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Bacillus coli communis Escherich 1885

Escherichia coli
Escherichia coli
(/ˌɛʃəˈrɪkiə ˈkoʊlɪ/ Anglicized to /ˌɛʃəˈrɪkiə ˈkoʊlaɪ/; commonly abbreviated E. coli) is a gram-negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some serotypes are pathogenic and can cause serious food poisoning in humans, and are occasionally responsible for product recalls.[1][2] E. coli
E. coli
are also responsible for a majority of cases of urinary tract infections. The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2,[3] and by preventing the establishment of pathogenic bacteria within the intestine.[4][5]

Contents

1 Introduction 2 Serotypes

2.1 O antigen 2.2 K antigen 2.3 H antigen

3 Role in disease

3.1 Gastrointestinal infection

3.1.1 Virulence properties 3.1.2 Epidemiology of gastrointestinal infection

3.2 Urinary tract
Urinary tract
infection 3.3 Neonatal
Neonatal
meningitis (NMEC) 3.4 Possible role in colorectal cancer 3.5 Animal diseases

4 Laboratory diagnosis 5 Antibiotic
Antibiotic
therapy and resistance

5.1 Beta-lactamase
Beta-lactamase
strains

6 Phage therapy 7 Vaccination 8 See also 9 References

Introduction[edit] E. coli
E. coli
and related bacteria constitute about 0.1% of gut flora,[6] and fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease. Cells are able to survive outside the body for a limited amount of time, which makes them ideal indicator organisms to test environmental samples for fecal contamination.[7][8] The bacterium can also be grown easily and inexpensively in a laboratory setting, and has been intensively investigated for over 60 years. E. coli
E. coli
is the most widely studied prokaryotic model organism, and an important species in the fields of biotechnology and microbiology, where it has served as the host organism for the majority of work with recombinant DNA. German paediatrician and bacteriologist Theodor Escherich
Theodor Escherich
discovered E. coli
E. coli
in 1885,[7] and it is now classified as part of the Enterobacteriaceae
Enterobacteriaceae
family of gamma-proteobacteria.[9] Serotypes[edit]

Structure of a lipopolysaccharide

Pathogenic E. coli
E. coli
strains can be categorized based on elements that can elicit an immune response in animals, namely:

O antigen: part of lipopolysaccharide layer K antigen: capsule H antigen: flagellin

For example, E. coli
E. coli
strain EDL933 is of the O157:H7 group. O antigen[edit] Main article: O antigen The outer membrane of an E. coli
E. coli
cell contains millions of lipopolysaccharide (LPS) molecules, which consists of:

O antigen, a polymer of immunogenic repeating oligosaccharides (1–40 units) Core region of phosphorylated nonrepeating oligosaccharides Lipid A
Lipid A
(endotoxin)

