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

. 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

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.

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

SIGNS AND SYMPTOMSIn

The IgA protease, showing its teeth in red!An Arms RaceSome bacteria have developed weapons that can cut our antibodies into small pieces so that they become unable to stick the invading bacteria into clumps. These anti-antibodies are called IgA proteases and are produced inside bacteria like the ones that cause meningitis and gonorrhoea

By blocking this protein enzyme it stops the release of viruses from the infected host cell and prevents new host cells from being infected.

phagosomes will fuse with lysosomes and pathogenic microorganisms are killed, but in this case acidification of the phagosome does not take place, and its membrane does not get late endosomal markers, like rab7 and LAMP-1.

personalized therapy with macrophages

macrophages (viruses of bacteria)

First, the presence of cell wall receptors enables K. pneumoniae to attach to the host cell, thereby altering the bacterial surface so that phagocytosis by polymorphonuclear leukocytes and macrophages is impaired and invasion of the non-phagocytic host cell is facilitated. Second, invasion of the host cell is also facilitated by the large polysaccharide capsule surrounding the bacterial cell; in addition this capsule acts as a barrier and protects the bacteria from phagocytosis. Third, K. pneumoniae produces an endotoxin that appears to be independent of factors that determine receptors and capsular characteristics.

cell wall receptors, capsular polysaccharide, and endotoxin

In gram-negative bacteria, relevance ratio of acinetobacter baumannii (AB) was the highest (18.4%) and followed by klebsiella pneumoniae (11.4%)

Pneumonia is the second leading reason for hospitalization of medicare beneficiaries and accounts for more than 600,000 medicare hospitalizations yearly [1,2]. It is common and potentially serious infected. The elderly are more susceptible to pneumonia and more likely to die from this infection than younger populations

between September to April.

The Yellow Fever Virus (YFV) is a flavivirus that is a member of a larger family of hemorrhagic fever viruses. YFV can cause characteristic yellowing (jaundice) of the whites of the eyes and skin due to damage in the liver cells. Spread by mosquitos, the virus has a 3-6 day incubation period with the first clinical signs appearing soon after. The first period’s signs include fever, vomiting, and muscle aches among other things. The second period is a remission period where a patient either experiences disappearance of initial symptoms or progresses to the third period, intoxication where the patient experiences continuing symptoms and can worsen to the point of death 7-10 days after initial onset of symptoms.

low threat Zika fever itself ge

Figure 1

s followed leading up to

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

It uses pili with the aid of protease enzymes in attachment to epithelial cells, such as in the respiratory tract.  The bacterium has capsules or slime layers that protect it from antibodies, lymphocytes, and phagocytes.  In order to invade tissues, it produces extracellular enzymes such as elastase and alkaline protease.  There are also three soluble proteins involved in invasion, which are cytotoxin (mw 25 kDa) and two hemolysins.  It produces the extracellular toxins Exoenzyme S and Exotoxin A and also LPS, which is characteristic of Gram-negative bacteria.  All of these characteristics lead to a wide variety of diseases.

The bacterium is very low-maintenance when it comes nutrition.  It does not require organic growth factors, and can use over seventy-five organic compounds for growth.  In a lab setting, acetate and ammonium sulfate in a medium will satisfy it.  The optimum growth temperature is 37 degrees C, but it can grow in temperatures up to 42 degrees C.  Not only is it tolerant to temperature, but also to salts and dyes, weak antiseptics, and antibiotics.

Table 2

They have no specific growth requirements and grow well on standard laboratory media, but grow best between 35 and 37 °C and at pH 7.2.

commercially available radioimmunoassay for bacterial antigen in urine is satisfactory, but is available only for serogroup 1 of L pneumophila

possesses pili (fimbriae), and most species are motile by means of a single polar flagellum

Treatment is with 3rd-generation cephalosporins, cefepime, carbapenems, fluoroquinolones, piperacillin/tazobactam, or aminoglycosides.

