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Ebola

Enterococcus faecalis Tropism for the Kidneys in the Urinary Tract of C57BL/6J Mice

Gram Stain of Escherichia coli

Treatments and drugs

Tests and diagnosis

Complications

Risk factorsBy Mayo Clinic Staff

Causes

Bacterial Urinary Tract Infections (UTIs)

Most strains of Enterobacter sp. were classified as moderate biofilm producer. Conc

Biofilm Formation of Enterobacteragglomerans

erious gram-negative bacillary infections (especially those due to Pseudomonas aeruginosa) Aminoglycosides are active against most gram-negative aerobic and facultative anaerobic bacilli but lack activity against anaerobes and most gram-positive bacteria, except for most staphylococci; however, some gram-negative bacilli and methicillin-resistant staphylococci are resistant.

oglycosides (see Table: Aminoglycosides) have concentration-dependent bactericidal activity. They bind to the 30S ribosom

e inhibited by the dyes eosin and methylene blue added to the agar. Based on a moderate rate of lactose fermentation and acid production, Enterobacter species produces large, muco

e isolation of Enterobacter aerogenes grown

Large, yellow to salmon color

. A diffuse slime layer of variable thickness (the M antigen) also may be produced but, unlike the K antigens, it is nonspecific and is serologically cross-reactive among different organisms.

he outer membrane also contains lipopolysaccharide (LPS), of which the lipid A portion is endotoxic and the O (somatic) antigen is serotype specific.

Blood Agar 5%, TSA Agar, Nutrient Agar. For selective isolation: MacConkey Agar, Hektoen Enteric (HE) Agar, EMB Agar. For maintenance: Blood Agar 5%, TSA Agar, Nutrient Agar.

Staphylococcus epidermidis.  Circular, pinhead colonies which are convex with entire margins.  The colonies of this gram-positive coccus appear either the color of the agar, or whitish.

ccus spp. in the periodontal pocket and 61.36% in the oral cavity, 27.27% presented thebacteria in both sites. S. epidermidis was the most prevalent specie in the periodontal pocket (15.9%) and oralcavity (27.27%).

n ofNitroreductase(Phenotypic & genotypic detection)The results of nitrate reduction test revealed that , all isolates (100%) of Enterobacterwere able to red

URL:http://www.uokufa.edu.iq/journals/index.php/ajb/indexEmail: biomgzn.sci@uokufa.edu.iqISSN: 2073-8854Magazin of Al-Kufa University for Biology/ VOL.5/ NO.2 / year: 2013It was found low percentages of Enterobacterisolates (E. cloacae , E. sakazakii) are able to produce bacteriocin only against sensitive bacteria E.coli. This low production of bacteriocin may be due to siderophore production that can inhibit the activity of bacteriocin such receptor for the uptake siderophore also functions as receptor for the bacteriocin (cloacin)[18].Enterobacterbacteriocin were active against E.coli, but were inactive against Klebsiella pneumoniae, this may be due to the growth inhibitor products of the Enterobacter strains for typing are different in nature [18,24].-Production of RpoSA-Detection of rpoS gene in Enterobacterspp. by PCR.Twenty six isolates (31%) out of 84 isolates of Enterobacter

e( 1): Virulence factors of Enterobacterspeci

hemolysin and extracellular protease

ut all isolates of Enterobacterspecies had a polysaccharide capsule surrounding the bacterial cell except one isolate of E.cloacaethat lack capsule structure (98.8% versus 1.2%) [

wo species of Enterobacterwere grew efficiently on CHROMTMagar medium and yield

lass 1 fimbriae

eing able to chelate iron to survive and spread within the ho

hey produce acid upon glucose fermentation , methyl red negative ,

cter, and Serratia: Biochemical Differentiation and Susceptibility to Ampicillin and

Cephalosporins at 20 μg/ml or less inhibited 90% of the Klebsiella strains but only 15% of the Enterobacter strains. Ampicillin inhibited 27% of Enterobacter strains

R and VP tests are particularly useful in the identification of the Enterobacteriacea

erial keratitis is usually treated with antibiotic dr

Chemicals in water such as those used in swimming pools may irritate the cornea and weaken the delicate surface tissue of the cornea (corneal epithelium),

