ss developed countries who have yet to implement these screening procedures continue to have higher rates of transmission

ecrease the frequenc

blood prior to 1990 at risk for contracting HCV

frequent screening vital to controlling the virus (S

80% of intravenous drug users (I

demographic factors

effects

HCV is typically spread from person to person by blood to blood contact, where the most common risk factors for contracting the virus are IV drug use and receiving a blood donation before 1990 (Lauer 41). There is also a risk of infection through sexual contact and needle sticks in the healthcare setting but these modes of transmission have a much lower rate of infection as compared to the other ways of spreading the virus (Lauer 41). Upon entering a newly infected host, HCV infects the liver when the envelope of the virus binds to receptors on the surface of the hepatocytes (Tang and Grisé 53). This causes endocytosis into the cell, which under the current understanding results in the pumping of hydrogen ions into the newly formed vesicle (Tang and Grisé 55). The acidification of this vesicle degrades the envelope and releases the RNA into the cytoplasm of the cell. From here it is translated and replicated creating new virus particles (Tang and Grisé 55).The large majority of people infected with HCV will develop viremia (74-86%), or the presence of virus within the bloodstream, and most of these individuals will go on to present with hepatic inflammation or fibrosis (Lauer 43). This involves swelling of the liver and addition of connective tissue to as a result of the trauma caused by the presence of the virus respectively. However, upon acute infection, individuals do not often present with symptoms, and can go as long as 30 years before showing signs of infection (Lauer 43). For this reason, it has been extremely difficult for researchers to track the history of the disease.

ntering a newly infected host, HCV infects th

to the other ways of spreading the vir

HCV is typically spread from person to person by blood to blood contact, where the most common risk factors for contracting the virus are IV drug use and receiving a blood donation before 19

Overview of Hepatitis C Virus

CV) is a member of the flaviviruses meaning it is composed of an envelope surrounding one continuous segment of RNA that codes for a single protein that is later processed to form all of the proteins needed by the virus (Lauer 42). T

fairly significant prevalence

Hosts that can carry the influenza virus are humans, horses, pigs, along with many avian species4. Many of the common influenza reservoirs that carry human infectious subtypes are either huma

n

tems the flu can cause death.

flu vaccine h

In humans influenza viruses are located in a person’s respiratory tract2. The most common portal of exit is by coughing or sneezing4. Direct contact, fomites, airborne, or transfer of bodily fluids are all modes of transmission for the influenza virus. This virus is easily spread and can be spread over a long period of time4. Adults can spread the virus for 3 to 5 days while children can spread it for up to 7 days4. Influenza enters the human body through the respiratory tract and its ultimate location depends on what kind of influenza it is. Human to human influenza infects the upper respiratory tract while avian influenza infects the lower respiratory tract. Once infected a person develops symptoms such as fever, sore throat, body aches, coughing, headaches, fatigue, along with vomiting and diarrhea5.

In humans influenza viruses are located in a person’s respiratory tract2. The most common portal of exit is by coughing or sneezing4. Direct contact, fomites, airborne, or transfer of bodily fluids are all modes of transmission for the influenza virus. This virus is easily spread and can be spread over a long period of time4. Adults can spread the virus for 3 to 5 days while children can spread it for up to 7 days4.

ducks, geese, and shorebirds

proteins

Spanish influenza, Asian influenza, and Hong-Kong influenza

mong humans

mainly strain A

greater

people each yea

Themostcommonmechanismofhigh-levelfluoroquino-loneresistanceisduetomutationinoneormoreofthegenesthatencodetheprimaryandsecondarytargetsofthesedrugs,thetypeIItopoisomerases(gyrA,gyrB,parC,andparE).TheregionwheremutationsariseinthesegenesthatencodefluoroquinoloneresistanceisashortDNAsequenceknownasthequinoloneresistance-deter-miningregion(QRDR)[28,29].MutationsintheQRDRofthesegenes,resultinginaminoacidsubstitutions,alterthetargetproteinstructureandsubsequentlythefluoroquin-olone-bindingaffinityoftheenzyme,leadingtodrugresis-tance[30,31].

