenteritis cases reported from 20 November to 4 December 2007. The causative agent was identified as Salmonella enterica subspecies enterica serotype Enteritidis for 14 out of 20 cases tested. The vehicle of transmission was traced to cream cakes produced by a bakery and sold at its retail outlets (P < 0.001, OR = 143.00, 95% Cl = 27.23–759.10). More than two-thirds of the 40 Salmonella strains isolated from hospitalized cases, food samples and asymptomatic food handlers were of phage type 1; the others reacted but did not conform to any phage type. The phage types correlated well with their unique antibiograms. The ribotype patterns of 22 selected isolates tested were highly similar, indicating genetic relatedness. The dendrogram of the strains from the outbreak showed distinct clustering and correlation compared to the non-outbreak strains, confirming a common source of infection.

2008

Diseases which result from pathogenic microorganisms are of two types: infection and intoxication. Foodborne infection is caused by the ingestion of food containing live bacteria which grow and establish themselves in the human intestinal tract. Foodborne intoxication is caused by ingesting food containing toxins formed by bacteria which resulted from the bacterial growth in the food item. The live microorganism does not have to be consumed.

National outbreak of Yersinia enterocolitica infections in military and civilian populations associated with consumption of mixed salad, Norway, 2014.

Growth; red slant, yellow butt, gas positive, black butt (H 2 S produced)

Infection: occurs when live bacterial cells are ingested. These bacterial cells can then grow in the digestive tract and cause symptoms. An example of a bacterial infection is Salmonella infection.

BIOCHEMICAL TESTS

Bismuth sulfite agar: Salmonellae produce black colonies. Blood Agar: S. typhi and S. paratyphi usually produce non-hemolytic smooth white colonies. MacConkey Agar: Non lactose fermenting smooth colonies i.e. pale colonies Deoxycholate Citrate Agar (DCA): Salmonella appear as pale colonies.

Azithromycin therapy would be a primary antibiotic choice for Campylobacter infections, when indicated (see Medical Care), [20] with a typical regimen of 500 mg/d for 3 days. However, erythromycin is the classic antibiotic of choice. Its resistance remains low, [21] and it can be used in pregnant women and children

Temperature range: 6-46 oC (43-115 oF) Optimum Temperature: 37oC (98.6oF) pH range: 4.1-9.0 Optimum pH: 6.5 - 7.5

Salmonella Enteritidis — the most common Salmonella serotype — accounted for 36 percent of infections resistant to nalidixic acid (resistance to nalidixic acid relates to decreased susceptibility to ciprofloxacin, a widely used fluoroquinolone drug).

binds to the wall of the intestine, and through some special proteins that it makes in response to the particular conditions in the intestine it actually penetrates the barrier between us and the outside. Once it has gained access to our insides, it is taken to the liver or spleen.

Susceptible to chloramphenicol, ciproflaxin, amoxicillin, co-trimoxazole, trimethprim-sulfonamid, cephalosporins and norfloxacin

Specificity of coloration

LIMITATIONS OF THE METHOD

chromID® Salmonella Media

Salmonella ASAP™ Chromogenic Media

chromID® Salmonella Ref 43621 (20 plates) Chromogenic media for the isolation and differentiation of Salmonella Direct from specimen Pink to mauve Click here to view product flyer.Click here for an evaluation sample of this media. chromID® Salmonella/Hektoen bi-plate Ref 43465 (20 bi-plates) Chromogenic media for the isolation and differentiation of Salmonella combined with Hektoen Optimized growth of Salmonella while still providing for the recovery of Shigella and other Gram negative organisms Click here for an evaluation sample of this media.

In the outbreak from May to September 2011, approximately 3,000 EHEC cases were observed with a median age of 46 years,

Sulfisoxazole (36%) had the most common antimicrobial resistance, followed by tetracycline (32%), streptomycin (29%), ampicillin (10%), trimethoprim (8%), cotrimoxazole (8%), chloramphenicol (7%), kanamycin (7%), piperacillin (6%), and neomycin (5%).

Stxs cross the intestinal barrier and bind to endothelial cells. At this point they presumably injure the host cell by inhibition of protein synthesis, stimulation of prothrombotic messages, or induction of apoptosis.