Fortunatelytheinfectionwascontrolledbytopicalsulphacetamideandgentamicindrops.Enterobactercloacaeisusuallyresistanttoampicillinandcanproduceacephalosporinasewhichmaydeactivatesomecephalosporins.'4Aminoglycosideshavebeenthemosteffectivedrugsagainsttheorganismandsepsishasbeentreatedwithcarbenicillinandanaminoglycoside.'H

nterobactercloacaewaspresentin4-12%ofallcasesofGram-negativebacteraemia.6I

terobacteriaceaesuchasKlebsiellacausecornealulceration.2AcaseofcornealulcerationduetoEnterobacterc

Book available

Antibiotic Susceptibility: Keratitis

On postoperative day 3, the organism was isolated to be an Enterobacter species, sensitive to ciprofl oxacin and gentamicin

Gram-negative organisms were found to be a rare cause of infectious keratitis, with only one case (due to Pseudomonas aeruginosa) in the literature. In an ASCRS survey of 338,550 LASIK pro-cedures, only 2 of 116 cases of infectious keratitis due to Gram-negative organisms were reported.

produce acid upon glucose fermentation, are methyl red negative, and Voges-Proskauer positive, with an optimal growth temperature of 30 °C(1). 80 % are encapsulated(1).

Editorial Note Editorial Note: In this investigation pasteurized milk was epidemiologically implicated as the vehicle of transmission of Y. enterocolitica. The temporal and geographic clustering of cases and the negative cultures of subsequent lots of milk are consistent with contamination of a single lot. The mechanism of contamination is unknown. Y. enterocolitica may be found in raw milk (1,2); contaminated raw milk was responsible for an outbreak of yersiniosis among children in Montreal (3). The organism has also been found in pasteurized milk (1,4) although not associated with illness. Y. enterocolitica generally does not survive standard pasteurization (5); however, if present in large enough numbers, viable Yersinia may persist after pasteurization (4-6). Once present in a pasteurized product, the organism grows well at refrigeration temperature (7). Therefore, pasteurization and proper handling of pasteurized milk may not ensure against enteric disease due to Y. enterocolitica. Only two other well documented food-borne outbreaks of Y. enterocolitica enteritis have been reported in the United States: one in New York state in 1976 caused by contaminated chocolate milk (8) and one in Washington state in 1982 caused by tofu (9). Food-borne transmission of yersiniosis has also been suspected in other outbreaks (10-12). This is the largest outbreak of yersiniosis ever reported in the United States.

Occasionally Y. enterocolitica infection occurs after contact with infected animals.

Virulence Factors of pYV-Bearing Strains of Y. enterocolitica [33]

he ability to penetrate the intestinal wall, which is thought to be controlled by plasmid genes, and the production of heat-stable enterotoxin, which is controlled by chromosomal genes.

attributed to the presence of a highly conserved 70-kb virulence plasmid, termed pYV/pCD and certain chromosomal genes.

Metabolism Y enterocolitica is non–lactose-fermenting, glucose-fermenting, and oxidase-negative facultative anaerobe that is motile at 25°C and nonmotile at 37°C. Most, but not all, Y enterocolitica isolates reduce nitrates. The presence of bile salts in the medium prevents the organism from fermenting lactose. Colonies of Y enterocolitica do not produce hy

of Y enterocolitica infection typically include the following: Diarrhea - The most common clinical manifestation of this infection; diarrhea may be bloody in severe cases Low-grade fever Abdominal pain - May localize to the right lower quadrant Vomiting - Present in app

if it spreads systemically, can also result in fatal sepsis

.7. Establishment of Yersiniosis Infection

e small conserved RNA chaperone protein, Hfq is required for full virulence of a variety of pathogenic bacteria, including both YE and YPT [90]. Hfq is required for expression of the heat-stable enterotoxin Yst in YE [91]

