0.6 cases per million per year. These data also show a rise inthe number of cases in 1999 over previous year

eral indicators suggest the incidence is rising particu-larly in the UK and efforts to curb the spread ofantimicrobial resistance, whilst well intended, may haveinadvertently led to a resurgence in this severe dise

1990–1995 and reported a combinedincidence of 2.3 cases per year per million person

ung abscesses often multiple in natureare a common sequelae t

101–1031F

utative virulencefactors are haemagglutinin, and haemolysin but little isknown about their actual role in pathogenesis

attle, sheep and wallabies

classical endotoxi

Severalvirulence mechanisms ofF. necrophorumhave beendescribed and probably the best understood of these isthe endotoxic lipopolysaccharide (LPS) in the cell wall

ncrease in the penetration of bacteria intothe tonsillar epithelium during cases of infectious mono-nucleosis and associations of IFND with Epstein Barr virusand the primary sore throat are due to reports of theMonospot or Paul–Bunnell tests for heterophile antibodybeing positive.

ted in textbooks thatF. necrophorumis acommensal in the human oro-pharynx but the actual hardevidence for this in the literature is conspicuously absent

ressed the need for anaerobic blood cultures

ram stained material from this patientshowed long threadlike Gram-negative bacil

calf diphtheria

factors that trigger the invasive process are not fullyunderstood.

usobacterium necrophorum was detected in 20.5% of patients and 9.4% of asymptomatic students

naerobic bacterium requiring special methods to grow it in a lab.

For an infection caused by F. necrophorum, aggressive therapy with antibiotics is appropriate, as the bacterium responds well to penicillin and other antibiotics

which in our study caused more sore throats than strep

6 percent of those contracting the Lemierre’s syndrome die.

a thrombophlebitis of tonsillar veins to the internal jugular vein and thence to septicemia and metastatic abscesses, and

evere pyrexial attack

tonsillar abscess

The ability to stimulate clot formation and multiply in the clot with subsequent embolic spread is clearly a fundamental feature of the pathogenesis of F. necrophorum infection.

dentified a thin gram-negative rod with filamentous forms at the border between the sound and necrotic tissues in stained sections of diphtheritic

virulence

persistent or recurrent tonsillitis

al infection begins in the oropharynx then spreads through the lymphatic vessels. Following this primary infection, thrombophlebitis (swelling) of the internal jugular vein (IJV) develops. The final phase of the disease occurs when septic emboli (pus-containing tissue) migrate from their original location in the body to various organs. The lungs are most co

90% of cases, Lemierre syndrome is caused by Fusobacterium necrophorum;

bacteria typically responsible for this disease is Fusobacterium necrophorum, a

am positive cocci in pairs and short

eutropenic patients with VGS bacteremia.

Dextran production results in glycocalyx deposition that promotes adherence

eptococci can be isolated from the blood, blisterfluid and from cultures of the infe

acteraemia is regu-larly seen in patients with necrotizing fascii

cytokines

ultivation of non-fastidious bacteria

Despite the overall low virulence, they may cause infective endocarditis, contribute to polymicrobic abscess, and invade the bloodstream during the state of neutropenia.

Viridans streptococci represent a group of 24 currently described Streptococcus species that are nutritionally fastidious

approximately 10% of viridans streptococci are bile-esculin positive.

ble 2. Pathogens associated with necrotizing fasciiti

led to attempts to treat such patients with higher doses of vancomycin

ototoxicity

“slow bactericidal”

red man” syndrome,

Alpha-hemolytic Streptococcus species “Viridans group” streptococci, including species such as the Streptococcus mutans, mitis, and salivarius groups display alpha hemolysis.

Vancomycin inhibits the second stage of cell wall synthesis in susceptible bacteria.

Rapid antigen tests

viridans streptococci are often susceptible to penicillin G and other β-lactams. Resistance is growing, and therapy for such strains should be dictated by results of in vitro susceptibility tests.

Necrotizing fasciitis should be treated in an ICU. Extensive (sometimes repeated) surgical debridement is required. A recommended initial antibiotic regimen is a β-lactam (often a broad-spectrum drug until etiology is confirmed by culture) plus clindamycin. Although streptococci remain susceptible to β-lactam antibiotics, animal studies show that penicillin is not always effective against a large bacterial inoculum because the streptococci are not rapidly growing and lack penicillin-binding proteins, which are the target of penicillin activity.

Shows key test in the differentiation of the virdidans streptoco

A,C,G, F, none

Viridans streptococci: most strains are α-hemolytic on blood agar media, are usually neither susceptible to optochin or bile soluble.

all viridans species are PYR negative

all strains of viridans streptococci have been sensitive to vancomycin

10% of viridans streptococci are bile-esculin positive

Viridans streptococci, mutans group Streptococcus mutans (human plaque) Streptococcus cricetus (rodent plaque, human) Streptococcus downei (monkey plaque) Streptococcus ferus(rodent plaque) Streptococcus macaccae (monkey plaque) Streptococcus ratti(rodent, human plaque) Streptococcus sobrinus(human plaque) Viridans streptococci, oral groupStreptococcus salivarius (human) Streptococcus vestibularius(human) Streptococcus sanguinis(human) Streptococcus parasanguinis(human) Streptococcus gordonii(human) Streptococcus anginosus(human) Streptococcus constellatus(human) Streptococcus intermedius(human) Streptococcus mitis(human) Streptococcus oralis(human) Streptococcus crista(human) Streptococcus infantis(human) Streptococcus perois (human)

viridans Streptococcus, or of unknown identity (basically includes all cultures other than pneumococci, ß-hemolytic streptococci, and nutritionally variant streptococci), inoculate the following media. Inoculate a trypticase soy 5% sheep blood agar plate by streaking a heavy inoculum onto one-fourth of the plate and streak the remaining portion for isolated colonies. Place a vancomycin disk on the heaviest part of the inoculum, and put the plate into a candle extinction jar or a CO2 incubator for 18 to 24 h at 35C.

enicillin susceptibility cannot be assumed

biotic usage drives resistance holds true for VGS, and there are numerous studies that have shown direct correlations between both penicillin and macrolide usage and the development of resistance in VGS.

pyrrolidonylarylamidase negative, and do not grow in 6.5% NaCl, and almost all species are negative for growth on bile esculin agar.

eucine aminopeptidase positive

catalase-negative,

heterogeneous group of organisms that can be both commensal flora and pathogens in humans

GS, the rates and patterns of antimicrobial resistance vary greatly depending upon the species identification and the patient populatio

Treatment includes isolation, rest, and antibiotic therapy

antimicrobials usually chosen empirically for bite wounds

animal bites, scratches or licks. Animals do not have to be ill to pass the bacterium to humans, as they can carry the organism without showing symptoms

meningitis, ocular infections, and respiratory infections, usually in patients with underlying pulmonary disease.

local wound infection

Human infections are usually contracted following exposure to domestic pets such as cats and dogs

avian cholera

Animal bites

Animal bites

super-spreader or whether she was also a super-shedder or possibly both

Nonetheless, it's important scientifically and for people and public health to understand index cases so that we know how diseases are coming into a community and how to stop their spread."