The O antigen
O antigen
is used for serotyping E. coli
E. coli
and these O group designations go from O1 to O181, with the exception of some groups which have been historically removed, namely O31, O47, O67, O72, O93 (now K84), O94, and O122; groups 174 to 181 are provisional (O174=OX3 and O175=OX7) or are under investigation (176 to 181 are STEC/VTEC).[10] Additionally subtypes exist for many O groups (e.g. O128ab and O128ac).[10] It should be noted though that antibodies towards several O antigens cross-react with other O antigens and partially to K antigens not only from E. coli, but also from other Escherichia
Escherichia
species and Enterobacteriaceae
Enterobacteriaceae
species.[10] The O antigen
O antigen
is encoded by the rfb gene cluster. rol (cld) gene encodes the regulator of lipopolysaccharide O-chain length. K antigen[edit] See also: Polysaccharide § Bacterial capsular polysaccharides The acidic capsular polysaccharide (CPS) is a thick, mucous-like, layer of polysaccharide that surrounds some pathogen E. coli. There are two separate groups of K-antigen groups, named group I and group II (while a small in-between subset (K3, K10, and K54/K96) has been classified as group III).[10] The former (I) consist of 100 kDa (large) capsular polysaccharides, while the latter (II), associated with extraintestinal diseases, are under 50 kDa in size.[10] Group I K antigens are only found with certain O-antigens (O8, O9, O20, and O101 groups), they are further subdivided on the basis of absence (IA, similar to that of Klebsiella species in structure) or presence (IB) of amino sugars and some group I K-antigens are attached to the lipid A-core of the lipopolysaccharide (KLPS), in a similar way to O antigens (and being structurally identical to O antigens in some instances are only considered as K antigens when co-expressed with another authentic O antigen).[10] Group II K antigens closely resemble those in gram-positive bacteria and greatly differ in composition and are further subdivided according to their acidic components, generally 20–50% of the CPS chains are bound to phospholipids.[10] In total there are 60 different K antigens that have been recognized (K1, K2a/ac, K3, K4, K5, K6, K7 (=K56), K8, K9 (=O104), K10, K11, K12 (K82), K13(=K20 and =K23), K14, K15, K16, K18a, K18ab (=K22), K19,K24, K26, K27, K28, K29, K30, K31, K34, K37, K39, K40, K41,K42, K43, K44, K45, K46, K47, K49 (O46), K50, K51, K52, K53, K54 (=K96), K55, K74, K84, K85ab/ac (=O141), K87 (=O32), K92, K93, K95, K97, K98, K100, K101, K102, K103, KX104, KX105,and KX106). H antigen[edit] See also: flagella The H antigen is a major component of flagella, involved in E. coli movement. It is generally encoded by the fliC gene. There are 53 identified H antigens, numbered from H1 to H56 (H13 and H22 were not E. coli
E. coli
antigens but from Citrobacter freundii, and H50 was found to be the same as H10).[11] Role in disease[edit] In humans and in domestic animals, virulent strains of E. coli
E. coli
can cause various diseases. In humans : gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hemolytic-uremic syndrome, peritonitis, mastitis, septicaemia and gram-negative pneumonia.[12] Gastrointestinal infection[edit]

Low-temperature electron micrograph of a cluster of E. coli
E. coli
bacteria, magnified 10,000 times. Each individual bacterium is a rounded cylinder.

Certain strains of E. coli, such as O157:H7, O104:H4, O121, O26, O103, O111, O145, and O104:H21, produce potentially lethal toxins. Food poisoning caused by E. coli
E. coli
can result from eating unwashed vegetables or poorly butchered and undercooked meat. O157:H7 is also notorious for causing serious and even life-threatening complications such as hemolytic-uremic syndrome. This particular strain is linked to the 2006 United States E. coli outbreak due to fresh spinach. The O104:H4 strain is equally virulent. Antibiotic
Antibiotic
and supportive treatment protocols for it are not as well-developed (it has the ability to be very enterohemorrhagic like O157:H7, causing bloody diarrhea, but also is more enteroaggregative, meaning it adheres well and clumps to intestinal membranes). It is the strain behind the deadly June 2011 E. coli outbreak in Europe. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. Earlier, poor hygienic methods of preparing meat in Scotland killed seven people in 1996 due to E. coli
E. coli
poisoning, and left hundreds more infected. E. coli
E. coli
can harbour both heat-stable and heat-labile enterotoxins. The latter, termed LT, contain one A subunit and five B subunits arranged into one holotoxin, and are highly similar in structure and function to cholera toxins. The B subunits assist in adherence and entry of the toxin into host intestinal cells, while the A subunit is cleaved and prevents cells from absorbing water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.[13] If E. coli
E. coli
bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or due to a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment. However, E. coli
E. coli
are extremely sensitive to such antibiotics as streptomycin or gentamicin. Recent research suggests treatment of enteropathogenic E. coli
E. coli
with antibiotics may not improve the outcome of the disease,[citation needed] as it may significantly increase the chance of developing haemolytic-uremic syndrome.[14] Intestinal mucosa-associated E. coli
E. coli
are observed in increased numbers in the inflammatory bowel diseases, Crohn's disease
Crohn's disease
and ulcerative colitis.[15] Invasive strains of E. coli
E. coli
exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.[16] Gastrointestinal infections can cause the body to develop memory T cells to attack gut microbes that are in the intestinal tract.Food poisoning can trigger an immune response to microbial gut bacteria. Some researchers suggest that it can lead to inflammatory bowel disease.[17] Virulence properties[edit] Enteric E. coli
E. coli
(EC) are classified on the basis of serological characteristics and virulence properties.[12] The major pathotypes of E. coli
E. coli
that cause diarrhea are listed below.[18]

Name Hosts Description

Enterotoxigenic E. coli
E. coli
(ETEC) causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses ETEC uses fimbrial adhesins (projections from the bacterial cell surface) to bind enterocyte cells in the small intestine. ETEC can produce two proteinaceous enterotoxins:

The larger of the two proteins, LT enterotoxin, is similar to cholera toxin in structure and function. The smaller protein, ST enterotoxin
ST enterotoxin
causes cGMP accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal lumen.