The ribosomal protection proteins have homology to elongation factors EF-Tu and EF-G (259, 292). The greatest homology is seen at the N-terminal area, which contains the GTP-binding domain. The Tet(M), Tet(O), and OtrA proteins reduce the susceptibility of ribosomes to the action of tetracyclines. The Streptomyces Otr(A) protein has greatest overall amino acid similarity to elongation factors.

being from the first outbreak in 1967

rotein-rich liquid that separates out when blood coagulates, called serum,

low blood pressure (

immediately

almost anyone

mmon in laboratories

the plasma membrane of the infected host cell (M

What is the Marburg virus?

Neisseria (N.) gonorrhoeae, the bacteria that cause the STD gonorrhea, has developed resistance to nearly all of the antibiotics used for gonorrhea treatment:  sulfonilamides, penicillin, tetracycline, and fluoroquinolones, such as ciprofloxacin.

The role of group G β-hemolytic streptococci (GGS) as significant human pathogens has been firmly established during the past 15 years. These organisms are normal inhabitants of the skin, oropharynx, and gastrointestinal and female genital tracts. Although cutaneous infections and pharyngitis are encountered most often, a wide variety of infections—including potentially life-threatening ones, such as septicemia, endocarditis, meningitis, peritonitis, pneumonitis, empyema, and septic arthritis—have been described.1

Streptococcal Infections

GGS

Overview

les virus s

ted with measles

s after the primary infection.

symptoms heightening wi

long

short

The measles virus is a spherical, envelope, non-segmented single stranded RNA virus that is member of the Morbillivirus genus and the Paramyxoviridae family. This virus contains approximately 16000 nucleotides and encodes for eight proteins (155). When first entering into the person the virus first comes into contact with the lung tissue where it attacks the immune system and its associated cells. These cells are macrophages and dendritic cells which serve as an early defense and warning system. From the lungs the virus migrate to the lymph nodes which contain B and T cells. The virus contains cell receptors CD26 and CD150 (SLAM) which are help to signal the lymphatic system into action. CD46 is a regulatory molecule found on cells with nucleus in the human body while SLAM can be found on active T and B lymphocytes (155). SLAM is also found on the surface on white blood cells and this functions as the point of entry. The virus then takes some of the host cell’s membrane to make its envelope allowing the virus to hide from the immune system. These infected T and B cells then migrate throughout the body thus infecting the whole body with the measles disease (156).

n areas which are densely populated with low vaccination coverage the virus primarily affects infants and young children.

153

ancestral zoonotic

OVERVIEW

s of January and M

outbreak,

Pteropus hypomelanus, P. vampyrus, Cynopterus brachyotis, Eonycteris spelaea, and an Insectivorous bat, Scotophilus kuhlii.

Pteropus

e same genus

es 3-14 days after infection

attention

1999

C5a peptidase

patient receives

8 to 10 days

general malaise

showing symptoms

Ro

sexual activity

direct parental transmission

EVB

contraction

or their blood

70 percent of infected persons died from Ebola.

wild animals

Erythromycin interferes with aminoacyl translocation, preventing the transfer of the tRNA bound at the A site of the rRNA complex to the P site of the rRNA complex

capsule of organisms such as B fragilis

collagenase, neuraminidase, deoxyribonuclease, deoxyribonuclease [DNase], heparinase, and proteinases)

A large amount of butyric acid in the absence of isobutyric or isovaleric acid indicates the presence of Fusobacterium.

Fusobacteria necrophorum produces a leukocidin and hemolyses erythrocytes of humans, horses, rabbits, and, much less extensively, sheep and cattle. Certain F necrophorum cells hemagglutinate the erythrocytes of humans, chickens, and pigeons. A bovine isolate of F necrophorum demonstrates phospholipase A and lysophospholipase activity.

