Pseudomonas aeruginosa is a gram negative, motile, aerophilic rod shaped bacteria which can happen as singles, in braces and on occasion in short ironss. P.aeruginosa is a omnipresent being which can proliferate under the sparest conditions such as sinks, lavatories, cosmetics, vaporizers, inhalators, inhalators, and anaesthesiology and dialysis equipment.
Infected patients and staff are besides possible primary beginnings of infection ( 2 ) . P.aeruginosa is a major timeserving pathogen of the immunocompromised doing a broad scope of nosocomial infections. These include infections of burn, station operative lesions, urinary piece of land ( particularly in patients with catheters ) , ears and eyes. Infection often leads to sepsis and deceases can happen ( 3 ) . This being is associated with the greatest morbidity and mortality in cystic fibrosis ( 4 ) and is prevailing among patients with burn lesions and endovenous drug users ( 5, 6 ) .
P.aeruginosa is able to prevail and multiply in moist environments and on most pieces of equipment in infirmary wards. This is of importance in transverse infection control ( 4 ) .P.
aeruginosa is the most of import, immune and unsafe being infecting burn patients ( 7 ) . It is the 5th common pathogen among hospital micro-organisms and causes 10 % of all infirmary acquired infections ( 8 ) . The rate of commensalisation additions as the continuance of infirmary stay additions ( 9 ) .
Epidermiologically, P.aeruginosa is ranked as the 4th cause of nosocomial infections in the United States ( 10 ) . A survey on assorted clinical isolates was conducted in Afghanistan at the Post Graduate Medical Institute ( PGMI ) Hayatabal Medical Complex to determine the prevalence and antimicrobic susceptibleness forms of P.aeruginosa infections. Among the positive isolates, 6.
67 % were P.aeruginosa with the highest rate of infection observed in orthopedic ward ( 24.61 % ) and 0PD ( 20 % ) . The highest per centum of P.aeruginosa isolates were observed in Pus ( 57.64 % ) ( 11 ) .
Pseudomonas aeruginosa is immune to many antimicrobic agents and has hence become dominant and of import when the more susceptible bacterium of the normal vegetations are suppressed ( 1 ) . With the widespread usage of quinolones both in the infirmary and in the common scene, drug immune P.aeruginosa isolates have emerged and go on to intensify quickly ( 12 ) . The antimicrobic agents are losing their efficaciousness due to indiscriminate usage of antibiotics, deficiency of consciousness, patient non conformity and unhygienic conditions ( 11 ) . Like most gram negative B, P.
aeruginosa has been reported to hold developed opposition to normally used antibiotics and germicides. It was originally sensitive to Carbernicillin, Pipracil, Gentamicin, Cipro and other drugs. However it is now immune to these antibiotics ( 13, 14 ) . The virulency factors associated with P.aeruginosa infections include cytotoxin production, the being ‘s ability to organize a biofilm, produce gelatinase, elastase and alkalic peptidase. These cause the devastation of connective tissue and debasement of host immunological factors ( 15, 16 ) . The primary purpose of this survey is to find the prevalence of P.
aeruginosa in lesion infections and its sensitiveness to normally used antibiotics in inmates at Parirenyatwa Group of Hospitals.
1.1.1 PSEUDOMONAS AERUGINOSA
Pseudomonas aeruginosa is one of the most common Gram-negative micro-organisms identified in the clinical specimens of infirmary admitted patients.
It is a rod that measures about 0.6 – 2µm and is motile by agencies of a individual polar scourge ( 1, 18 ) .P. aeruginosa is noted for its metabolic versatility and its exceeding ability to colonise a broad assortment of environments and besides for its intrinsic opposition to a broad assortment of antimicrobic agents. It is an obligate aerobe that grows good at temperatures between 37-42 & A ; deg ; C. Due to its omnipresent nature, P. aeruginosa grows readily on any type of media ( 1 ) .
On Blood agar they are frequently ?-haemolytic while on MacConkey agar they produce pale settlements because they do non ferment lactose. P.aeruginosa is oxidase positive ( 17 ) .Pseudomonas aeruginosa is good known for its production of two soluble pigments, pyocyanin which is a non-fluorescent blue pigment and the fluorescent pigment pyoverdin, which gives a light-green coloring material to the media. P. aeruginosa besides produces a sweet grape-like smells due to the production of 2-aminoacetophenone ( 1, 17 ) .