ETEC strains are noninvasive, and they do not leave the intestinal lumen. ETEC is the leading bacterial cause of diarrhea in children in the developing world, as well as the most common cause of traveler's diarrhea. Each year, ETEC causes more than 200 million cases of diarrhea and 380,000 deaths, mostly in children in developing countries.[19]

Enteropathogenic E. coli
E. coli
(EPEC) causative agent of diarrhea in humans, rabbits, dogs, cats and horses Like ETEC, EPEC also causes diarrhea, but the molecular mechanisms of colonization and aetiology are different. EPEC lack ST and LT toxins, but they use an adhesin known as intimin to bind host intestinal cells. This pathotype has an array of virulence factors that are similar to those found in Shigella. Adherence to the intestinal mucosa causes a rearrangement of actin in the host cell, causing significant deformation. EPEC cells are moderately invasive (i.e. they enter host cells) and elicit an inflammatory response. Changes in intestinal cell ultrastructure due to "attachment and effacement" is likely the prime cause of diarrhea in those afflicted with EPEC.

Enteroinvasive E. coli
E. coli
(EIEC) found only in humans EIEC infection causes a syndrome that is identical to shigellosis, with profuse diarrhea and high fever.

Enterohemorrhagic E. coli
E. coli
(EHEC) found in humans, cattle, and goats The most infamous member of this pathotype is strain O157:H7, which causes bloody diarrhea and no fever. EHEC can cause hemolytic-uremic syndrome and sudden kidney failure. It uses bacterial fimbriae for attachment ( E. coli
E. coli
common pilus, ECP),[20] is moderately invasive and possesses a phage-encoded shiga toxin that can elicit an intense inflammatory response.

Enteroaggregative E. coli
E. coli
(EAEC) found only in humans So named because they have fimbriae which aggregate tissue culture cells, EAEC bind to the intestinal mucosa to cause watery diarrhea without fever. EAEC are noninvasive. They produce a hemolysin and an ST enterotoxin
ST enterotoxin
similar to that of ETEC.

Adherent-Invasive E. coli
E. coli
(AIEC) found in humans AIEC are able to invade intestinal epithelial cells and replicate intracellularly. It is likely that AIEC are able to proliferate more effectively in hosts with defective innate immunity. They are associated with the ileal mucosa in Crohn's disease.[21]

Epidemiology of gastrointestinal infection[edit] Transmission of pathogenic E. coli
E. coli
often occurs via fecal–oral transmission.[22][23][24] Common routes of transmission include: unhygienic food preparation,[23] farm contamination due to manure fertilization,[25] irrigation of crops with contaminated greywater or raw sewage,[26] feral pigs on cropland,[27] or direct consumption of sewage-contaminated water.[28] Dairy and beef cattle are primary reservoirs of E. coli
E. coli
O157:H7,[29] and they can carry it asymptomatically and shed it in their feces.[29] Food products associated with E. coli
E. coli
outbreaks include cucumber,[30] raw ground beef,[31] raw seed sprouts or spinach,[25] raw milk, unpasteurized juice, unpasteurized cheese and foods contaminated by infected food workers via fecal–oral route.[23] According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, instituting health care policies so food industry employees seek treatment when they are ill, pasteurization of juice or dairy products and proper hand washing requirements.[23] Shiga toxin-producing E. coli
E. coli
(STEC), specifically serotype O157:H7, have also been transmitted by flies,[32][33][34] as well as direct contact with farm animals,[35][36] petting zoo animals,[37] and airborne particles found in animal-rearing environments.[38] Urinary tract
Urinary tract
infection[edit]