Symptoms

Oral antibiotics such as β-lactams are appropriate first-line therapy for most patients. A proportion of H. influenzae isolates produce β-lactamase (this varies markedly between different locations) and in this circumstance, extended spectrum cephalosporins, amoxicillin-clavulinic acid, trimethoprim-sulfamethoxazole, tetracyclines, quinolones and macrolide antibiotics are appropriate therapeutic choices.

On an agar medium which included ornithine, raffinose, and Koser citrate, K. pneumoniae strains grew as yellow mucoid colonies at 24 h and there was some increase in colony size at 48 h.

The growth and appearance of these bacteria were not influenced by pH changes over a pH range of 5.2 to 6.4.

Their capsule allows them to resist phagocytosis and complement-mediated lysis in the nonimmune host.

The organism enters the body through the nasopharynx. Organisms colonize the nasopharynx and may remain only transiently or for several months in the absence of symptoms (asymptomatic carrier).

In this review, we summarize the current “state of the art” of carbapenem antibiotics and their role in our antimicrobial armamentarium

among Klebsiella pneumoniae isolates ESBL producers increased from 1.5% to 4.0%

Discussion

Those who are living in long-term care facilities or are currently hospitalized and breathing with mechanical ventilators are at even higher risk of developing a lung infection from Klebsiella.

Empiric treament of severe nosocomial infections in critically ill patients or in ICU

Cephalosporins are bactericidal (kill bacteria) and work in a similar way to penicillins. They bind to and block the activity of enzymes responsible for making peptidoglycan, an important component of the bacterial cell wall. They are called broad-spectrum antibiotics because they are effective against a wide range of bacteria.

) through target-site modification by methylation or mutation that prevents the binding of the antibiotic to its ribosomal target, (2) through efflux of the antibiotic, and (3) by drug inactiva

The third generation cephalosporins have a marked activity against gram-negative bacteria due to enhanced beta-lactamase stability and the ability to penetrate the gram-negative cell wall. They have more favorable pharmacologic properties than previous generations.

Effective therapy for severe community acquired K. pneumoniae pneumonia consists of empiric treatment with coverage against Gram negative organisms, aggressive ventilation, and clinical and radiologic surveillance for surgically treatable entities such as pulmonary gangrene, lung abscess and empyema (111, 141, 180). Third generation cephalosporins or quinolones would provide coverage against most community acquired K. pneumoniae. Macrolides (including azithromycin) have no useful activity against K. pneumoniae. The superiority of combinations of third generation cephalosporins and aminoglycosides has been demonstrated in one study (111) but not in others (129, 131). The clinical outcome when chloramphenicol and aminoglycosides are used in combination has been poor (118).

Critically ill patients with nosocomial Klebsiella bacteremia should probably be treated with antibiotics active against ESBL producers until the absence of an ESBL is definitively established.

Selection of antimicrobial therapy for Klebsiella bacteremia should be based on local susceptibility patterns of isolates causing bacteremia. In particular, the likelihood that an isolate may be an ESBL producer is an important consideration.

It is not an active fermenter of carbohydrates and produces acid, but no gas, in glucose and is lactose-negative. The oxidase and catalase test for P.aeruginosa are positive.

Haemophilus influenzae type b bacteria can’t survive on surfaces or in the environment. The bacterium’s only known reservoir is humans, who may carry it without becoming ill.

Figure 1. . Klebsiella pneumoniae antimicrobial drug resistance, United States, 1998–2010. ATM, aztreonam; SXT, trimethoprim/sulfamethoxazole; CAZ, ceftazidime; CIP, ciprofloxacin; TET, tetracycline; TOB, tobramycin; TZP, piperacillin/tazobactam; CPM, cefepime; AMK, amikacin; IPM, imipenem. Ceftriaxone and gentamicin were not included for better data presentation.

Figure 2. . Prevalence of antimicrobial cross-resistance among imipenem-resistant Klebsiella pneumoniae isolates, United States, 2010. TET, tetracycline; AMK, amikacin; GEN, gentamicin; CPM, cefepime; SXT, trimethoprim/sulfamethoxazole; CRO, ceftriaxone; TOB, tobramycin; CIP, ciprofloxacin; TZP, piperacillin/tazobactam; CAZ, ceftazidime; ATM, aztreonam.