YE pathogenicity depends on the presence of the 70-kb plasmid associated with Yersinia virulence, pYV [67, 77–79]. The pYV plasmid differentiates pathogenic from non-pathogenic strains, because it is essential for virulence [79]. The highly pathogenic Y. enterocolitica biotype 1B also harbors the chromosomal high-pathogenicity island (HPI), as do almost all European strains of Y. pseudotuberculosis serotype O1 [69]. HPI encodes proteins that are involved in the biosynthesis, regulation, and transport of the siderophore yersiniabactin [80, 81] and has thus been referred to as an “iron capture island” [63, 69]. There are five main genes within this island (psn, irp1, irp2, ybtP, and ybtQ) that are involved in the yersiniabactin system [80, 82, 83]. This system is positively regulated by YtbA, which is, itself, negatively regulated by the iron-responsive regulator F

For instance, strain 1B/O:8 has been the predominant version of pathogenic YE in the United States

Subsequently, YE bacilli replicate in Peyer’s patches and can sometimes spread to more distant lymphoid tissues, such as the mesenteric lymph nodes [16–18]. Dissemination from the distal ileum to the spleen and liver is relatively common, followed by extracellular replication and formation of monoclonal microabscesses [19]

The most common infection is acute gastroenteritis, mainly observed in children and infants on account of being somewhat immunocompromised due to an immature immune system

nfection is usually characterized by a self-limiting acute infection beginning in the intestine and spreading to the mesenteric lymph nodes. However, more serious infections and chronic conditions can also occur, particularly in immunocomp

Natural antibiotic susceptibility of biovars (some examples) 

Ninety-nine percent of all Yersinia strains were resistant to amoxycillin, but bi

The fluoroquinolones are the only direct inhibitors of DNA synthesis; by binding to the enzyme-DNA complex, they stabilize DNA strand breaks created by DNA gyrase and topoisomerase IV. Ternary complexes of drug, enzyme, and DNA block progress of the replication fork. Cytotoxicity of fluoroquinolones is likely a 2-step process involving (1) conversion of the topoisomerase-quinolone-DNA complex to an irreversible form and (2) generation of a double-strand break by denaturation of the topoisomerase. The molecular factors necessary for the transition from step 1 to step 2 remain unclear, but downstream pathways for cell death may overlap with those used by other bactericidal antimicrobials. Studies of fluoroquinolone-resistant mutants and purified topoisomerases indicate that many quinolones have differing activities against the two targets. Drugs with similar activities against both targets may prove less likely to select de novo res

entration-dependent bactericidal activity (see Effectiveness) by inhibiting the activity of DNA gyrase and topoisomerase, enzymes essential for bacterial DNA replication.

Foodborne Diseases

eak of illness caused by Yersinia enterocolitica O:9 in Norway was linked to ready-to-eat salad mix, an unusual vehicle for this

safety measures to minimize human infection are of increasing interest to the scientific and medical community.

Table 1. Biochemical Characteristics(a) of Yersinia species (2, 9 ,10 ,52)

Yersinia are oxidase-negative, Gram-negative rods. Use Tables 1 and 2 to identify species and biotype of Yersinia isolates. Currently only strains of Y. enterocolitica biotypes 1B, 2, 3, 4, and 5 are known to be pathogenic. These biotypes and Y. enterocolitica biotype 6 and Y. kristensenii do not rapidly (within 24 h) hydrolyze esculin or ferment salicin (Tables 1 and 2). However, Y. enterocolitica biotype 6 and Y. kristensenii are relatively rare; they can be distinguished by failure to ferment sucrose, and they are pyrazinamidase-positive (28). Hold Y. enterocolitica isolates which are within biotypes 1B, 2, 3, 4, and 5 for further pathogenicity tests.

e Esculin agar

ensen's Urea agar

. enterocolitica on YSA (CIN) a

MacConkey agar plates

nvasion of host cells (ail for Y. enterocolitica and inv for Y. pseudotuberculosis), iron complexing and uptake proteins (irps), and heat-stable enterotoxin (ystA). Factors carried on the 70 kb virulence plasmid (pYV for Y. enterocolitica and pIB1 for Y. pseudotuberculosis) include: the Yersinia outer proteins (yops), low calcium response (lcr), Yersinia adherence protein (yadA), and the temperature dependent transcriptional regulator of many of the other plasmid genes (virF) (38).