E. coli
E. coli
bacteria

Uropathogenic E. coli
E. coli
(UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy.[12] In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder as well as to the kidneys (causing pyelonephritis),[39] or the prostate in males. Because women have a shorter urethra than men, they are 14 times more likely to suffer from an ascending UTI.[12] Uropathogenic E. coli
E. coli
use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood-group antigen of erythrocytes and uroepithelial cells.[12] Approximately 1% of the human population lacks this receptor,[citation needed] and its presence or absence dictates an individual's susceptibility or non-susceptibility, respectively, to E. coli
E. coli
urinary tract infections. Uropathogenic E. coli
E. coli
produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells. Another virulence factor commonly present in UPEC is the Dr family of adhesins, which are particularly associated with cystitis and pregnancy-associated pyelonephritis.[40] The Dr adhesins bind Dr blood group antigen (Dra) which is present on decay accelerating factor (DAF) on erythrocytes and other cell types. There, the Dr adhesins induce the development of long cellular extensions that wrap around the bacteria, accompanied by the activation of several signal transduction cascades, including activation of PI-3 kinase.[40] UPEC can evade the body's innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs).[41] They also have the ability to form K antigen, capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli
E. coli
are recalcitrant to immune factors and antibiotic therapy, and are often responsible for chronic urinary tract infections.[42] K antigen-producing E. coli
E. coli
infections are commonly found in the upper urinary tract.[12] Descending infections, though relatively rare, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream. Neonatal
Neonatal
meningitis (NMEC)[edit] It is produced by a serotype of Escherichia coli
Escherichia coli
that contains a capsular antigen called K1. The colonization of the newborn's intestines with these strains, that are present in the mother's vagina, lead to bacteremia, which leads to meningitis.[43] And because of the absence of the IgM
IgM
antibodies from the mother (these do not cross the placenta because FcRn
FcRn
only mediates the transfer of IgG), plus the fact that the body recognizes as self the K1 antigen, as it resembles the cerebral glycopeptides, this leads to a severe meningitis in the neonates. Possible role in colorectal cancer[edit] Some E. coli
E. coli
strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA. About 20% of humans are colonized with E. coli
E. coli
that harbor the pks island.[44] Colibactin can cause cellular senescence[45] or cancer by damaging DNA.[46] However, the mucosal barrier prevents E. coli
E. coli
from reaching the surface of enterocytes. Mucin
Mucin
production diminishes in the presence of inflammation.[47] Only when some inflammatory condition co-occurs with E. coli
E. coli
infection the bacterium is able to deliver colibactin to enterocytes and induce tumorogenesis.[48] Animal diseases[edit] In animals, virulent strains of E. coli
E. coli
are responsible of a variety of diseases, among others septicemia and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs. Most of the serotypes isolated from poultry are pathogenic only for birds. So avian sources of E. coli
E. coli
do not seem to be important sources of infections in other animals.[49]