Cells of F necrophorum often are elongated or filamentous, are curved, and possess spherical enlargements and large, free, round bodies.

1 Human diseases

Isolation and identification of N. gonorrhoeae

Spectinomycin Resistance

uoroquinolone resistance (53.2%) in Neisseria gonorrhoeae

. These data suggest that large noncharged amino acids alter the rRNA structure near the tetracycline-binding site, leading to a lower affinity of the antibiot

Metronidazole is reduced to disrupt energy metabolism of anaerobes by hindering the replication, transcription and repair process of DNA results in cell death. Presence of oxygen prevents reduction of metronidazole and so reduces its cytotoxicity.

In order to establish infection, the bacteria need to escape the host immune response, and in streptococci, a varied arsenal of bacterial strategies have been described. The M-protein aids in immune evasion by inhibiting phagocytosis and inactivating the complement system.[1] Furthermore, Streptococcus dysgalactiae possesses Protein G, a virulence factor binding circulating immunoglobulins, and thus interfering with the host antibody response.[49] DrsG, a virulence protein abrogating the effect of antimicrobial peptides secreted by human immune cells, is also harboured by a subset of SDSE-strains.[50][51]

It is important that testing first be performed to determine that the organism is in the Streptococcus genus. Only group A streptococci and group D enterococci are PYR-positive. Other streptococci are negative; however additional testing, using a pure culture, may be necessary to separate group A streptococci (S. pyogenes) from beta-hemolytic enterococci.

INTERPRETATION OF RESULTS A bright pink or cherry red color will appear within one minute if the test is positive. A negative test is indicated by no color change. The development of an orange, salmon, or yellow color should be interpreted as a negative reaction. Organisms expected to give a positive result: Group A streptococci (Streptococcus pyogenes) Group D enterococci (Enterococcusspp.) Coagulase-negative Staphylococcus spp.: haemolyticus, lugdunensis and schleiferi Citrobacter, Klebsiella, Yersinia, Enterobacter and Serratia spp.

Traditionally, streptococci are classified by the use of Lancefield group antigens and by hemolysis on blood agar. Lancefield group antigen does not correlate with the species. Classification by hemolysis is imprecise. The molecular taxonomic studies have improved classification. The beta-hemolytic isolates under Lancefield group A, C, F, and G are subdivided into large and small colony forming groups. The large colony groups possess numerous virulence mechanisms, and are labeled "pyogenic". Large colony group C streptococci are usually resistant to bacitracin. This is the method used by many clinical laboratories from Group A Streptococci (GABHS) in many clinical laboratories. However, some Group C Streptococci (GCS) are susceptible to bacitracin and may result in misidentification if Lancefield serologic typing is not performed. Among the Group G streptococci (GGS), Bacitracin susceptibility has been reported to be as high as 67% (87). Trimethoprim/sulfamethoxazole (SXT) disk testing has been added to improve in the identification. Both GCS and GGS are susceptible and GABHS are resistant. For specific identification, a serogrouping reagent is used. The large colony Lancefield GCS are variably classified into some of several possible species, namely, S. dysgalactiae, S. equisimilis, S. zooepidemicus, and S. equi (36). These species can be differentiated by microbiological and biochemical characteristics. All but S.dysgalactiae commonly cause beta-hemolysis in blood agar. S. equisimilis is the most common GCS to cause infection in humans but may also infect domestic animals. The other species primarily infect animals. Most clinical laboratories do not speciate GCS isolates.

