VZV is transmitted through respiratory droplets, direct and indirect contact.

probably involves either endocytosis

being neurotropic

The other anaerobes tested – A. vaginae, M. mulieris, P. bivia, Veillonella, Peptostreptococcus and Peptoniphilus – demonstrated significantly lower biofilm formation relative to G. vaginalis (Student's t-test, P<0.0001).

Analysis of adherence, biofilm formation and cytotoxicity suggests a greater virulence potential of Gardnerella vaginalis relative to other bacterial-vaginosis-associated anaerobes

Many mycoplasmal pathogens exhibit filamentous or flask-shaped appearances and display prominent and specialized polar tip organelles that mediate attachment to host target cells (43,44). These tip structures are complex, composed of a network of interactive proteins, designated adhesins, and adherence-accessory proteins (Figure 1, [14,43]).

Once they attach to a host cell in the body, their unique plasma and protein coating can then mimic the cell wall of the host cell and the immune system can not differentiate the mycoplasma from the body’s own host cell (1).

Trich can cause genital inflammation that makes it easier to become infected with the HIV virus or to pass the HIV virus on to a sex partner.

A health care provider will examine your vagina for signs of vaginal discharge. Your provider can also perform laboratory tests on a sample of vaginal fluid to determine if BV is present.

When 10% ferric chloride is added to phenylalanine deaminase medium inoculated with Proteus mirabilis, the presence of phenylpyruvic acid causes the media to turn dark green.  This is a positive result.

Proteus mirabilisATCC 14153 Growth good to excellent; colonies medium-sized, pale to beige, surrounded by an amber to brown halo; in areas of dense growth, the medium may be completely amber to brown. Swarming is partially to completely inhibited.

Deposited Name:Proteus vulgaris Hauser emend. Judicial CommissionProduct Description: Quality control strainMediumATCC® Medium 3: Nutrient agar or nutrient brothGrowth ConditionsTemperature: 37°CAtmosphere: AerobicPropagation Procedure1. Open vial according to enclosed instructions.2. Using a single tube of #3 broth (5 to 6 mL), withdraw approximately 0.5 to 1.0 mL with a Pasteur or1.0 mL pipette. Rehydrate the entire pellet.3. Aseptically transfer this aliquot back into the broth tube. Mix well.4. Use several drops of the suspension to inoculate a #3 agar slant and/or plate.5. Incubate the tubes and plate at 37°C for 24 hours.Colonies on #3 agar are cream, translucent, circular, low convex, entire, and smooth. Swarming occurs withextended incubation. Cells are motile rods in singles and pairs that vary in size

Contact lens wearers are more prone to bacterial infection, especially with Gram-negative organisms. The contact lens induces hypoxia, increases corneal temperature and decreases tear flow over the corneal surface. The adhering 21 of microorganisms (Staphylococci, Moraxella, Candida) to the contact lens and epithelium 22–24 is aided by mucus and proteins. The risk of developing corneal infections is 9–15 times greater with overnight use of contact lenses compared to daytime use. Aphakic eyes are more prone to microbial keratitis with extended wear soft contact lenses. There is a higher risk of bacterial keratitis with disposable contact lenses used overnight.24 The most common organisms associated with contact lens related bacterial keratitis are Pseudomonas aeruginosa and Staphylococci. Bandage soft contact lenses are more often associated with polymicrobial infections (Staphylococci, Streptococci, Serratia). Extended wear soft cosmetic lenses are more prone to Pseudomonas infections.25While Gram-negative organisms like Pseudomonas, Haemophilus and Moraxella cause infectious keratitis in extended wear cosmetic contact lens users, therapeutic soft contact lens wearers on the other hand are prone to corneal ulcers caused by Gram-positive bacteria especially Streptococci.

Pathophysiology

Selective & Differential Media for Proteus

monella spp. (-) (99)

Salmonella enterica ATCC® 14028 A 24hr 35°C Aerobic Growth; colorless to amber colonies

