Penicillin V 500 mg PO BID for 10d or Benzathine penicillin G 1.2 million U IM once or Amoxicillin 500-875 mg PO q12h or 250-500 PO q8h for 10d

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.

human upper airway and frequently are asymptomatic colonizers of the skin, gastrointestinal tract, and female genital tract.

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 overall average length of stay for all patients with GGS was 9.4 days, with longer stays for those with underlying diabetes mellitus (14.6 days) than for those without diabetes (6.7 days).

noted above, typical exudative pharyngitis with fever and adenopathy indistinguishable from GAS tonsillopharyngitis can be caused by large colony group C and G organisms, especially S. dysgalactiae subsp. equisimilis.

Groups C and G streptococci are typical chaining cocci that are Gram positive, facultative anaerobes which produce small or large colonies on sheep blood agar.

Zaoutis et al reported vancomycin tolerance in 54% of 32 GCS and GGS isolates

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.

2% of GCS and 4% of GGS exhibiting resistance.

One mechanism of resistance to vancomycin involves the alteration to the terminal amino acid residues of the NAM/NAG-peptide subunits, under normal conditions, D-alanyl-D-alanine, to which vancomycin binds.

Two mechanisms of bacitracin resistance are understood. One mechanism relies on a protein called a BcrABC transporter which pumps bacitracin out after it has entered the cell. Another mechanism relies on another protein called BacA which provides the active phosphorylated bactoprenol from a different synthetic pathway.

Erythromycin Resistance by Ribosome Modification

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.

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).

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

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.

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.

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

. 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

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