Most patients reported with GCS and GGS infections have received apenicillin or cephalosporin (often with an aminoglycoside). Small numbers of patients have been treated with other antimicrobial agents (vancomycin, erythromycin, clindamycin, or chloramphenicol). On the basis of in vitro data as well as reported clinical experience, penicillin G is the preferred antibiotic (8, 10, 13, 43, 75, 87, 89). Alternative agents with relatively uniform activity include ampicillin, cefotaxime,imipenem, and vancomycin. In vitro testing should be performed if clindamycin or the macrolides are considered for therapy in light of the recent reports of resistance to these agents.

Strain Identification to the Species and Subspecies Levels

linical features of upper respiratory tract infection and pyogenic pharyngitis as well as colony counts were tabulated for each patient according to throat culture results.

rare emergence of penicillin-resistant strains with β-lactamase activity

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

Fusobacterium is ubiquitous in the normal flora of the oropharyngeal, gastrointestinal, and genitourinary tracts of healthy humans.

Additional physical findings included a temperature of 38.6°C,

chills and sweats

All isolates were susceptible to penicillin and levofloxacin, 6 (26.1%) showed resistance or reduced susceptibility to erythromycin [1 mef(A), 3 erm(TR), 1 mef(A)+erm(TR) and 1 erm(TR)+erm(B)] and 7 (30.4%) were resistant or exhibited reduced susceptibility to tetracycline [2 tet(M), 5 tet(M)+tet(O)]. The prevalence in Argentina was of at least 23 invasive infections by SDSE. A wide genetic diversity was observed. All isolates carried speJ and ssa genes. Similarly to other studies, macrolide resistance (26.1%) was mainly associated to the MLSB phenotype.

-/- Other Enzymes: Esculinase -, lipase -, Tryptophanase + (= indole +).

Smells like rancid butter (or boiled cabbage).

All the F. necrophorum strains were susceptible to penicillin and metronidazole. Susceptibility was usually read within 24 h.

7.4 ± 0.1.

selective agar

5% H2, 10% CO2 and 85% NO2

obligate anaerobe pleomorphic rod

where it may account for more than 20% of acute pharyngitis

RECOMMENDED MEDIA For culture: Brain Heart Infusion (BHI) Agar, Chocolate Agar, Brucella with H & K Agar, Cooked Meat Medium, Thioglycollate Broth with Supplements, and complex media containing peptone promotes optimum growth. For selective isolation: LKV Agar or BBE Agar. For maintenance: Cooked Meat Medium, Thioglycollate Broth with Supplements, Brucella Agar with H & K, or Brain Heart Infusion (BHI) Agar. Skim Milk Media may be used for long-term storage at -70 degrees C. INCUBATION Temperature: 35 degrees C. Time: 48 hours. Atmosphere: Anaerobic with 5% CO 2 . pH: Near 7.

Catalase-variable. Lipase-negative. Indole-variable. Esculin-hydrolysis-negative. Mannose, Lactose, Fructose, and Glucose production from fermentation positive for F. mortiferum . Mannose production from fermentation positive for F. varium . Mannose, Lactose, Fructose, and Glucose production from fermentation negative for F. necrophorum and F. nucleatum . Metronidazole-sensitive.

Virulence Factor

invasion of host cell barriers such as the epithelial and endothelial cells

OUTER MEMBRANE CONSTITUENTS ASSOCIATED WITH GONOCOCCAL VIRULENCE

thoseharboringgroupBweremorelikelytohaveenlargedtonsils(P<0.001),exudate(P<0.02),andtenderenlargedanteriorcervicallymphnodes(P<0.01)

DetectionofGBScanbe determined directly from broth media using latex agglutination, probes or nucleic acid amplification tests (NAAT) such as PCR

Procedures for processing clinical specimens for culture of group B Streptococcus (GBS) (s

Group B strep disease is usually treated with penicillin or other common antibiotics

gastrointestinal tract (the part of your body that digests food, including the stomach and intestines) of men and women and may be a source of some infection.