m may survive and grow during refrigerated

For detection and direct differentiation of pathogenic Yersinia enterocolitica  

osis is usually made by a faecal specimen or by detecting Yersinia using a PCR (polymerase chain reactio

Colonial growth pattern displayed by Yersinia enterocolitica bacteria

CDC recommends the use of cefsulodin-irgasan-novobiocin (CIN) agar for isolation of Yersinia spp. from nonsterile sites.   Incubation at 25° C is recommended to prevent loss of the virulence plasmid in Y. enterocolitica. In addition, the lower temperature favors the growth of Yersinia over some other members of the Enterobacteriaceae family that can grow on CIN agar.  

virulence plasmid

. They can also be transmitted by direct or indirect contact with animals.

The incidence of yersiniosis in FoodNet(https://www.cdc.gov/foodnet/index.html) sites in 2014 was 0.28 cases per 100,000 population. This met the U.S. Healthy People 2020 target for yersiniosis of 0.30 or fewer cases per 100,000.

Antibiotics should be given for severe cases. Y. enterocolitica isolates are usually susceptible to trimethoprim-sulfamethoxazole, aminoglycosides, third-generation cephalosporins, fluoroquinolones, and tetracyclines; they are typically resistant to first-generation cephalosporins and most penicillins. They are typically resistant to first-generation cephalosporins and most penicillins. Antimicrobial therapy has no effect on postinfectious sequelae.

culture on cefsulodin-irgasan-novobiocin (CIN) or other specific for growing it.

Yersiniosis is caused by a facultative anaerobic gram-negative coccobacilli

Yersiniosis usually is diagnosed by detecting the organism in the stool of an infected person. Many laboratories do not routinely test for Yersinia, so it is important to notify laboratory personnel when yersiniosis is suspected so that special tests can be done. The organism can also be recovered from other sites, including the throat, lymph nodes, joint fluid, urine, bile, and blood.

Complications are rare and can include skin rash, joint pains, or spread of bacteria to the bloodstream

ersiniosis usually goes away on its own without antibiotic tre

etecting the bacteria in the stool of an infected person

eople occasionally become infected after drinking contaminated milk or untreated water, or after contact with infected animals or their feces. On rare occasions, people become infected through person-

Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms and may be confused with appendicitis. Complications are rare, and may include skin rash, joint pains, or spread of bacteria to the bloodstream.

Pigs are the major animal reservoir for the few strains of Y. enterocolitica that cause human illness, but rodents, rabbits, sheep, cattle, horses, dogs, and cats also can carry strains that cause human illness.

ating raw or undercooked pork contaminate

117,000 illnesses, 640 hospitalizations, and 35 death

USA and Australia showed case–fatality rates of 14% for nosocomial infections and 5–10% for community-acquired infections (Benin et al., 2002;Howden et al., 2003). In Europe, the overall case–fatality rate is about 12%

It is involved in attachment and adherence to host cells as well as natural competence of L. pneumophila.

FeoB is required for efficient killing of macrophages and full virulence in a mouse model of Legionnaires’ disease.

Finally, secreted phospholipases connect Legionella virulence to host lipid

Interruption of gyrase activity by quinolones

zithromycin inhibits bacterial protein synthesis by binding to the 50S ribosomal

egionellagrows bestin warm water that is not moving or that does not have enough disinfectant to kill germs.

asons external to the building itself, like nearby constructio

Current or former smokers and people with a chronic lung disease, such as emphysem

) through target-site modification by methylation or mutation that prevents the binding of the antibiotic to its ribosomal target, (2) through efflux of the antibiotic, and (3) by drug inactiva

L. pneumophila8 (14%)00017 (30%)39 (70%)

Rifampin specifically inhibits bacterial RNA polymerase, the enzyme responsible for DNA transcription, by forming a stable drug-enzyme complex with a binding constant of 10(-9) M at 37 C. T

binding inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. Erythromycin may be bacteriostatic or bactericidal depending on the organism and drug concentration.

macrolide antibiotic

erythromycin [ĕ-rith″ro-mi´sin] a broad-spectrum antibiotic produced by a strain

iew OriginalDownload .ppt

irect fluorescent antibody (DFA) testing has the ability to provide results in a time frame able to influence clinical management and has a specificity of close to 100% (5). However, DFA is technically demanding and insensitive. As with sputum culture, DFA has limited usefulness when patients cannot produce sputum.