8% of Klebsiella spp. isolates were carbapenem resistant in

specific for ferric iron and thus supply iron to the bacterial cells

54Journal of Thi-Qar University No.4 Vol.3 Mar/2008K.pneumoniaehave many virulence factors that make it pathogenicity, these factors are :

Antibiotics

Infection with carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings.[11] One of many CREs is carbapenem-resistant Klebsiella pneumoniae (CRKP). Over the past 10 years, a progressive increase in CRKP has been seen worldwide; however, this new emerging nosocomial pathogen is probably best known for an outbreak in Israel that began around 2006 within the healthcare system there.

Klebsiella pneumoniae is a Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. It appears as a mucoid lactose fermenter on MacConkey agar.

If the specific Klebsiella in a particular patient does not show antibiotic resistance, then the antibiotics used to treat such susceptible isolates include ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate, ceftazidime, cefepime, levofloxacin, norfloxacin, gatifloxacin, moxifloxacin, meropenem, and ertapenem. Some experts recommend the use of meropenem for patients with ESBL-producing Klebsiella. The claim is that meropenem produces the best bacterial clearing.

A number of mechanisms cause carbapenem resistance in the Enterobacteriaceae. These include hyperproduction of ampC beta-lactamase with an outer membrane porin mutation, CTX-M extended-spectrum beta-lactamase with a porin mutation or drug efflux, and carbapenemase production. The most important mechanism of resistance by CRKP is the production of a carbapenemase enzyme, blakpc. The gene that encodes the blakpc enzyme is carried on a mobile piece of genetic material (a transposon; the specific transposon involved is called Tn4401), which increases the risk for dissemination. CRE can be difficult to detect because some strains that harbor blakpc have minimum inhibitory concentrations that are elevated, but still within the susceptible range for carbapenems. Because these strains are susceptible to carbapenems, they are not identified as potential clinical or infection control risks using standard susceptibility testing guidelines. Patients with unrecognized CRKP colonization have been reservoirs for transmission during nosocomial outbreaks. Depending on the type of infection and the mode of infectivity, cells of Klebsiella spp. may adhere and attack upper respiratory tract epithelial cells, cells in gastrointestinal tract, endothelial cells, or uroepithelial cells, followed by colonization of mucosal membranes (phac-aspc.gc.ca).[15]

Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates plasmids as the primary source of the resistance genes.[9] Klebsiella species with the ability to produce extended-spectrum beta-lactamases (ESBL) are resistant to many classes of antibiotics. The most frequent are resistance to aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[10]

are seen mostly in people with a weakened immune system

alcoholism

It naturally occurs in the soil,

Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium

As a general rule, Klebsiella infections are seen mostly in people with a weakened immune system. Most often, illness affects middle-aged and older men with debilitating diseases. This patient population is believed to have impaired respiratory host defenses, including persons with diabetes, alcoholism, malignancy, liver disease, chronic obstructive pulmonary diseases, glucocorticoid therapy, renal failure, and certain occupational exposures (such as papermill workers). Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection). Feces are the most significant source of patient infection, followed by contact with contaminated instruments.[citation needed]

ceftazidime (92-95%), ceftriaxone (96-98%), cefotaxime (96%), piperacillin-tazobactam (90-97%), imipeneum (98-100%), gentamicin (95-96%), amikacin (98-99%), triethoprimsulfamethoxazole (SXT) (88-90%).

a high transmission rate in East and Southeast Asian countries. The most affected countries include Taiwan, Singapore, Vietnam, India and China (Mao). This disease tends to occur in areas with fluctuating cli

opulation. It is a non zoonotic disease as it can not be transmitted to animals(CDC).

