Proteus mirabilis causes 90% of Proteus infections and can be considered a community-acquired infection

species are most commonly found in the human intestinal tract as part of normal human intestinal flora

An Outbreak of Yersinia enterocolitica O:8 Infections Associated with Pasteurized Mil

Such symptoms are followed by watery, mucoid diarrhea (78-96%); fever (43-47%); colicky abdominal pain (22-84%); bloody stools (< 10%); and white blood cells (WBCs) in the stool (25%).

They’re also looking into how the affected communities treat their sick and bury their dead—practices that could affect the spread of Ebola.

The cases have all occurred in the Likati-Aketi territory—a hard-to-access part of the northern Bas-Uélé province

The country has experienced eight outbreaks since 1976, most recently in 2014

five have been tested and only one has been confirmed for Ebola. (It is not clear whether the five tests included all three deaths.)

Three of those people have died, one of whom tested positive for Ebola Zaire—the most dangerous of the virus’s several species

Ebola virus has emerged again in the Democratic Republic of Congo, and brought along two of its primary symptoms: confusion and misinformation.

Resistance arises when the PBPs-and particularly the transpeptidases-are modified, or when they are protected by beta-lactamases or 'permeability barriers'.

Relevant β-lactams and aminoglycosides remain active against 70%–98% of P. aeruginosa isolates in the United States and the United Kingdom

Drugs of Choice The choices for treatment for P. aeruginosa infections include the following antimicrobial agents, with the fluroquinolones being the only oral options:                • Aminogylcosides (amikacin, tobramycin, gentamicin)                • Carbapenems (imipenem, meropenem, doripenem)                • Cephalosporins, third-generation (cefoperazone, cefsulodin, ceftazidime, but not cefotaxime or ceftriaxone)                • Cephalosporins, fourth-generation (cefepime, cefpirome, cefclidin)                • Fluoroquinolones (ciprofloxacin, levofloxacin)                • Monobactam (aztreonam)                • Extended-spectrum penicillins (ticarcillin and/or ticarcillin-clavulanate, piperacillin and/or piperacillin–tazobactam,azlocillin).                • Polymyxin B/Colistin

The aminoglycosides can be inactivated by acetylation of an amino group by acetyltransferases, by adenylation of a hydroxyl group by adenyltransferases, or by phosphorylation of a hydroxyl group by phosphotransferases

including first-, second-, and many third-generation cephalosporin, penicillins, and macrolide

cephalosporins (cefoperazone, cefsulodin and ceftazidime, but not cefotaxime or ceftriaxone), fourth generation cephalosporins (cefepime, cefpirome, cefclidin), extended spectrum penicillins (ticarcillin, piperacillin, azlocillin), monobactams (aztreonam); carbapenems (imipenem, meropenem), quinolones (ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin), and aminoglycocides (gentamycin, amikacin, tobramycin, colimycin).

 polar flagella, which are critical for motility in initial stages of pulmonary infection, activate IL-8 production by binding to toll-like receptor on the surface of airway epithelial cells, and facilitate adherence to epithelial and eukaryotic cells with pile/ non-piling adhesions (polar pili)

Inhibition of protein synthesis. Once inside the bacterial cell, aminoglycosides bind to the 30s ribosomal sub-unit and cause a misreading of the genetic code.  This subsequently leads to the interruption of normal bacterial protein synthesis.

wo major adhesins have been identified in P. aeruginosa, flagella and type IV pili (Tfp) [10]–[12]. The single polar flagellum is a polymer composed of flagellin,

biofilm which anchors the cells to their environment and in medical situations, it protects the bacteria from the host defenses such as lymphocytes, phagocytes, the ciliary action of the respiratory tract, antibodies and complement.

surface-bound exoenzyme S could serve as an adhesin for glycolipids on respiratory cells.

These adhesins appear to bind to specific galactose or mannose or sialic acid receptors on epithelial cells. Colonization of the respiratory tract by Pseudomonas requires pili adherence and may be aided by production of a protease enzyme that degrades fibronectin in order to expose the underlying pilus receptors on the epithelial cell surface

inability to ferment lactose, a positive oxidase reaction, its fruity odor, and its ability to grow at 42°C.

It grows well on most laboratory media and commonly is isolated on blood agar or eosin-methylthionine blue agar

including fluoroquinolones, gentamicin and imipenem

both R-factors and RTFs, and it is able to transfer these genes by means of the bacterial mechanisms of horizontal gene transfer (HGT), mainly transduction and conjugation.

Clinical samples, in general, yield one or another of two smooth colony types. One type has a fried-egg appearance which is large, smooth, with flat edges and an elevated appearance. Another type, frequently obtained from respiratory and urinary tract secretions, has a mucoid appearance, which is attributed to the production of alginate slime. The smooth and mucoid colonies are presumed to play a role in colonization and virulence

biofilm

According to the CDC, the overall incidence of P. aeruginosa infections in U.S. hospitals averages about 0.4 percent (4 per 1000 discharges), and the bacterium is the fourth most commonly-isolated nosocomial pathogen accounting for 10.1 percent of all hospital-acquired infections.

Pseudomonas aeruginosa infection is a serious problem in patients hospitalized with cancer, cystic fibrosis, and burns. The case fatality rate in these patients is near 50 percent.

opportunistic pathogen, meaning that it exploits some break in the host defenses to initiate an infection.

outer membrane protects it from antibiotics it has developed resistance because it lives among antibiotic producing bacteria and fungi in the soil

10% of all hospital-acquired infections

it is found mostly in hospitals; in food, sinks, toilets, mops, instruments such as respiratory equipment, or even transferred from the hands of healthy visitors or hospital staff

low antibiotic susceptibility

Because it thrives on moist surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It

generally in the immunocompromised

rude prevalence of multidrug-resistant bloodstream P. aeruginosa isolates in our institution from 2005 to 2007 was 14%

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).

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.

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

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.

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,

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

Pathogenicity

Streptococcus Penicillinplusclindamycin 2–4 million units every 4–6 h IV (adult)600–900 mg every 8 h IV 60 000–100 000 units/kg/dose every 6 h IV10–13 mg/kg/dose every 8 h IV Vancomycin, linezolid, quinupristin/dalfopristin, daptomycin Staphylococcus aureus Nafcillin 1–2 g every 4 h IV 50 mg/kg/dose every 6 h IV Vancomycin, linezolid, quinupristin/dalfopristin, daptomycin Oxacillin 1–2 g every 4 h IV 50 mg/kg/dose every 6 h IV Cefazolin 1 g every 8 h IV 33 mg/kg/dose every 8 h IV Vancomycin (for resistant strains) 30 mg/kg/d in 2 divided doses IV 15 mg/kg/dose every 6 h IV  

NOVOBIOCIN (

Catalase mediates the breakdown of hydrogen peroxide H2O2 into oxygen and water. 

grape-like clusters when viewed through a microscope, and has round, usually golden-yellow colonies

The disease is spread through contact with an infected cat (a bite or scratch) or exposure to cat fleas

Bump (papule) or blister (pustule) at site of injury (usually the first sign)FatigueFever (in some people)HeadacheLymph node swelling (lymphadenopathy) near the site of the scratch or biteOverall discomfort (malaise)

bartonella bacteria