L pneumophila by urinary antigen testing (LPUAT) is a rapid tool for early diagnosis of Legionella infection (6-14). An enzyme immunoassay (EIA) for detecting L pneumophila serogroup 1, which accounts for between 50% and 70% of cases of Legionella p

Sputum culture is favoured by many because it has the ability to detect all species and subgroups of Legionella and has a specificity of 100%

under UV light. Incubated aerobically for 72 hours at 35ºC.

On BCYE and BCYE Selective Agars, colonies of Legionella pneumophila appear white-gray to blue-gray and fluoresce yellow-green under long-wave UV light.

Incubate plates at 35 +/- 2ºC. for a minimum of 3 days. Growth is typically visible after 3-4 days, but may take up to 2 weeks.

nother factor that favors the survival of Legionella in natural or treated waters is its relative resistance to the effects of chlorine and heat; Legionella can find refuge in relatively inhospitable environments such as hot-water tanks.

may appear that we are defenseless against Legionella infection, because the most effective type of host defense shows only very modest bactericidal abilities in vitro. In fact most infections are subclinical, and mortality is low in patients who are not immunocompromised. Similarly, even susceptible experimental animals survive infection unless moderately large doses of bacteria are given. The defense mechanisms probably function better in vivo than in vitro. The action of host defenses may also be additive in vivo. One can construct a scenario by which bacteria are increasingly phagocytosed by cells that do not permit bacterial growth. The net result is a decreasing number of extracellular bacteria and hence a decreased source of infection for a decreasing population of permissive cells. Obsolescent inflammatory cells in the lungs are removed by the mucociliary escalator and expectorated as sputum. Therefore, the infection may begin with a bang, but it ends in most cases with a whimper.

erythromycin and rifampin inhibit the growth of Legionella organisms in infected macrophages, but do not kill the bacteria

tibiotics used to treat the Pennsylvania legionnaires suggests that erythromycin was the most effective agen

The preferred drug for symptomatic Legionella infections is erythromycin. If the patient is seriously ill, it is important to deliver the antibiotic intravenously at first; subsequently, oral therapy may be used. Rifampin is sometimes added as a second antibiotic in seriously ill patients

his medium contains yeast extract, iron, L-cysteine, and α-ketoglutarate for bacterial growth; activated charcoal to inactivate toxic peroxides that develop in the media; and buffer with a pK at pH 6.9, the optimum for growth of Legionella organisms. Addition of albumin to the media may further facilitate growth of species other than L pneumophila. For contaminated specimens such as sputum, antibiotics should be added. Morphologically distinctive bacterial colonies can usually be detected within 3 to 5 days and identified presumptively as Legionella species if the isolated bacteria depend on cysteine for growth. The identification can be confirmed by specific immunologic typing of the isolated bacteria or, in problematic cases, by molecular analysis.

Direct detection of bacterial antigen in clinical specimens is potentially much faster than culturing

Serologic diagnosis

charcoal-yeast extract - α-ketoglutarate medium.

poradic or epidemic, community acquired or nosocomial. There is great geographic variation in the frequency of infection even within communities

air-cooling equipment that generates aerosols.

Aerosols are produced in numerous ways in our environment, from taking a shower to flushing the toilet.

The only documented source of Legionella species is water, particularly the surface waters of rivers and lakes and drinking water.

The classic pathway of the complement system is activated by L pneumophila, enhancing phagocytosis still furthe

Virulence appears to be multifactorial. An outer membrane protein that functions as a metalloprotease and a cytoplasmic membrane heat-shock protein elicit protective immune responses, but are not essential for expression of virulence. A gene that encodes a 29 Kd protein and plays a role in cellular infection has been identified. Mutations of the gene are associated with decreased virulence.

ymptoms of Legionella infection undoubtedly result from a combination of physical interference with oxygenation of blood, ventilation-perfusion imbalance in the remaining lung tissue, and release of toxic products from bacteria and inflammatory cells. Bacterial factors include a protease that may be responsible for tissue damage. Cellular factors include interleukin-1, which produces fever after it is released from monocytes, and tumor necrosis factor, which may be responsible for some of the systemic symptoms.