categorized alongside p

, as mentioned earlier it is primarily symptom based, consisting of rest, fluid intake, platelet, or red blood cell transfusion, thus depending on the severity of the condition, and typically with a better prognosis and low risk of death if diagnosed early (1). In regards to how this virus is transmitted, it is done by getting bitten by the female Aedes aegypti o

Viruses of the family flaviviridae are single stranded, positive, enveloped RNA viruses that are most commonly found in certain arthropod species, sometimes transferring over and infecting humans via bites or stings (6).Within the spectrum of Dengue Virus, it has been found that there are approximately 4 different serotypes (viral classification based on presence of certain antigens) called; DENV-1, DENV-2, DENV-3, and DENV-4 (1). In regards to the DENV structure; it is a 50nm virus enclosed in a lipid membrane with about 180 copies of envelope E protein attached to the surface of the membrane via transmembrane segment (1). The viral genome is about 11,000 bases, and consists of a polyprotein that is divided into three structural proteins, C, prM, E; seven nonstructural proteins, NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5, and short non-coding regions on both the 5’ and 3’ ends (1).

As mentioned earlier, dengue virus is a type of virus that hails from a group of viruses that are from the the family flaviviridae. These types of viruses also include other similar type viruses such as West Nile, Yellow Fever and Zika viruses.

The virus has a classification system that has been imposed by the World Health Organization (WHO) in 1974 in order to assist in its treatment and diagnosis, which has gone through revisions in the years 2009 and 2011, which classifies the disease’s severity as dengue fever, and dengue hemorrhagic fever grades 1-4 (3) The virus has a variety of symptoms with severities depending on its subtype. Typical symptoms of dengue fever include; joint pain, high fever, nausea, low white blood cell count, whereas the more severe version of dengue hemorrhagic fever entails

flavivirus

us is quite prevalent in t

Herpes simplex virus can affect everyone all over the world and cause major life-threatening diseases.

e herpes simplex virus can also cause mortality. Meningitis can result from HSV-2 (Engleberg). Also, HSV-1 can enter the central nervous system causing fatal encephalitis (Engleberg), or inflammation of the brain.

Americas, and the Western Pacific (WHO)

Almost all humans have HSV-1, but the majority do not show symptoms (Engleberg). In fact, only about one third of people with the virus see symptoms (Engleberg). Globally, approximately 67% of people have HSV-1

he treatment reduces symptoms, but does not prevent the infected person from having symptoms ever again.

HSV-1 affects the face and skin and HSV-2 affects the genital area

Prevalence and Diagnosis

r over a long period of time,

infected, further transmission of the virus is a result of contact from bodily fluids such as breast milk, blood, vomit, stool, urine, and others. (Mog

ebola. (Center of D

The virus encodes its genetic material in RNA and uses it to infect the host

The other clinical form of rabies, known as the numb type or the non-classical or paralytic type, is characterized by feelings of weakness or paralysis

nues to find improved methods of prevention and treatment.

genetically engineered live attenuated human rotavirus strains or hybrid human-bovine reassortment rotavirus strains

Geographical Distribution

diversity in strains o

Common symptoms include vomiting, diarrhea, and fever for three to eight days. The incubation period for the virus is two days, and diagnosis is often executed by the detection of rotavirus antigen in stool samples

of contaminated food or water.

so it is primarily transmitted via the fecal-oral route

Rotavirus molecules are non enveloped and double-shelled, and have a similar appearance to that of a wheel.

Selected Virulence Factors

7-14% of pneumonia,

who have diabetes or who suffer from alcoholisms due to a weakened immune system

Capsular Polysaccharide and Lipopolysaccharide O Side Chain

Hospital-acquired infections rely on the urinary tract, lower respirator tract, biliary tract, and surgical wounds to set up colonization

Klebsiella infections are most well-known in hospitals spread through person-to-person contact by contaminated hands of surrounded people in the hospitals, whether it be an employee or a patient. Klebsiella is spread very easily and rapidly, but not through the air. Healthcare settings are most vulnerable to Klebsiella infections due to the nature of procedures that allow easy access of bacteria into the body. Patients who are on ventilators, catheters, or surgery wounds are highly prone to catching this deadly infection

pH range of 5.2 to 6.4

Klebsiellae are lactose-fermenting, urease-positive, and indole-negative organisms,

They have no special culture requirements. Most species can use citrate and glucose as sole carbon sources; thus, they grow well on most ordinary media.