SPI-1 is required for bacterial invasion into intestinal epithelial cells, while systemic infections and intracellular accumulation of Salmonella spp. are dependent on the function of SPI-2 (Valle

Resistance of Salmonella spp. to the lytic action of complement (part of the immune response) is directly related to the length of the O side chain (Jay et al. 2003).

Salmonella enterica is estimated to cause 1.2 million illnesses each year in the United States and to be the leading cause of hospitalizations and deaths from foodborne disease

Growth; blue to blue-green colonies with black centers

being able to execute N-linked glycosylation of more than 30 proteins related to colonization, adherence, and invasion. Moreover, the flagellum is not only depicted to facilitate motility but as well secretion of Campylobacter invasive antigens (Cia). The only toxin of C. jejuni, the so-called cytolethal distending toxin (CdtA,B,C), seems to be important for cell cycle control and induction of host cell apoptosis and has been recognized as a major pathogenicity-associated factor. In contrast to other diarrhoea-causing bacteria, no other classical virulence factors have yet been identified in C. jejuni.

The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear.

Many types of media have been used to culture C. jejuni. Mueller-Hinton medium, blood agar, Columbia blood agar, and BBL medium are commonly used. However, Mueller Hinton (MH) has the highest recovery rate and is recommended in this unit

C. jejuni is also able to grow in anaerobic conditions.

Significant loss of viable bacteria occurs when the bacteria are left at room temperature and atmosphere for only 10 min.

All Campylobacter species are inherently resistant to vancomycin, rifampin, and trimethoprim.

Erythromycin has once again come to be considered the optimal drug for treatment of Campylobacter infections. Despite decades of use, the rate of resistance of Campylobacter to erythromycin remains quite low. Other advantages of erythromycin include its low cost, safety, ease of administration, and narrow spectrum of activity. Unlike the fluoroquinolones and tetracyclines, erythromycin may be administered safely to children and pregnant women and is less likely than many agents to exert an inhibitory effect on other fecal flora.

However, in the past few years, a rapidly increasing proportion of Campylobacter strains all over the world have been found to be fluoroquinolone-resistant

Maintenance of hydration and electrolyte balance, not antibiotic treatment, is the cornerstone of treatment for Campylobacter

contaminated water, contact with pets (especially birds and cats)

Fecal leukocytes and RBCs are detected in the stools of 75% of infected persons

Clinically, Campylobacter infection is indistinguishable from acute gastrointestinal infections produced by other bacterial pathogens, such as Salmonella, Shigella, and Yersinia species.

They grow best at 42°C. Because most Campylobacter species are resistant to cephalothin (an agent to which most other stool flora are susceptible), the usual method for isolation from stool samples is use of a medium that contains cephalothin.

Campylobacter species are motile by means of unipolar or bipolar flagellae. The organisms grow quite slowly; 72–96 h are required for primary isolation from stool samples

ampylobacter infections were found to cause diarrheal disease >2–7 times as frequently as infections with Salmonella species, Shigella species, or Escherichia coli O157:H7

Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection

Azithromycin and fluoroquinolones (e.g., ciprofloxacin) are commonly used for treatment of these infections, but resistance to fluoroquinolones is common. Antimicrobial susceptibility testing can help guide appropriate therapy.

What are public health agencies doing to prevent or control campylobacteriosis?

Do not drink unpasteurized milk or untreated surface water.

Surface water and mountain streams can become contaminated from infected feces from cows or wild birds.

Most cases of campylobacteriosis are associated with eating raw or undercooked poultry meat or from cross-contamination of other foods by these items. Outbreaks of Campylobacter have most often been associated with unpasteurized dairy products, contaminated water, poultry, and produce. Animals can also be infected, and some people get infected from contact with the stool of an ill dog or cat.

Almost all persons infected with Campylobacter recover without any specific treatment. Patients should drink extra fluids as long as the diarrhea lasts. Antimicrobial therapy is warranted only for patients with severe disease or those at high risk for severe disease

Campylobacter jejuni grows best at 37°C to 42°C, the approximate body temperature of a bird (41°C to 42°C), and seems to be well adapted to birds, who carry it without becoming ill. These bacteria are fragile. They cannot tolerate drying and can be killed by oxygen. They grow only in places with less oxygen than the amount in the atmosphere. Freezing reduces the number of Campylobacter bacteria on raw meat.