Pneumonia(https://www.cdc.gov/pneumonia/index.html) (lung infection) symptoms include: Fever and chills Cough Rapid breathing or difficulty breathing Chest pain

Asymptomatic carriage in gastrointestinal and genital tracts is common. Intrapartum transmission via ascending spread from the vagina occurs. Mode of transmission of disease in non-pregnant adults is unknown.

Neurologic sequelae include sight or hearing loss and cerebral palsy. Death occurs in 5% of infants and adults.

S. pneumoniae cultures are α-hemolytic on blood agar medium

Gram-Positive, Catalase-Negative Genera

A clearing of the turbidity in the bile tube but not in the saline control tube indicates a positive test, i.e., the pneumococcal cells have lysed ("solubilized").

. The group C antigen is found with several different species and the S. anginous group of bacteria, Table 2, page 67. Group G streptococci: The ß-hemolytic streptococci with group G antigen have not had an official taxonomic name. Some have suggested that these strains be called S. canis but this has not gained approval officially or in practical use. ß-hemolytic streptococci with group G antigen should be reported simply as Lancefield's group G streptococci.

Gram-Positive, Catalase-Negative Genera Streptococcus, GPC-ChainsBeta hemolytic

Resistance of Group B Streptococcus to Selected Antibiotics, Including Erythromycin and Clindamycin

Concerns about potential antibiotic tolerance in GCS and GGS and reports of clinical failures in patients with severe infections have led many authors to recommend combination therapy for synergy (aminoglycoside plus a cell wall-active agent) in the initial treatment of these patients (1, 17, 18, 27, 28, 31, 33, 35). Our in vitro findings suggest that among high-risk patients with invasive GCS and GGS infections who cannot be treated with penicillin, tolerance of other antimicrobial agents, including vancomycin, should be closely monitored.

The majority of GCS and GGS strains demonstrate in vitro susceptibility to penicillins, vancomycin, erythromycin, and cephalosporins (3,30). Antimicrobial tolerance, defined as a minimum bactericidal concentration (MBC) 32 or more times higher than the MIC, among GCS and GGS has been reported for penicillin and other agents (24, 27,29).

Up to 90 percent of pharyngeal gonorrhea in men and women may be asymptomatic

The oxidase test uses the tetramethyl derivative of the oxidase reagent

The catalase test (3% hydrogen peroxide) or superoxol (30% hydrogen peroxide) are other rapid tests used in the presumptive identification of N gonorrhoeae. A drop of the reagent is placed in the centre of a clean glass slide and the suspect colony is picked with a loop and emulsified in the reagent. N gonorrhoeae will produce a positive reaction with bubbling within 1 s to 2 s. Weak bubbling or bubbling after 3 s indicates a negative reaction (5) (Table ​(Table2).2).

The inoculated plates should be incubated at 35°C to 37°C in a moist atmosphere enriched with CO2 (3% to 7%) (5). An 18 h to 24 h culture should be used as the inoculum for additional tests. Plates should not be incubated for longer than 48 h because most old cultures would not survive storage conditions.

intracellular Gram-negative kidney-shaped diplococci in polymorphonuclear leukocytes

The laboratory diagnosis of Neisseria gonorrhoeae

ceftriaxone in a single 125-mg dose intramuscularly or ciprofloxacin (Cipro) in a single 500-mg dose orally,

usually do not cause adverse sequelae

Symptoms

cteriacarryingatetracyclinemodifi-cationresistancegeneproducea44-kDaenzymethatchemicallymodifiestetracycline(T)toaninactiveform

cytoplasmicproteininteractsorassociateswiththeribosome,makingitinsensitivetotetra-cyclineinhibitio

Bacteriacarryinganeffluxtypeofresistancegeneproduceacytoplasmicmembraneprotein(rectan-gularbox),whichpumpstetracyclineo

Penicillin kills susceptible bacteria by specifically inhibiting the transpeptidase that catalyzes the final step in cell wall biosynthesis, the cross-linking of peptidoglycan.