Virulence Properties of the Legionella Pneumophila Cell Envelope

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.

Legionella pneumophila is responsible for 1% to 4% of cases of community-acquired pneumonia requiring hospitalization

emperatures of 20 to 50 degrees Celsius (optimal 35 degrees Celsius

s illnesses have occurred after short exposures and 3 or more km from the source of outbreaks

Legionella pneumophila and related species are commonly found in lakes, rivers, creeks, hot springs and other bodies of wate

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.

When bacteria such as Klebsiella pneumoniae produce an enzyme known as a carbapenemase (referred to as KPC-producing organisms), then the class of antibiotics called carbapenems will not work to kill the bacteria and treat the infection. Klebsiella species are examples of Enterobacteriaceae, a normal part of the human gut bacteria, that can become carbapenem-resistant. CRE, which stands for carbapenem-resistant Enterobacteriaceae, are a family of germs that are difficult to treat because they have high levels of resistance to antibiotics. Unfortunately, carbapenem antibiotics often are the last line of defense against Gram-negative infections that are resistant to other antibiotics.

Klebsiella bacteria have developed antimicrobial resistance, most recently to the class of antibiotics known as carbapenems(https://www.cdc.gov/hai/organisms/cre/index.html).

How Klebsiella bacteria are spread

Patients whose care requires devices like ventilators (breathing machines) or intravenous (vein) catheters, and patients who are taking long courses of certain antibiotics are most at risk for Klebsiella infections. Healthy people usually do not get Klebsiella infections.

normally found in the human intestines (where they do not cause disease). They are also found in human stool (feces).

Biochemical Tests

On Blood Agar: translucent, low, convex or flat pin point colonies, Satellitism. On Chocolate Agar: Grayish, Transparent, smooth, low, convex or flat with a slightly splayed out, entire edge, mucoid, pale

Slender, short, gram negative rods or coccobacillus 3-0.5 um X 0.5-1 um with rounded ends.

carbenicillin, cephalosporins, ceftazidime, and ciprofloxacin

P. aeruginosa have been found to survive within droplet nuclei and can remain in aerosols for long periods of time, thus there is evidence of potential airborne transmission Footnote 20. Contact with contaminated water is also a major route, but since the oral infectious dose is thought to be very high, routes that pose the greatest health risk are skin exposure (for example, in contaminated hot tub water) and lung exposure from inhaling aerosols discharged from infected respiratory tracts Footnote 13. The bacterial can often enter the body through injuries and wounds Footnote 3. The use of contaminated mechanical respiratory ventilators in hospital settings is also a common source of nosocomial infections Footnote 12.

Humans, animals (wild, domestic, livestock), and plants (flora and fungi)

P. aeruginosa infections account for 20% of pneumonia and 16% of urinary tract infections Footnote 16. Prevalence in the community is less than in the hospital, and cases of severe community-acquired infection are rare

The common site of infection is the lower respiratory tract,

opportunistic pathogens,

P. aeruginosa can produce a large variety of extracellular toxins, including exotoxin A and enterotoxins

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

Many P. aeruginosa isolates are resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment

Identification[edit] Test Results Gram Stain - Oxidase + Indole Production - Methyl Red - Voges-Proskaeur - Citrate + Hydrogen Sulfide Production - Urea Hydrolysis + Phenylalanine Deaminase - Lysine Decarboxylase - Motility + Gelatin Hydrolysis + Acid from lactose - acid from glucose - acid from maltose - acid from mannitol + acid from sucrose - nitrate reduction + DNAse - Lipase + Pigment + (bluish green pigmentation) Catalase +

the blue-green color of laboratory cultures

citrate, catalase, and oxidase positive.