The organism is isolated from infants and young adults more frequently than from persons in other age groups and from males more frequently than females.

The diarrhea may be bloody

Most people who become ill with campylobacteriosis get diarrhea, cramping, abdominal pain, and fever within two to five days after exposure to the organism.

How do people get infected with this germ?

nonspore-forming, Gram-negative, microaerophilic, nonfermenting bacterium

The vast majority of cases occur as isolated events, not as part of recognized outbreaks.

grow optimally at 37 to 42 °C.[5][6][7][8] When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form

oxidase-positive

C. jejuni is also commonly found in animal feces.

14 cases are diagnosed each year for each 100,000 persons in the population.

Yst, included on the genes ystA and ystB, is a membrane-acting virulence factor. It is a heat-stable enterotoxin that is important in causing diarrhea in the host

These plasmids include an outer membrane protein, YadA, that is used for adhesion and can resist phagocytosis by host cell with the help of Yops proteins

Although host gastric acid act as a substantial barrier to prevent infection from the pathogen, Y. enterocolitica utilizes plasmids

4–6 days (range, 1–14 days)

Yersiniosis usually goes away on its own without antibiotic treatment. However, antibiotics may be used to treat more severe or complicated infections.

bacteria are found naturally in the intestines of poultry, cattle, swine, rodents, wild birds and household pets like cats and dogs. The bacteria have also been found in untreated surface water (caused by fecal matter in the environment) and manure.

They’re also looking into how the affected communities treat their sick and bury their dead—practices that could affect the spread of Ebola.

The cases have all occurred in the Likati-Aketi territory—a hard-to-access part of the northern Bas-Uélé province

The country has experienced eight outbreaks since 1976, most recently in 2014

five have been tested and only one has been confirmed for Ebola. (It is not clear whether the five tests included all three deaths.)

Three of those people have died, one of whom tested positive for Ebola Zaire—the most dangerous of the virus’s several species

Ebola virus has emerged again in the Democratic Republic of Congo, and brought along two of its primary symptoms: confusion and misinformation.

Salmonellae are capable of producing biofilms providing the organism with an exopolysaccharide matrix that inhibits chemical attack against chlorine [132–134]

Salmonella is considered to be mesophilic with some strains being able to survive at extremely low or high temperatures (2°C to 54°C).

In the US, Salmonella is the leading foodborne pathogen, causing the largest number of deaths and has the highest cost burden [12]. The annual costs associated with salmonellosis for 2010 were estimated at $2.71 billion for 1.4 million cases [13]. The highest numbers of Salmonella outbreaks from the past decade are related to land animals, with poultry as a main reservoir (Table 2). More than 70% of human salmonellosis in the US has been attributed to the consumption of contaminated chicken, turkey, or eggs [14]. From 1998 to 2008, approximately 145 Salmonella outbreaks have been associated with poultry while 117 outbreaks were associated with eggs, causing illnesses in 2580 and 2,938 people, respectively [14].

The main niche of Salmonella serovars is the intestinal tract of humans and farm animals. It can also be present in the intestinal tract of wild birds, reptiles, and occasionally insects. Feedstuff, soil, bedding, litter, and fecal matter are commonly identified as sources of Salmonella contamination in farms [7–10]. As Salmonella colonizes the gastrointestinal tract, the organisms are excreted in feces from which they may be transmitted by insects and other animals to a large number of places and are generally found in polluted water. Salmonellae do not originate in water; therefore their presence denotes fecal contamination [6]. Humans and animals that consume polluted water may shed the bacteria through fecal matter continuing of the cycle of contamination.

Current recommendations are to treat most patients with uncomplicated Salmonella infection with supportive therapy and no antimicrobial agents. Antimicrobial therapy should be considered for patients who are severely ill (for example, those with severe diarrhea, high fever, or manifestations of extraintestinal infection) and for gastroenteritis caused by Salmonella species in people at increased risk of invasive disease (infants aged <3 months, older adults aged ≥60 years, and the debilitated or immunosuppressed). Fluoroquinolones are often employed for empiric treatment of patients with moderate to severe travelers’ diarrhea; azithromycin and rifaximin are also commonly used. Resistance to antimicrobial agents varies by serotype and geographic region. Resistance to older antimicrobial agents (chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole) has been present for many years, and resistance to both fluoroquinolones and third-generation cephalosporins has increased.