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

only actively multiplying cells are susceptible to bactericidal effects of the antibiotic,

inhibit bacterial cell wall synthesis, and interact with penicillin binding proteins, leading to bacterial lysis.

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

Streptococcal bacteria use an enzyme called streptokinase to block the blood clotting response and allow themselves to move more freely around the human host's circulatory system.

M protein

directly to the cell surface or components of surface structures, e.g., pili projected away from the confines of the cell wall. The protein subunits of pili may themselves mediate adherence, or they may carry the adhesins along their lengths or at their tips. The specificity of microbial adherence is often associated with protein-carbohydrate (lectin-like) reactions.

These are usually proteins that recognize specific receptors, often sugars or oligosaccharides, expressed at various body sites. The keratinized epithelial cells at the buccal mucosal surface display different receptors from, for example, those present within the salivary pellicle formed on the tooth surface. This provides selectivity for the adherence of different streptococcal species

Although deep infections can easily be treated with antibiotics, we know that some people can die from this type of infection, especially when the bacteria have spread into the bloodstream (bacteremia).

group C and G streptococci most commonly live on animals such as horses and cattle and can spread to humans through raw milk or contact with animals. However, both types can live in people’s throats and probably spread like the group A strep. F

Usually group C pharyngitis affects an older population, particularly teenagers and young adults. Several studies have demonstrated that group C streptococci are a relatively common cause of acute pharyngitis among college students and among adults seeking care in an emergency room

Although a group C streptococcus has a prevalence of less than 5% in adult pharyngitis patients,

rapid streptococcal antigen test and monospot test were negative

complaining of sore throat, high fever, and neck swelling

Severe Acute Pharyngitis Caused by Group C Streptococcus

Ampicillin is an acceptable alternative, but penicillin is preferred because it has a narrower spectrum of antimicrobial activity and may be less likely to select for resistant organisms.

Serious group B strep infections in adults can be fatal. On average, 8% of adults with invasive group B strep infections (infections where the bacteria have entered a part of the body that is normally not exposed to bacteria) die. Risk of death is lower among younger adults, and adults who do not have other medical conditions.

If infection is discovered to be caused by F. nucleatum or F. necrophorum, treatment should be started promptly as these two species have been linked to deaths as a result of severe cases of Lemierre’s disease

SURVIVAL OUTSIDE HOST: Fusobacteria have been known to persist in soil for up to 18 weeks (16). They survive well in wet soil with high manure content (17), however, studies of aerated fecal slurry showed that the levels of Fusobacterium were below the level of detection after 24 hours (18). In non-aerated fecal slurry, no change in Fusobacterium levels were observed in the first 24 hours, and Fusobacteria were no longer present after 6 days. Survival on BHIA medium exposed to air ranges from six hours to seven days depending on species

RUG RESISTANCE: Fusobacterium may be resistant to penicillin and there is widespread resistance to erythromycin and other macrolides

Metronidazole, piperacillin/tazobactum, ticarcillin/clavulanate, amoxicillin/sulbactum, ampicillin/sulbactum, ertupenem, imipenem, meropenem, clindamycin, and cefoxitin are all used therapeutically to treat infections associated with Fusobacterium (6, 10)

ZOONOSIS: Yes - Fusobacterium can be passed to humans from animal bites or handling of animals with open sore

RESERVOIR: Humans and animals, including horses, cattle, sheep, cats, dogs, goats, pigs, cows

Infections can occur by contact with mucous membranes as well as accidental inoculation and transfer of bodily fluids

HOST RANGE: Humans and animals, including horses, cattle, sheep, goats, pigs, fowl

It is also associated with Lemierre disease, which presents as acute jugular vein septic thrombophlebitis, often with complications including sepsis, and metastastic abscesses in the lungs, liver, joints and pleural spaces.

these two species have been linked to deaths as a result of severe cases of Lemierre’s disease.