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

Laboratory testing Gram staining of body fluids from various sites of infection Bacterial culture (blood, other body fluids): The most confirmatory method of establishing the diagnosis; slide agglutination with type-specific antisera is used for serotyping H influenzae Immunologic studies: Detection of the polyribosyl ribitol phosphate (PRP) polysaccharide capsule via countercurrent immunoelectrophoresis, latex particle agglutination, co-agglutination, and enzyme-linked immunosorbent assay; important adjuncts to culturing for rapid diagnosis Cerebrospinal fluid (CSF) studies (eg, Gram stain, culture, glucose/protein levels) Blood cell counts: Assessment for anemia, leukocytosis, thrombocytosis, and/or thrombocytopenia Acute phase reactants: Characteristic elevated erythrocyte sedimentation rates (ESRs) and C-reactive protein (CRP) levels in patients with septic arthritis

Haemophilus influenzae is a small (1 µm × 0.3 µm), pleomorphic, gram-negative coccobacillus.

The most common types of disease caused by H. influenzae type b (Hib) include pneumonia, bacteremia, meningitis, epiglottitis, septic arthritis, cellulitis, otitis media, purulent pericarditis, and other less common infections such as endocarditis and osteomyelitis. Non-b H. influenzae can cause disease similar to Hib infections. Nontypeable H. influenzae commonly causes ear infections in children and bronchitis in adults, but also causes invasive disease, such as bacteremia and bacteremic pneumonia.

H. influenzae, including Hib, are spread person-to-person through respiratory droplets that occur when someone who has the bacteria in their nose or throat coughs or sneezes.

H. influenzae, including Hib, disease occurs mostly in babies and children younger than five years old. Adults 65 years or older, American Indians, and Alaska Natives are also at increased risk for getting sick with invasive H. influenzae disease.

It is also an opportunistic pathogen for patients with chronic pulmonary disease, enteric pathogenicity, nasal mucosa atrophy, and rhinoscleroma.

Klebsiella pneumoniae is a Gram-negative, non-motile, encapsulated, lactose fermenting, facultative anaerobic, rod shaped bacterium found in the normal flora of the intestines

blood or body fluids of a person who is sick with or has died from Ebola, coming in contact with contaminated objects like needles and touching infected animals, their blood or other body fluids, or bush meat.

Regarding the current EBOV outbreak, it is hypothesized that the index case most likely originated via animal — human contact (e.g., ingestion of undercooked ‘bush meat’, animal bite, or inadvertent contact with body fluids or blood from an animal)

rate of invasive disease is about 10 cases out of every 100,000 non-pregnant adults

Most cases of group B strep disease in adults are among those who have other medical conditions that put them at increased risk, such as:

normal residents of the vaginal flora in 25% of healthy women

Clinical manifestations of adult GBS infection are varied and include skin, soft tissue and urinary tract infections, bacteremia, pneumonia, arthritis and endocarditis

Group B Streptococcus (GBS) are generally beta hemolytic on blood agar plates (right hand side)

Bacteria under Microscope Streptococcus agalactiae Group B streptococcus, GBS

moxicillin/clavulanic acid for 14 days

Amoxicillin acts by inhibiting bacterial cell wall synthesis. Lack of bacterial cell wall results in death due to lysis of bacteria. So amoxicillin is useful only for actively growing and cell wall synthesizing bacteria.

A total of 5,093 isolates were collected in 2014. Of these, 25.3% were resistant to tetracycline, 19.2% to ciprofloxacin, and 16.2% to penicillin (plasmid-based, chromosomal, or both)

n 2010, 27.2% of all GISP isolates were resistant to penicillin, tetracycline, ciprofloxacin, or some combination of those antimicrobials and 6.9% of isolates were resistant to all three antimicrobial

62 million new cases of gonorrhea occur globally each year

Disseminated infection is rare but can occur 1 to 3 percent of adults

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 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).

C. Pathogenesis

Viral and Host Factors in Human Respiratory Syncytial Virus Pathogenesis

necrobacillosis,

10-20% Mortality

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