P. aeruginosa is infective when introduced to countries missing normal host defense mechanisms for illustration when there is tissue harm and during malignant neoplastic disease therapy where there is neutropaenia ( 1 ) . P.aeruginosa is a major timeserving pathogen of the immunocompromised doing a broad scope of nosocomial infections. These include infections of burn, station operative lesions, urinary piece of land ( particularly in patients with catheters ) , ears and eyes ( in users of extended-wear soft contact lenses ) . Infection often leads to sepsis and deceases can happen ( 3 ) .
This being is associated with the greatest morbidity and mortality in cystic fibrosis ( 4 ) and is prevailing among patients with burn lesions and endovenous drug users ( 5, 6 ) .It produces cytotoxins, peptidases and hemolysins. Isolates from patients with Cystic fibrosis produce a polyose, alginate. The alginate, pili and outer membrane mediate adhesion to host epithelial tissues ( 19 ) .
3 VIRULENCE FACTORS
The ability of Pseudomonas aeruginosa to do a broad scope of infections is due to its ability to bring forth a figure of cell-associated ( adhesions, alginate, pili, scourge and lipopolysaccharide ) and extracellular ( elastase, exoenzyme S, exotoxin A, haemolysins, Fe binding proteins, leukocidins and peptidases ) virulency factors. These mediate a figure of procedures including adhesion, alimentary acquisition, immune system equivocation, leucocyte violent death, tissue adhesion and blood watercourse invasion ( 20, 21 ) .
CELL-ASSOCIATED VIRULENCE FACTORS
P.aeruginosa requires a breach in first-line defense mechanisms to originate infection. This can ensue from change of the immunologic defense mechanism mechanisms for illustration in chemotherapy-induced immunosuppression and AIDS, break of the protective balance of mucosal normal vegetations by broad-spectrum antibiotics, or breach of normal mucosal barriers for illustration injury and Burnss ( 21, 23 ) .
Attachment of P. aeruginosa to host epithelial tissue is mediated by type 4 pili, that extend from the cell surface ( 1, 22 ) . Flagella, chiefly responsible for motility may besides move as adhesins to epithelial cells ( 23 ) . Lipopolysaccharides are responsible for endotoxic belongingss of the being while the exopolysacharride is responsible for the mucoid settlements from patients with Cystic fibrosis ( 1 ) .
Extracellular VIRULENCE FACTORS
These are extracellular merchandises produced by P. aeruginosa that can do extended tissue harm. They include exotoxin A, exoenzyme S, elastase, alkalic peptidase but the part of a given factor varies with the type of infection ( 24 ) .
Exotoxin A catalyses ADP-ribosylation and inactivation of elongation factor 2, taking to suppression of protein biogenesis and cell decease ( 25 ) . It is besides responsible for local tissue mortification ( 1 ) . Exoenzyme S is besides an ADP-riboslytransferase that ribosylates GTP adhering proteins ensuing in direct tissue harm ( 26 ) . Phospholipase C and rhamnolipid are haemolysin produced by P. aeruginosa. They breakdown lipoids and lecithin and both have cytotoxic effects ( 27 ) .
Pseudomonas aeruginosa besides produces toxins which include Las B elastase, Las A elastase and alkalic peptidase ( 28 ) . Las A elastase and Las B elastase have elastolytic activity. Elastin is a major constituent of lung tissue and blood vass. Las B elastase is a zinc metalloprotease while Las A is a peptidase.
Alkaline peptidase lyses fibrin ( 29 ) .
Pseudomonas aeruginosa is besides able to organize biofilms. Biofilms are complex communities of surface-attached sums of micro-organisms embedded in a self-secreted extracellular polyose matrix or sludge ( alginate ) ( 30, 31 ) . These act as efficient barriers against antimicrobic agents ( aminoglycosides, ? lactamases, fluoroqunilones and germicides ) and the host immune system ensuing in relentless colonization and loss of action at the site of infection ( 32, 33 ) .
1.1.4 CELL TO CELL SIGNALLING
Cell to cell signalling systems control extracellular virulency factors required for tissue invasion by P.
THE LAS CELL TO CELL SIGNALLING SYSTEM
The Las cell to cell signalling system regulates the look of Las B elastase ( 34 ) . It regulates Las B look and is required for optimum production of other extracellular virulency factors such as Las A elastase and exotoxin A ( 35 ) .