Leaky capillaries allow the transudation of serum and deposition of fibrin in the alveoli. The result is a destructive pneumonia that obliterates the air spaces and compromises respiratory function

The bacteria bind to alveolar macrophages via the complement receptors and are engulfed into a phagosomal vacuole. However, by an unknown mechanism, the bacteria block the fusion of lysosomes with the phagosome, preventing the normal acidification of the phagolysosome and keeping the toxic myeloperoxidase system segregated from the susceptible bacteria. The bacilli multiply within the phagosome. Thus, a cellular compartment that should be a death trap instead becomes a nursery. Eventually, the cell is destroyed, releasing a new generation of microbes to infect other cells.

Person-to-person transmission has never been demonstrated, and Legionella is not a member of the bacterial flora of humans.

Important antigens include outer membrane proteins, some of which are species specific antigens, and the lipopolysaccharide that is the major serogroup specific antigen.

rimary growth factor required is L-cysteine, a nutrient that is also essential for Francisella tularensis. Ferric iron is also essential, and other compounds are necessary for optimal growth. Energy is derived from amino acids rather than carbohydrates.

fastidious only in regard to the media commonly used in laboratories

Gram-negative bacilli

Bacteremia occurs during Legionella pneumonia, and symptomatic infection outside the lungs occasionally develops

acute pneumonia, which varies in severity from mild illness that does not require hospitalization (walking pneumonia) to fatal multilobar pneumonia. Typically, patients have high, unremitting fever and cough but do not produce much sputum. Extrapulmonary symptoms, such as headache, confusion, muscle aches, and gastrointestinal disturbances, are common. Most patients respond promptly to appropriate antimicrobial therapy, but convalescence is often prolonged (lasting many weeks or even months).

infections are primarily respirator

drug of choice is erythromycin

method is culturing on special charcoal-containing agar.

Disease may be sporadic or epidemic and may occur in the community or in hospitals. People with compromised host defenses are at increased risk.

most common presentation of Legionella pneumophila is acute pneumonia

L. pneumophila is divided into 15 serogroups, among which serogroup 1 is the most prevalent disease-causing variant

k available

Footrot and Foot Abscess of Ruminants

penicillins remain the treatment of choice in most cases of LS, cephalosporins (such as cefoxitin and cefotetan), metronidazole, or clindamycin monotherapy can sometimes be used as first-line drugs owing to the rare emergence of penicillin-resistant strains with β-lactamase activity

acyclines inhibit bacterial protein synthesis by blocking the attachment of the transfer RNA-amino acid to the ribosome. More

he association between erythromycin and the ribosome is reversible and takes place only when the 50 S subunit is free from tRNA molecules bearing nascent peptide chains. Gram-positive bacteria accumulate about 100 times more

considered to be a commensal of the human upper respiratory tra

Some older studies report on beta-lactamase-producing strains of Fusobacterium isolates

cteriacarryingatetracyclinemodifi-cationresistancegeneproducea44-kDaenzymethatchemicallymodifiestetracycline(T)toaninactiveform

cytoplasmicproteininteractsorassociateswiththeribosome,makingitinsensitivetotetra-cyclineinhibitio

Bacteriacarryinganeffluxtypeofresistancegeneproduceacytoplasmicmembraneprotein(rectan-gularbox),whichpumpstetracyclineo

binding

nhibiting bacterial protein synthesis at the level of the 50S ribos

selectively toxic effect of nitroimidazole drugs towards anaerobic bacteria and protozoa depends on a number of factors.

Beta-lactams

nhibiting the transpeptidase that catalyzes the final step in cell wall biosynthesis,

Figure 2.