Colibacillosis in domestic chicken

Mastitis
Mastitis
in cows

Laboratory diagnosis[edit] In stool samples, microscopy will show gram-negative rods, with no particular cell arrangement. Then, either MacConkey agar
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
TSI slant
with a (A/A/g+/H2S-) profile. Also, IMViC
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). Tests for toxin production can use mammalian cells in tissue culture, which are rapidly killed by shiga toxin. Although sensitive and very specific, this method is slow and expensive.[50] Typically, diagnosis has been done by culturing on sorbitol-MacConkey medium and then using typing antiserum. However, current latex assays and some typing antisera have shown cross reactions with non-E. coli O157
O157
colonies. Furthermore, not all E. coli
E. coli
O157
O157
strains associated with HUS are nonsorbitol fermentors. The Council of State and Territorial Epidemiologists recommend that clinical laboratories screen at least all bloody stools for this pathogen. The U.S. Centers for Disease Control and Prevention recommend that "all stools submitted for routine testing from patients with acute community-acquired diarrhea (regardless of patient age, season of the year, or presence or absence of blood in the stool) be simultaneously cultured for E. coli
E. coli
O157:H7 ( O157
O157
STEC) and tested with an assay that detects Shiga toxins to detect non-O157 STEC".[51][52] Antibiotic
Antibiotic
therapy and resistance[edit] Main article: Antibiotic
Antibiotic
resistance Bacterial infections are usually treated with antibiotics. However, the antibiotic sensitivities of different strains of E. coli
E. coli
vary widely. As gram-negative organisms, E. coli
E. coli
are resistant to many antibiotics that are effective against gram-positive organisms. Antibiotics
Antibiotics
which may be used to treat E. coli
E. coli
infection include amoxicillin, as well as other semisynthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin and the aminoglycosides. Antibiotic
Antibiotic
resistance is a growing problem. Some of this is due to overuse of antibiotics in humans, but some of it is probably due to the use of antibiotics as growth promoters in animal feeds.[53] A study published in the journal Science in August 2007 found the rate of adaptative mutations in E. coli
E. coli
is "on the order of 10−5 per genome per generation, which is 1,000 times as high as previous estimates," a finding which may have significance for the study and management of bacterial antibiotic resistance.[54] Antibiotic-resistant E. coli
E. coli
may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as Staphylococcus aureus, through a process called horizontal gene transfer. E. coli
E. coli
bacteria often carry multiple drug resistance plasmids, and under stress, readily transfer those plasmids to other species. Mixing of species in the intestines allows E. coli
E. coli
to accept and transfer plasmids from and to other bacteria. Thus, E. coli
E. coli
and the other enterobacteria are important reservoirs of transferable antibiotic resistance.[55] Beta-lactamase
Beta-lactamase
strains[edit] 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.[56] These beta-lactamase enzymes make many, if not all, of the penicillins and cephalosporins ineffective as therapy. Extended-spectrum beta-lactamase–producing E. coli
E. coli
(ESBL E. coli) are highly resistant to an array of antibiotics, and infections by these strains are difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective. In 2009, a gene called New Delhi metallo-beta-lactamase
New Delhi metallo-beta-lactamase
(shortened NDM-1) that even gives resistance to intravenous antibiotic carbapenem, were discovered in India
India
and Pakistan
Pakistan
on E. coli
E. coli
bacteria. Increased concern about the prevalence of this form of "superbug" in the United Kingdom
United Kingdom
has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths.[57] Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture. Phage therapy[edit] Phage therapy—viruses that specifically target pathogenic bacteria—has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by E. coli.[58] Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and in Poland.[59] However, on January 2, 2007, the United States FDA gave Omnilytics approval to apply its E. coli
E. coli
O157:H7 killing phage in a mist, spray or wash on live animals that will be slaughtered for human consumption.[60] The enterobacteria phage T4, a highly studied phage, targets E. coli
E. coli
for infection. Vaccination[edit] Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli
E. coli
infection.[61] In March 2006, a vaccine eliciting an immune response against the E. coli O157:H7 O-specific polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa
Pseudomonas aeruginosa
(O157-rEPA) was reported to be safe in children two to five years old. Previous work had already indicated it was safe for adults.[62] A phase III clinical trial to verify the large-scale efficacy of the treatment is planned.[62] In 2006, Fort Dodge Animal Health (Wyeth) introduced an effective, live, attenuated vaccine to control airsacculitis and peritonitis in chickens. The vaccine is a genetically modified avirulent vaccine that has demonstrated protection against O78 and untypeable strains.[63] In January 2007, the Canadian biopharmaceutical company Bioniche announced it has developed a cattle vaccine which reduces the number of O157:H7 shed in manure by a factor of 1000, to about 1000 pathogenic bacteria per gram of manure.[64][65][66] In April 2009, a Michigan State University researcher announced he had developed a working vaccine for a strain of E. coli. Dr. Mahdi Saeed, Professor of epidemiology and infectious disease in MSU's colleges of Veterinary Medicine and Human
Human
Medicine, has applied for a patent for his discovery and has made contact with pharmaceutical companies for commercial production.[67] See also[edit]

List of strains of Escherichia
Escherichia
coli

References[edit]

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v t e

Escherichia
Escherichia
coli

Outbreaks

1993 Jack in the Box 1996 Odwalla 2000 Walkerton 2005 South Wales (O157) 2006 North American (spinach; O157:H7) 2006 North American (multiple; O157:H7) 2009 United Kingdom 2011 Germany (O104:H4) 2015 United States

Genes

CPS operon DnaG Fis FNR regulon OmpT RecBCD RpoE RpoF RpoN RpoS

Strains

Enterohemorrhagic Enteroinvasive Enterotoxigenic O104:H21 O104:H4 O121 O157:H7 Verotoxin-producing

Related

Aerobactin Coliform index Long-term evolution experiment EcoCyc Enteroaggregative Molecular biology Hok/sok system LacUV5 Min System Pathogenic EnvZ/OmpR Rho factor T4 rII system Theodor Escherich

v t e

Infectious diseases Bacterial disease: Proteobacterial G−

primarily A00–A79, 001–041, 080–109

α

Rickettsiales

Rickettsiaceae/ (Rickettsioses)