About 90% of isolates are obtained from routine stool culture, but isolates are also obtained from blood, urine, and material from sites of infection. Isolates of salmonellae are needed for serotyping and antimicrobial susceptibility testing.

Gastroenteritis is the most common clinical presentation of nontyphoidal Salmonella infection. The incubation period of nontyphoidal salmonellosis is 6–72 hours, but illness usually occurs within 12–36 hours after exposure. Illness is commonly manifested by acute diarrhea, abdominal pain, fever, and sometimes vomiting. The illness usually lasts 4–7 days, and most people recover without treatment. Approximately 5% of people develop bacteremia or focal infection (such as meningitis or osteomyelitis). Salmonellosis outcomes differ by serotype. Infections with some serotypes, including Dublin and Choleraesuis, are more likely to result in invasive infections. Rates of invasive infections and death are generally higher among infants, older adults, and people with immunosuppressive conditions (including HIV), hemoglobinopathies, and malignant neoplasms.

Nontyphoidal salmonellae are a leading cause of bacterial diarrhea worldwide; they are estimated to cause 94 million cases of gastroenteritis and 115,000 deaths globally each year. The risk of Salmonella infection among travelers returning to the United States varies by region of the world visited. In one analysis, the incidence of laboratory-confirmed infections from 2004 through 2009 was 7.1 cases per 100,000 among travelers to Latin American and Caribbean, 5.8 cases per 100,000 among travelers to Asia, and 25.8 cases per 100,000 among travelers to Africa. The true number of illnesses is much higher, because most ill people do not have a stool specimen tested. Travelers with salmonellosis were most likely to report visiting the following countries: Mexico (38% of travel-associated salmonellosis), India (9%), Jamaica (7%), the Dominican Republic (4%), China (3%), and the Bahamas (2%). Salmonella infection and carriage has been reported among internationally adopted children.

Usually through the consumption of food or water contaminated with animal feces. Transmission can also occur through direct contact with infected animals or their environment and directly between humans.

SURVEILLANCE: Monitor for symptoms. Confirm diagnosis by isolation from stool or blood and by serotyping to identify the serotype (7, 8). Note: All diagnostic methods are not necessarily available in all countries. FIRST AID/TREATMENT: Treatment depends on the clinical symptoms presented by the patient. Gastrotenteritis: Fluid and electrolyte replacement as well as control of the nausea and vomiting are the usual treatments for these symptoms (7, 8). Antibiotic treatment is not usually used; however, it may be necessary for neonates, children, the elderly, and the immunosuppressed, in which case ciproflaxin, co-trimoxazole, ampicillin, and cephalosporins may be used (4, 7, 8).

SURVIVAL OUTSIDE HOST: Serotype Choleraesuis can survive in wet swine feces for at least 3 months and in dry swine feces for at least 13 months (21). Serotype Dublin can survive in feces spread on concrete, rubber, and polyester for almost six years (17). Serotype Typhimurium can survive in cattle slurry for 19-60 days, cattle manure for 48 days, soil for 231 days, and water for up to 152 days (22, 23). Flies have been shown to excrete certain serotypes for 8 days and bed bugs can excrete bacilli for up to 21 days (15, 24). Certain serotypes have been shown to survive on fingertips for up to 80 minutes, depending on the inoculum size (25). Salmonella serotypes have been found to live up to 63 days on lettuce, 231 days on parsley, 32 weeks in pecans, 10 months on refrigerated cheddar cheese, 9 months in butter, up to 63 days in frozen yogurt, and up to 20 weeks on frozen minced beef and chicken (26-28).

DRUG SUSCEPTIBILITY: Susceptible to chloramphenicol, ciproflaxin, amoxicillin, co-trimoxazole, trimethprim-sulfonamid, cephalosporins and norfloxacin (4, 8). Some resistance to chloramphenicol has been reported and, in 1989, 32% of strains were multi-drug resistant (2, 4, 17).