Salmonella enterica ATCC® 14028 A 24hr 35°C Aerobic Growth; colonies colorless

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

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

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

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

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

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

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

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

Specificity of coloration

LIMITATIONS OF THE METHOD

chromID® Salmonella Media

Salmonella ASAP™ Chromogenic Media

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

High adherence and biofilm formation were positively correlated with bacterial surface hydrophobicity, type 3 fimbriae expression but not with type 1 pili expression and were not dependent upon the strain's origin. The K. pneumoniae CF3051 reference strain expressing only type 1 fimbriae adhered slightly to glass and polypropylene and did not form biofilm on polystyrene. K. pneumoniae IA565 and CF3097 reference strains producing type 1 and type 3 fimbriae showed efficient adherence to both glass and polypropylene and biofilm formation on polystyrene. Moreover, transformation of the afimbriated, weakly-adherent CF3172 strain with the recombinant pFK10 plasmid carrying the mrk gene cluster resulted in type 3 fimbriae expression, increased surface hydrophobicity, increased adherence to abiotic surfaces and biofilm formation. Thus, type 3 pili constitute the main K. pneumoniae adhesive factor, facilitating adherence and biofilm formation on abiotic surfaces of strains of different origins.

The role of the LPS O side chain in bacterium-cell interactions and cytokine production still remains unclear. However, for mo-DCs exposed to LPS-deficient mutants, in particular the ΔwecA strain, which was barely affected in CPS synthesis, a clear increase in cytokine production was observed. It is therefore likely that the LPS O antigen per se plays a specific role in DC activation.

This observation, combined with the decrease in DC-SIGN previously observed, confirmed that K. pneumoniae CPS can impair the host immune response, probably allowing the bacteria to avoid the host defense and thus to multiply more easily. Yoshida et al. previously found that deletion of CPS increases the levels of TNF-α and IL-6 in bronchoalveolar lavage fluid of mice infected with K. pneumoniae strains, thus allowing a more efficient immune response and a decrease in murine mortality (47).

. Theguideline panel agreed that the use of local antibiograms to in-form antibiotic selection is the preferred approach to initiatingearly appropriate antibiotic coverage while avoiding superfluoustreatment

They are responsible for destructive changes to human lungs inflammation and hemorrhage with cell death, necrosis that sometimes produces a thick, bloody, mucoid sputum .

Several virulence factors have been demonstrated to mediate K. pneumoniae infectivity and include, but are most likely not limited to, adherence factors, capsule production, lipopolysaccharide presence, and siderophore activity.

The results of this study indicate that resistance to hLF1-11 and colistin are not strictly associated, and suggest an hLF1-11-induced sensitizing effect of K. pneumoniae to antibiotics, especially to hydrophobic antibiotics, which are normally not effective on Gram-negative bacteria. Altogether, these data indicate that hLF1-11 in combination with antibiotics is a promising candidate to treat infections caused by MDR-K. pneumoniae strains.

The designations "group C Streptococcus" (GCS) and "group G Streptococcus" (GGS) are used by clinical microbiology laboratories to denote clinical isolates of streptococci that react with Lancefield group C or G typing serum and, like Streptococcus pyogenes (group A Streptococcus), form large colonies on sheep blood agar, typically surrounded by a zone of beta-hemolysis.

Hemolysis should not be used as a stringent identification criterion. Bacitracin susceptibility is a widely used screening method for presumptive identification of S pyogenes; however, some S pyogenes are resistant to bacitracin (up to 10%) and some group C and G streptococci (about 3-5%) are susceptible to bacitracin. Some of the group B streptococci also may be bacitracin sensitive, but are presumptively identified by their properties of hippurate hydrolysis and CAMP positivity. S pneumoniae can be separated from other α-hemolytic streptococci on the basis of sensitivity to surfactants, such as bile or optochin (ethylhydrocupreine hydrochloride). These agents activate autolytic enzymes in the organisms that hydrolyze peptidoglycan.

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

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.

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.

SURVIVAL OUTSIDE HOST: The bacterium can survive on a dry surface for 3 days to 6.5 months (22). It has been found to survive in ice cream (18 days), raw and pasteurized milk at 15-37 ºC (96 hrs), room temperature butter (48 hrs), and neutralized butter (12-17 days) (17). GAS has been found to last several days in cold salads at room temperature (18).

MODE OF TRANSMISSION: Transmission via respiratory droplets, hand contact with nasal discharge and skin contact with impetigo lesions are the most important modes of transmission (5, 9, 13). The pathogen can be found in its carrier state in the anus, vagina, skin and pharynx and contact with these surfaces can spread the infection (5, 14, 15) The bacterium can be spread to cattle and then back to humans through raw milk as well as through contaminated food sources (salads, milk, eggs); however, cattle do not contract the disease (16-18). Necrotizing fasciitis is usually because of contamination of skin lesions or wounds with the infectious agent (12).

