2.1.1 HISTORY OF PSEUDOMONAS AERUGENOSA Pseudomonas aerogenosa was first recognized in the study “On the blue and green coloration of bandages” in 1882, conducted by Carle Gessard a French pharmacist. In his study he discovered that P.aerugenosa was a water-soluble pigment, which under exposure to ultraviolet light, illuminated green-blue.
Carle Gessard, back in 1882, concluded that P.aerugenosa was of a pathogenic, infectious nature, after classifying the strand; due to the similarity between the strand and other similar microbes.Since the discovery of this opportunistic pathogen, breakthroughs have been made, sighting the severity of its power to fester rapidly and oppose treatment. This pathogen is constantly monitored, and its genome is continually updated into data bases, due to the potential for it to be used as a biological weapon2.
1.1.1 HISTORY OF ESCHERICHIA COLIIn 1885, the German-Austrian pediatrician Escherichia disc overfed this organism in the feces of healthy individuals. He called it Bacterium coli commune because it is found in the colon. Early classifications of prokaryotes placed these in a handful of genera based on their shape and motility (at that time Ernst Haeckel’s classification of bacteria in the kingdom Monera was in place).
Bacterium coli was the type species of the now invalid genus Bacterium when it was revealed that the former type species (“Bacterium triloculare”) was missing. Following a revision of Bacterium, it was reclassified as Bacillus coli by Migula in 1895 and later reclassified in the newly created genus Escherichia, named after its original discoverer. Bacterium coli has since been used for biological lab experiment research, infection can lead to hemolytic uremic syndrome (HUS), characterized by hemolytic anemia, thrombocytopenia, and renal injury.1996 the world’s worst outbreak of E. coli food poisoning occurred in Wishaw, Scotland, killing 20 people.
2.1.1.
2 EPIDEMIOLOGY AND CONTROL OF PSEUDOMONAS AERUGENOSA P. aeruginosa is primarily a nosocomial pathogen, and the methods for control of infection are similar to those for other nosocomial pathogens. Because pseudomonas thrives in moist environments, special attention should be paid to sinks, water baths, showers, hot tubs, and other wet areas. For epidemiologic purposes, strains can be typed using molecular typing techniques. 2.1.1.
3 EPIDEMIOLOGY PREVENTION AND CONTROL OF ESCHERICHIA COLIThe enteric bacteria establish themselves in the normal intestinal tract within a few days after birth and from then on constitute a main portion of the normal aerobic (facultative anaerobic) ssmicrobial flora. E. coli is the prototype. Enteric that are mostly found in water found in water or milk are accepted as proof of fecal contamination from sewage or other sources.Control measures are not feasible as far as the normal endogenous flora is concerned. Enteropathogenic E .coli serotypes should be controlled like salmonellae. Some of the enteric constitute a major problem in hospital infection.
It is particularly important to recognize that many enteric bacteria are “opportunists” that cause illness when they are introduced into debilitated patients. Within hospitals or other institutions, these bacteria commonly are trans-mitted by personnel, instruments, or parenteral medications. Their control depends on hand washing, rigorous asepsis, sterilization of equipment, disinfection, restraint in intravenous therapy, and strict precautions in keeping the urinary tract sterile (i.e. closed drainage).2.1.
1.4. MICROBIOLOGY AND DIAGNOSIS OF PSEUDOMONAS AERUGENOSAA. SpecimensSpecimens from skin lesions, pus, urine, blood, spinal fluid, sputum, and other material should be obtained as indicated by the type of infection.B. SmearsGram-negative rods are often seen in smears. No specific morphologic characteristics differentiate pseudomonads in specimens from enteric or other gram-negative rods.
C. CultureSpecimens are plated on blood agar and the differential media commonly used to grow the enteric gram-negative rods. Pseudomonads grow readily on most of these media, but they may grow more slowly than the enteric. P. aeruginosa does not ferment lactose and is easily differentiated from the lactose-fermenting bacteria. Culture is the specific test for diagnosis of P aeruginosa infection. (Henry et al,. 2011).
2.2. PATHOGENESIS OF PSEUDOMONASP. aeruginosa is pathogenic only when introduced into areas devoid of normal defenses, such as when mucous membranes and skin are disrupted by direct tissue damage as in the case of burn wounds; when intravenous or urinary catheters are used; or when neutropenia is present, as in cancer chemo-therapy. The bacterium attaches to and colonizes the mucous membranes or skin, invades locally, and produces systemic disease.
These processes are promoted by the pili, enzymes, and toxins described earlier. Lipopolysaccharide plays a direct role in causing fever, shock, oliguria, leukocytosis and leukopenia, disseminated intravascular coagulation, and adult respiratory distress syndrome.P.
aeruginosa and other pseudomonads are resistant to many antimicrobial agents and therefore become dominant and important when more susceptible bacteria of the normal microbiota are suppressed. May lead to rapid destruction of the eye, occurs most commonly after injury or surgical procedures. In infants or debilitated persons, P .aeruginosa may invade the bloodstream and result in fatal sepsis; this occurs commonly in patients with leukemia or lymphoma who have received antineoplastic drugs or radiation therapy and in patients with severe burns. 2.
2.1 PATHOGENESIS AND CLINICAL MANIFESTATION OF ESCHERICHIA COLIThe clinical manifestations of infections with E coli and the other enteric bacteria depend on the site of the infection and cannot be differentiated by symptoms or signs from processes caused by other bacteria.A. E coli1.
Urinary tract infection—E coli is the most common cause of urinary tract infection and accounts for approximately 90% of first urinary tract infections in young women. The symptoms and signs include urinary frequency, dysuria, hematuria, and pyuria. Flank pain is associated with upper tract infection.
None of these symptoms or signs is specific for E. coli infection. Urinary tract infection can result in bacteremia with clinical signs of sepsis. Most of the urinary tract infections that involve the bladder or kidney in an otherwise healthy host are caused by a small number of O antigen types that have specifically elaborated virulence factors that facilitate colonization and sub-sequent clinical infections. These organisms are designated as uropathogenic E coli. Typically, these organisms produce hemolysin, which is
