PROTEUS-PROVIDENCIA-MORGANELLA GENERA

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1 Gram-negative rods Proteus & Pseudomonas DR. HUDA ABO-ALEES Objectives: Describe the morphology & physiology for Proteus & Pseudomonas. Determine the virulence factors of proteus and pseudomonas. Analyze the diseases & pathogenicity for proteus and pseudomonas. Over view about the epidemiology. Outline the laboratory diagnosis. Describe the treatment for each. PROTEUS-PROVIDENCIA-MORGANELLA GENERA According to recent genetic studies many species of proteus genus have been transferred to genus providencia and morganella. Such as: Proteus morganii = Morganella morganii and Proteus rettgeri = Providencia rettgeri. That s leaves only two species in proteus genus these are: Proteus vulgaris and Proteus mirabilis. GENERAL CHARACTERISTICS Gram-negative rods that are distinguished from other members of the Enterobacteriaceae by their ability to produce the enzyme phenylalanine deaminase. Produce the enzyme urease, which cleave urea to form NH3 and C02.

2 Certain species are very motile and produce a striking swarming effect on blood agar, characterized by expanding rings (waves) of organisms over the surface of the agar.(swarming Phenomenon). The cell wall O antigens of certain strains of Proteus, such as OX-19, OX-K and OX-2, cross-react with antigens of several species of Rickettsiae (which cause typhus fever). These Proteus antigens can be used in laboratory test to detect the presence of antibodies against certain rickettsiae in patient's serum. This test, called the Weil-Felix. When treated serum of person infected with typhus fever with Proteus Ag from spp (OX-19, OX-K and OX-2) will give +ve reaction, means that the patient has typhus fever. HABITAT AND TRANSMISSION The organisms are present in the human colon (normal flora) as well as in soil and water. Transmission usually endogenous, to urinary tract by ascending spared of fecal flora. Proteus. mirabilis is the species that cause most community and hospital-acquired infections.

3 PATHOGENESIS AND VIRULENCE FACTORS 1. Endotoxin causes fever and shock associated with sepsis. 2. The vigorous motility of Proteus organism may contribute to their ability to invade the UT. 3. The Production of Urease enzyme urease is an important feature of the pathogenesis of UTI by Proteus. Urease hydrolyzes the urea in urine to form ammonia, which raises the PH resulting to alkaline urine. This encourages the formation of stones (calculi) (struvite) composed of magnesium ammonium phosphate. Stones in the UT obstruct urine flow, damage urinary epithelium, and serve as a nidus for recurrent infection by trapping bacteria within the stone. Because alkaline urine also favors growth of the organisms and more extensive renal damage, treatment involves keeping the urine at a low ph. PREDISPOSING FACTORS FOR UTI Some conditions enhance the chances of getting UTI: 1. The colonization of the vagina. 2. Urinary catheters. 3. Abnormalities of the urinary tract such as strictures, valves, and stones. CLINICAL FINDINGS AND DISEASES Urinary tract infection. Pneumonia. Wound infection. Septicemia.

4 LABORATORY DIAGNOSIS 1. Staining by Gram stain : Gram ve rods. 2.. Culture: a. On MacConkey and EBM ager produce non-lactose fermenter (colorless) colony. b. On blood ager produce characteristic Swarming phenomena which considered as diagnostic feature for Proteus however, can cause misdiagnosis for other bacteria as it can cover other colonies and cannot obtain pure culture. How it can be prevented. 3. P. vulagaris and p. mirabilis produce H2S which blacken the butt of TSI agar. 4. P. mirabilis is indole negative, while others are indole positive. 5. Ferment glucose producing acid and gas. 6. Urea agar (urease test) =: Pink (+); Yellow (-). TREATMENT It is best to do antibiotics sensitivity test antibiotics before using antibiotics to reduce drug resistance. Trimethoprim-sulfamethoxazole or ampicillin is often used for uncomplicated UIT. Third generation cephalosporin should be used for serious infections.

5 Many important species: Pseudomonas aeruginosa Burkholderia cepacia Burkholderia mallei Burkholderia pseudomallei GENERAL CHARACTERISTICS PSEUDOMONAS Pseudomonades are Gram-negative rods. Motile. Strict aerobic means that they drive their energy only by oxidation of sugar rather than fermentation. Non-lactose fermenter. Oxidase-positive. P. aeruginosa isolated from patients with cystic fibrosis have prominent slime layer (Glycocalyx) which give their colony very mucoid appearance. P. aeruginosa produces two pigments useful in clinical and laboratory diagnosis: 1- Pyocyanin, which can color the pus in a wound blue not produced by other species. 2- Pyoverdin (fluorescein). It is a greenish yellow pigment produced by many other species. EPIDEMIOLOGY AND TRANSMISSION P aeruginosa is widely distributed in soil and water. 1 0% of people carry it as normal flora of the colon. Opportunistic pathogens, cause infection in patients with severe burns and chronic respiratory diseases.

6 Important cause of hospital acquired infection as it have remarkable ability to withstand disinfectants, also its ability to grow in simple aqueous solutions resulted in contamination of respiratory therapy and anesthesia equipment, intravenous fluid, and even distilled water. PATHOGENESIS AND VIRULENCE FACTORS Pathogenesis based on multiple virulence factors: Endotoxin, exotoxins, and enzymes Endotoxin cause symptoms of sepsis and septic shock, the best known exotoxin is Exotoxin A which cause tissue necrosis. Enzymes such as elastase and proteases, which are histotoxic and facilitate invasion of the organism into the blood stream. Pyocyanin damages the cilia and the mucosal cells of the respiratory tract. CLINICAL FINDINGS AND DISEASES P. aeruginosa can cause infections anywhere in the body. And it is one of the important cause of gram-negative nosocomial infection Urinary tract infection. Pneumonia the most common cause of gram negative nosocomial pneumonia, especially in cystic fibrosis patient. Wound infection especially burns. Sepsis. Endocarditis.

7 CLINICAL FINDINGS AND DISEASES Malignant otitis externa, which is sever external otitis. especially in diabetic patients Corneal infection in contact lens users. Bone infection as osteochondiritis. Folliculitis and other skin infections as ecthyma gangrenosum. LABORATORY DIAGNOSIS 1. Oxidase positive. 2. Culture: a. On MacConkey agar: No lactose fermentation give pale colonies. b. Nutrient agar: Demonstrate pigment production like pyocyanin and pyoverdin that diffuse into the agar. c. blood agar: Spreading flat pigmented, sometime with Betahemolysis mucoid, confluent growth. TREATMENT Pseudomonas.aeruginosa usually resistant to many antimicrobial agents. 1. The drugs of choice are B-lactam compounds as penicillin, pipracillin, ticarcillin. 2. Aminoglycosides such as gentamycin and tobramycin. 1&2 often given in combination to provide potential effect and reduce drug resistance. 3. Ciprofloxacin.

8 PREVENTION Prevention is easier than cure. 1. Patients at risk as patients with severe burns should be kept in isolated ward to reduce the chance of infection. 2. Therapeutic substances and medical instrument should be kept sterile and screened frequently for contamination especially if they are used for many patients. REFERENCES. Jawetz, Melnick and Adelberg's Medical Microbiology (Brooks, Butel, Morse). 25th ed. Copyright Medical microbiology by David Greenwood 17 th ed Levinson W. Review of Medical Microbiology and Immunology.12 th ed. Copyright 2012, McGraw-Hill.