Staphylococcus and Streptococcus species:

Numerous epidemiological studies have identified high rates of invasive S. pyogenes infection in men rather than women, a pattern that can be observed for many other invasive bacterial infections and one that is not fully understood. Age-specific incidence rates show a typical J-shaped distribution, with highest rates in the elderly, followed by infants. Assessment of rates of disease according to patient ethnicity show generally higher rates of disease in individuals of non-white European descent. These observations have been made in a diverse range of populations, including indigenous populations of Australia, New Zealand, the Pacific Islands, and circumpolar regions of the northern hemisphere. The reasons behind these excesses in risk are poorly understood and could reflect differential access to healthcare or general living conditions—but could also encompass some genetic predisposing factors.

Puerperal Sepsis: Puerperal sepsis occurs during pregnancy or during an abortion, when group A streptococcus colonizing the patient invades the endometrium and surrounding structures as well as the lymphatics and bloodstream. Endometritis and septicemia result and can be complicated by pelvic cellulitis, thrombophlebitis, peritonitis, or pelvic abscess. Therapy consists of aggressive surgical exploration and parenterally administered penicillin or clindamycin (see section on myositis/myonecrosis). Patients allergic to penicillin can be treated with a first generation cephalosporin, clindamycin, or vancomycin (8).  

only five are known to commonly cause disease in immune-competent human beings: Group A, Group B, both members of Group D, and two groups that lack the Lancefield carbohydrate antigen: Streptococcus pneumoniae and Viridans streptococci.[5]

FORMULA Ingredients per liter of deionized water:* Pancreatic Digest of Casein 15.0gm Peptic Digest of Soybean Meal 5.0gm Sodium Chloride 5.0gm Sheep Blood 50.0ml Agar 12.0gm Final pH 7.3 +/- 0.2 at 25ºC.

SUPPORT PROTOCOLS FOR DIFFERENTIAL IDENTIFICATION OF S. PYOGENES (GAS) (adapted from microbelibrary.org)

NOTE: All steps should be performed using sterile technique. GAS will remain viable on plates for only 5–7 days after streaking if stored at room temperature. GAS does not survive at 4°C.

is a facultative anaerobe and is grown at 37°C in either ambient air or in 5–10% CO2. Like all streptococci, GAS is both catalase and oxidase negative. GAS lacks the necessary enzymes for a functional TCA cycle and oxidative-cytochromes for electron transport; therefore, relies completely on fermentation of sugars for growth and energy production. It is a member of the lactic acid bacteria and is homofermentative for lactic acid production from glucose fermentation. Specific components of a rich growth medium for GAS include neo peptone extracts, glucose as carbon source, and a complex mixture of nutrients from beef heart infusion as first described by Todd & Hewitt (Todd and Hewitt, 1932). GAS is considered a multiple amino acid auxotroph requiring nearly all amino acids to be present in its growth media. A Chemically Defined Medium has been developed for GAS containing all of the necessary amino acids for GAS growth (van de Rijn, 1980).

To identify S. pyogenes in clinical samples, blood agar plates are screened for the presence of β-hemolytic colonies. The typical appearance of S. pyogenes colonies after 24 hours of incubation at 35-37°C is dome-shaped with a smooth or moist surface and clear margins. They display a white-greyish color and have a diameter of > 0.5 mm, and are surrounded by a zone of β-hemolysis that is often two to four times as large as the colony diameter. Microscopically, S. pyogenes appears as Gram-positive cocci, arranged in chains (Figure 1).

The infection is transmitted to humans by animals through direct contact with infected materials like afterbirth or indirectly by ingestion of animal products and by inhalation of airborne agents. Consumption of raw milk and cheese made from raw milk (fresh cheese) is the major source of infection in man. Most of the fresh cheeses are sheep and goat cheese.

This modeof transmissionoccurs whena herd owner buys replacementcattle or domestic bisonthat are infected or have been exposed to infected animals, animal tissues or animal dischargespriortopurchase

can affect almost any part of your body, including your reproductive system, liver, heart and central nervous system

very rare in the United States

bacteria may be spread from animals to people

Long-term signs and symptoms

Signs and symptoms are similar to those of the flu

relieve symptoms, prevent a relapse of the disease and avoid complications

usually confirm a diagnosis of brucellosis by testing a sample of blood or bone marrow for the brucella bacteria or by testing blood for antibodies to the bacteria