35 °C

olation of F. necrophorum from cerebral abscess pus was successful only for the portion of sample inoculated immediately into semisolid medium which had been gassed out.

characteristic morphology should be known to all microbiologists and should immediately suggest the diagnosis of necrobacillosis and guide the treatment.”

volatile fatty acid profile containing a single major peak of butyric acid (with minor peaks of acetic and propionic acid) is highly indicative of a member of the genus Fusobacterium (49). Unfortunately, these days it is rare for a routine diagnostic

of neck pain and sometimes s

Lipopolysaccharide is an important virulence factor

Leukotoxin

Unfortunately, the relevance of the work to human necrobacillosis is limited

cquired immunity might play a role in determining the age-related decline in disease incidence

a break in the mucosa was required to allow entry

thought that the majority of cases of postanginal sepsis originated in abscesses which were found in the proximity of the tonsil and that these pus collections spread deeper into the loose connective tissue of the pharynx and attach themselves to the walls of the veins, producing purulent periphlebitis and endophlebitis

Erythromycin resistance is common in F. necrophorum

male preponderance

0/12 patients were aged between 18 and 29 years. This has been a consistent observation in all later series (Table ​(Table4).4). In the current case series, of 222 cases fitting the Lemierre's syndrome case definition, the median age was 19 years and 89% of patients were aged 10 to 35 years.

o convincing culture evidence exists to confirm that F. necrophorum is a part of the normal oral flora.

ta and concluded that F. necrophorum was probably a normal inhabitant of the mucous membranes of humans and commented that “the fact that B. necrophorum has not been found in the normal colon does not indicate that it is not present here but probably that it is present in insufficient numbers to be detected.” I am

e it binds the CD14/TLR4/MD2 receptor complex in many cell types, but especially in monocytes, dendritic cells, macrophages and B cells, which promotes the secretion of pro-inflammatory cytokines, nitric oxide, and eicosanoids.[15]

LPS is secreted

(PMNs)

major virulence factor is leukotoxin

enicillin remains the drug of choice because most Fusobacterium infections have in vitro sensitivity to penicillins but not to macrolides

mall percentage of theformer may progress to IFND and become severely il

There is a paucity of susceptibility data in the literatureon which to base empirical treatment. However, resistanceto metronidazole has never been reported and susceptibilitydata from 100 human isolates ofF. necrophorumsubmittedto the UK ARL identified 15% resistance to erythromycin,with 2% resistance to penicillin and 1% resistance totetracycline. There was no resistance to metronidazole, co-amoxiclav, chloramphenicol, cefoxitin, clindamycin orimipenem[36]. The level of 15% resist

ot been possible to conductstatistically valid trials to evaluate optimum treatmentregimens. C

real-time PCR

strict anaerobic protocols paying particularattention to minimise the exposure to air of recentlyinoculated agar plates. It is important not to expose micro-colonies ofF. necrophorumto air after overnight incuba-tion; preferably they should have 48 h uninterruptedincubation. In mixed culture, colonies ofF. necrophorummay easily be overlooked particularly by staff unfamiliarwith their typical appearance.

recent study of 248 throat swabs examinedat the University College Hospital in London. This studyfoundF. necrophorumin 10% of patients with sore throats,second only to the incidence of Group A streptococci

lite that can be rapidly detected direct from colonieson an agar plate by using the spot indole reagentp-dimethylcinnamaldehyde. Another readily detectable fea-ture ofF. necrophorumis the production of lipase on anagar medium sup

fFusobacterium necrophorumpleomorphis

our, smooth or umbonate, round andentire with an odour redolent of over-

Basic blood agar medium is usually insufficient andrequires additional supplementation with vitamin K,haemin and menadion

Such a result is available after a15 min assa

s–liquid chromatography(GLC

is very unlikely that it would berecognised by this characteristic alone

necrophorumis a shortcocco-bacillus with occasional very long fil

Severalreports stress that inappropriate antibiotics at this stagecould seriously compromise clinical outcome

markedly in favour of youngadults in the 16–23 years age band and many other studieshave reported a similar peak incidence in teenagers andyoung adults.

Referrals ofF. necrophorumto UK Anaerobe ReferenceLaboratory 1992–2004