MODE OF TRANSMISSION: Human infection usually occurs when consuming contaminated foods and water, contact with infected feces, as well as contact with infective animals, animal feed, or humans (2, 4, 7, 8, 16). Foods that pose a higher risk include meat, poultry, milk products, and egg products (7-9). In hospitals, the bacteria have been spread by personnel in pediatric wards, either on their hands or on inadequately disinfected scopes (5, 17). Flies can infect foods which can also be a risk for transmission to humans (18, 19). INCUBATION PERIOD: For non-typhoidal salmonellosis, the incubation period is variable, depends on the inoculum size, and usually ranges between 5 and 72 hours (8). For typhoid fever, the incubation period can be between 3 and 60 days, although most infections occur 7-14 days after contamination (4). The incubation period for typhoid fever is highly variable and depends on inoculum size, host susceptibility, and the bacterial strain (2, 4). COMMUNICABILITY: Humans can spread the disease for as long as they shed the bacterium in their feces (20). Certain carriers shed the bacteria for years and 5 % of patients recovering from non-typhoidal salmonellosis can shed the bacteria for 20 weeks (7). Animals can have a latent or carrier state where they excrete the organism briefly, intermittently or persistently (4).

HOST RANGE: For serotypes causing non-typhoidal salmonellosis, the primary hosts are domestic and wild animals such as cattle, swine, poultry, wild birds, and pets (particularly reptiles) as well as flies (8, 14, 15). Humans are usually the final host (8). For Salmonella Typhi, humans are the only known host (7).

EPIDEMIOLOGY: Infections with Salmonella enterica occur worldwide; however, certain diseases are more prevalent in different regions. Non-typhoid salmonellosis is more common in industrialized countries whereas enteric fever is mostly found in developing countries (with the most cases in Asia) (4, 12). There are about 1.3 billion cases of non-typhoid salmonellosis worldwide each year and the WHO estimates that there are 17 million cases and over 500,000 deaths each year caused by typhoid fever (4, 10). There is a peak in disease in the summer and fall, and it is most common in children (2, 7, 9). In the developing world, salmonellosis contributes to childhood diarrhoea morbidity and mortality as bacteria are responsible for about 20% of cases (4, 13). Epidemics of salmonellosis have been reported in institutions such as hospitals and nursing homes (7).

PATHOGENICITY/TOXICITY: Salmonella enterica can cause four different clinical manifestations: gastroenteritis, bacteremia, enteric fever, and an asymptomatic carrier state (7). It is more common in children under the age of 5, adults 20-30 year olds, and patients 70 years or older (7). Gastroenteritis: Gastroenteritis or “food poisoning” is usually characterized by sudden nausea, vomiting, abdominal cramps, diarrhea, headache chills and fever up to 39 ºC (6-9). The symptoms can be mild to severe and may last between 5-7 days (7, 8). The Typhimurium serotype is the most common cause of gastroenteritis and there are an estimated 1.3 billion cases and 3 million deaths annually (1.4 million cases and 600 deaths in the US alone) due to non-typhoidal Salmonella (2, 9, 10). In well resourced countries with low levels of invasive complications, the mortality rate due to non-typhoidal Salmonella is lower then 1% (10); however, in developing countries, the mortality rate can be as high as 24% (10).

Salmonella enterica is a facultative anaerobe and is a gram negative, motile and non-sporing rod that is 0.7-1.5 by 2.0-5.0 µm in size (4-6).

The usual habitat for subspecies enterica (I) is warm-blooded animals (1-3).

Salmonella enterica causes ≈1 million illnesses and >350 deaths annually in the United States (1). Among >2,500 known serotypes, S. enterica serotype Enteritidis is one of the most commonly reported causes of human salmonellosis in most industrialized countries (2).

Secreted proteins are of major importance for the pathogenesis of infectious diseases caused by Salmonella enterica. A remarkable large number of fimbrial and non-fimbrial adhesins are present in Salmonella, and mediate biofilm formation and contact to host cells. Secreted proteins are also involved in host cell invasion and intracellular proliferation, two hallmarks of Salmonella pathogenesis.[4]

L pneumophila is responsible for approximately 1% to 3% of community-acquired pneumonias