Fusobacterium can be transmitted from human-to-human by bite wounds (8). There is also some evidence that Fusobacterium can be transferred in bodily fluids (6).

Infections can occur by contact with mucous membranes as well as accidental inoculation and transfer of bodily fluids

Infections may occur after surgical or accidental trauma, edema, anoxia, tissue destruction, and animal bites

difficult to culture, requiring a longer incubation period than other bacteria.

he mean duration of antibiotic treatment was 4 weeks, but it ranged from 10 days to 8 weeks.

Over 10% of non-group A beta-hemolytic streptococci (groups C and G) can also show sensitivity.

Pathogenicity

Detection of the organism by polymerase chain reaction in the study does not prove that fusobacterium is the cause of the pharyngitis, especially since it’s found in a not insignificant proportion of asymptomatic individuals (9%).

Most pharyngitis is causes by respiratory viruses. There is no way to detect fusobacterium as a cause of pharyngitis in clinical practice

From the perspective of patient management, there are two interpretations circulating about this paper — one that it encourages antibiotic prescribing, the other that it does no such thing.

F. necrophorum contains particulary powerful endotoxic lipopolysaccharides in its cell wall and produces a coagulase enzyme that encourages clot formation. Additionally, it produces a variety of exotoxins, including leukocidin, hemolysin, lipase, and cytoplasmic toxin, all of which likely contribute to its pathogenicity.

The species is generally susceptible to penicillin, clindamycin, and chloramphenicol and resistant to erythromycin and macrolides.

normal inhabitants of all mucosal surfaces, including the mouth, upper respiratory tract, gastrointestinal tract, and urogenital tract

Table 1.   Identification of F. necrophorum   Indole  Positive   Lipase  Positive   Hydrogen sulfide  Negative   Catalase  Negative   Esculin  Negative   Catalase  Negative

characterized by slender or fusiform rods with tapered ends, though some species may be pleomorphic

leukotoxin and endotoxin are believed to be more important than other toxins in overcoming the host's defence mechanisms to establish the infection.

Several toxins, such as leukotoxin, endotoxin, haemolysin, haemagglutinin and adhesin, have been implicated as virulence factors.

It is hard to differentiate a viral and a bacterial cause of a sore throat based on symptoms alone.[25] Thus often a throat swab is done to rule out a bacterial cause.

Fusobacterium necrophorum is a normal inhabitant of the oropharyngeal flora and can occasionally create a peritonsillar abscess. In 1 out of 400 untreated cases, Lemierre's syndrome occurs.

Lemierre's syndrome occurs most often when a bacterial (e.g. Fusobacterium necrophorum) throat infection progresses to the formation of a peritonsillar abscess. Deep in the abscess, anaerobic bacteria can flourish. When the abscess wall ruptures internally, the drainage carrying bacteria seeps through the soft tissue and infects the nearby structures.

treatment with penicillin or metronidazole, but penicillin treatment for persistent pharyngitis appears anecdotally to have a higher relapse rate, although the reasons are unclear.

Pathogenicity

sore throats

rod-shaped species of Gram-negative bacteria. It is an obligate anaerobe

common inhabitant of the alimentary tract within humans and animals.

Presumptive diagnosis of gonorrhea is made on the basis of one of the following three criteria:typical gram-negative intracellular diplococci on microscopic examination of a smear of urethral exudate from men or endocervical secretions from women*;growth of a gram-negative, oxidase-positive diplococcus, from the urethra (men) or endocervix (women), on a selective culture medium, and demonstration of typical colonial morphology, positive oxidase reaction, and typical gram- negative morphology;detection of N. gonorrhoeae by a nonculture laboratory test (Antigen detection test (e.g., Gonozyme [Abbott]), direct specimen nucleic acid probe test (e.g., Pace II [GenProbe]), nucleic acid amplification test (e.g., LCR [Abbott]).

DRUG SUSCEPTIBILITY:

cultured anaerobically,