Typhus

Rickettsia typhi

Murine typhus

Rickettsia prowazekii

Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus

Spotted fever

Tick-borne

Rickettsia rickettsii

Rocky Mountain spotted fever

Rickettsia conorii

Boutonneuse fever

Rickettsia japonica

Japanese spotted fever

Rickettsia sibirica

North Asian tick typhus

Rickettsia australis

Queensland tick typhus

Rickettsia honei

Flinders Island spotted fever

Rickettsia africae

African tick bite fever

Rickettsia parkeri

American tick bite fever

Rickettsia aeschlimannii

Rickettsia aeschlimannii infection

Mite-borne

Rickettsia akari

Rickettsialpox

Orientia tsutsugamushi

Scrub typhus

Flea-borne

Rickettsia felis

Flea-borne spotted fever

Anaplasmataceae

Ehrlichiosis: Anaplasma phagocytophilum

Human
Human
granulocytic anaplasmosis, Anaplasmosis

Ehrlichia chaffeensis

Human
Human
monocytotropic ehrlichiosis

Ehrlichia ewingii

Ehrlichiosis ewingii infection

Rhizobiales

Brucellaceae

Brucella abortus

Brucellosis

Bartonellaceae

Bartonellosis: Bartonella henselae

Cat-scratch disease

Bartonella quintana

Trench fever

Either B. henselae or B. quintana

Bacillary angiomatosis

Bartonella bacilliformis

Carrion's disease, Verruga peruana

β

Neisseriales

M+

Neisseria meningitidis/meningococcus

Meningococcal disease, Waterhouse–Friderichsen syndrome, Meningococcal septicaemia

M−

Neisseria gonorrhoeae/gonococcus

Gonorrhea

ungrouped:

Eikenella corrodens/Kingella kingae

HACEK

Chromobacterium violaceum

Chromobacteriosis infection

Burkholderiales

Burkholderia pseudomallei

Melioidosis

Burkholderia mallei

Glanders

Burkholderia cepacia complex Bordetella pertussis/Bordetella parapertussis

Pertussis

γ

Enterobacteriales (OX−)

Lac+

Klebsiella pneumoniae

Rhinoscleroma, Klebsiella pneumonia

Klebsiella granulomatis

Granuloma inguinale

Klebsiella oxytoca

Escherichia
Escherichia
coli: Enterotoxigenic Enteroinvasive Enterohemorrhagic O157:H7 O104:H4

Hemolytic-uremic syndrome

Enterobacter aerogenes/Enterobacter cloacae

Slow/weak

Serratia marcescens

Serratia infection

Citrobacter koseri/Citrobacter freundii

Lac−

H2S+

Salmonella enterica

Typhoid fever, Paratyphoid fever, Salmonellosis

H2S−

Shigella
Shigella
dysenteriae/sonnei/flexneri/boydii

Shigellosis, Bacillary dysentery

Proteus mirabilis/Proteus vulgaris Yersinia pestis

Plague/Bubonic plague

Yersinia enterocolitica

Yersiniosis

Yersinia pseudotuberculosis

Far East scarlet-like fever

Pasteurellales

Haemophilus:

H. influenzae

Haemophilus
Haemophilus
meningitis Brazilian purpuric fever

H. ducreyi

Chancroid

H. parainfluenzae

HACEK

Pasteurella multocida

Pasteurellosis Actinobacillus

Actinobacillosis

Aggregatibacter actinomycetemcomitans

HACEK

Legionellales

Legionella pneumophila/Legionella longbeachae

Legionnaires' disease

Coxiella burnetii

Q fever

Thiotrichales

Francisella tularensis

Tularemia

Vibrionaceae

Vibrio cholerae

Cholera

Vibrio vulnificus Vibrio parahaemolyticus Vibrio alginolyticus Plesiomonas shigelloides

Pseudomonadales

Pseudomonas aeruginosa

Pseudomonas infection

Moraxella catarrhalis Acinetobacter baumannii

Xanthomonadaceae

Stenotrophomonas maltophilia

Cardiobacteriaceae

Cardiobacterium hominis

HACEK

Aeromonadales

Aeromonas hydrophila/Aeromonas veronii

Aeromonas infection

ε

Campylobacterales

Campylobacter jejuni

Campylobacteriosis, Guillain–Barré syndrome

Helicobacter pylori

Peptic ulcer, MALT lymphoma, Gastric cancer

Helicobacter cinaedi

Helic

.