THE RHL CELL TO CELL SIGNALLING SYSTEM
The rhl cell to cell signalling system controls the production of rhamnolipid. The system regulates the look of the rhl AB operon that encodes a rhamnosyltransferase required for rhamnolipid production. It is besides of import for Las B elastase, peptidase, pyocyanin and alkalic transferase production ( 36 ) .
5 ANTIMICROBIAL REACTIVITY OF P. AERUGINOSA
Like most gram negative B, P.aeruginosa has been reported to hold developed opposition to normally used antibiotics and germicides. It was originally sensitive to Carbernicillin, Pipracil, Gentamicin, Cipro and other drugs. Degrees of cross-resistance between these agents have been reported nevertheless ( 13, 14 ) . Treatment of infections by P. aeruginosa is frequently hard because of its virulency and limited pick of antimicrobic agents.
P. aeruginosa has the capacity to transport multiresistance plasmids, and this characteristic has led to the visual aspect of some strains that are immune to all dependable antibiotics ( 37 ) . In a survey carried out at the Post Graduate Medical Institute Hayatabad Medical composite in Afghanistan on the prevalence and opposition form of P. aeruginosa against assorted antibiotics, the highest opposition was observed against Principen, ampicillin/ sulbactam, co-amoxiclave and ofloxacin and least opposition was observed against amikacin. Similarly the MIC for Principen, ampicillin/sulbactam and co-amoxiclave against clinical isolates of Pseudomonas aeruginosa was besides high ( 11 ) . A similar survey carried out at Dhaka Medical College Hospital in 2006 showed that about all of the P. aeruginosa isolates were immune to cefixime and co-trimoxazole, bulk were immune to ceftazidime, gentamycin and Cipro.
The consequence of the survey showed that imipenem is the most effectual drug against P. aeruginosa, followed by amikacin and Cipro ( 39 ) .
MECHANISM OF ACTION OF COMMONLY USED ANTIBIOTICS
The commonly used antibiotics in the intervention of P.
aeruginosa infections are Aminoglycosides ( for illustration Gentamicin and amikacin ) , Penicillins ( such as cabernicillin ) , Quinolones ( for illustration Nalidixic acid, Cipro and levofloxacin ) , Cephalosporins ( Fortaz ) and Carbapenemes ( meropenem and imipenem ) ( 37 ) .Penicillins, Cephalosporins and Carbapenemes inhibit bacterial cell wall synthesis. They are ?-lactam agents. Aminoglycosides and Tetracyclines are inhibitors of protein synthesis. Quinolones are inhibitors of bacterial nucleic acid synthesis ( 17 ) .
Resistance TO ANTIBIOTICS
The antimicrobic opposition conferred by P. aeruginosa is due to mutants in the being ‘s familial stuff.
No individual mutant is responsible for multidrug opposition. Mutants to topoisomerase 2 and 4 confer fluoroquinolone opposition. Derepression of the chromosomal AmpC ?-lactamase reduces susceptibleness to penicillins and Mefoxins. Up-regulation of MexAB-OprM compromises the fluoroquinolones, penicillins, Mefoxins and it besides enhances opposition to many other drugs that lack utile anti-pseudomonal actions ( 38 ) .
2 STATEMENT OF THE PROBLEM
Sing the ability of Pseudomonas aeruginosa to prevail and multiply in damp topographic points and in most pieces of equipment in infirmary wards ( 4 ) , antimicrobic opposition is a turning concern. This is attributed to the fact that the being is able to defy conditions such as high temperature and high concentrations of salts and antiseptic ( 10 ) . It is hence imperative to invariably measure the pathogenesis and sensitiveness forms of P.aeruginosa so as to forestall farther spread and return of infection in the infirmary set up.
Null Hypothesis ( H0 )
The prevalence of P. aeruginosa in lesion and Pus swab specimens at Parirenyatwa infirmary is 6.7 % .
Alternate Hypothesis ( H1 )
The prevalence of P. aeruginosa in lesion and Pus swab specimens at Parirenyatwa infirmary is greater than 6.7 % .
The purposes of this survey are:
To find the prevalence of P. aeruginosa in lesion and Pus swab specimens of patients admitted at Parirenyatwa infirmary.To find the antimicrobic susceptibleness forms of the isolates.