Proteus spp.

Proteus spp.

1. Enterobacteriaceae Proteus

2. General characteristics Proteus species are widespread in the environment. Are normal inhabitants of the human intestinal tract . N itrate-positive . Facultative anaerobic. O xidase-negative. Ferment glucose ( lac - ) The two species to most commonly produce infections in humans are P. mirabilis and P. vulgaris .

3. Characteristics of Pathogenic Enterobacteriaceae

4. pathology P. mirabilis causes urinary tract infections ( make stones) and occasionally other infections, such as bloodstream infection and respiratory tract infections. P. vulgaris is probably more frequently implicated in wound and soft tissue infections than UTIs. Antibiotic Profile P. mirabilis is resistant to nitrofurantoin (used for UTI). P. vulgaris is generally more resistant to various antibiotics (specifically ampicillin, amoxicillin.. etc ).

5. P . mirabilis Indole test positive . ( t o convert tryptophan into  indole) P. Vulgaris Indole test negative . They have ability to swarm over the surface of media. ( motile ) H2S positive Non Lactose ferment. Urease positive. Oxidase negative Catalase positive . phenylalanine deaminase

6. Microorganisms capable of producing  phenylalanine deaminase remove the amine (NH2) from phenylalanine and releases the amine group as free ammonia This enzyme removes the amine group from the amino acid

7. Proteus syndrome is genetic disorder not bacterial infection

8. Gram-negative bacilli Pseudomonas

9. Pseudomonas: Other Opportunistic Gram-negative Bacilli Family Pseudomonadaceae, which contains over 200 species. Most of them are pathogenic to plants, insects, and reptiles. A few species cause disease in humans. P. aeruginosa is the most important. These organisms are notorious because of the potency to develop innate resistance to many antibiotics . Are obligatory aerobic. Non fermented Sugar. Mostly oxidase-positive bacteria . Most of them are motile by presence of one or two flagella

10. Pseudomonas: Other Opportunistic Gram-negative Bacilli is found in soil, water, plants, and animals. it may colonize healthy humans without causing disease( normal flora )   . Is major cause of nosocomial infections . P. Aeruginosa can even grow in laboratory water baths, hot tubs, wet IV tubing, and other water-containing vessels. This explains why the organism is responsible for so many nosocomial infections P.  aeruginosa secretes a  capsule-like polysaccharide called alginate. P. aeruginosa produces numerous toxins Has ability to grow at 42C. Pseudosel Agar

11. Antigenic Structure and Toxins Pathogenesis is based on multiple virulence factors: endotoxin, exotoxins, and enzymes. adhesins, pili . Its endotoxin , like that of other gram-negative bacteria, causes the symptoms of sepsis and septic shock. The best known of the exotoxins is exotoxin A , which causes t issue necrosis . It inhibits by the same mechanism as diphtheria eukaryotic protein synthesis exotoxin (Corynebacterium) .

12. Antigenic Structure and Toxins Strains of P. aeruginosa that have a “type III secretion system” are significantly more virulent than those that do not. This secretion system transfers the exotoxin from the bacterium directly into the adjacent human cell, which allows the toxin to avoid neutralizing antibody. - cause cell death or interfere with the host immune response to infection

13. Clinical significance P. aeruginosa causes both localized and systemic illness Localized infections : These may occur in the eye Ear elderly diabetic patients or trauma patients skin (wound sepsis) Urinary tract (particularly in hospitalized patients) Respiratory tract (pneumonia) Gastrointestinal tract meningitis

14. Clinical significance 2. Systemic infections: Infections reflecting systemic spread of the organism include bacteremia (most common in patients whose immune system has been compromised). secondary pneumonia. bone and joint infections. Endocarditis.

15. Antibiotic Resistance P. aeruginosa is intrinsically resistant to many antimicrobial agents, and can acquire additional resistance to many other antimicrobial agents via horizontal gene transfer or mutations . The mechanisms responsible for intrinsic resistance include various multidrug efflux pumps ( affecting β- lactams, fluoroquinolones, macrolides, and other antibiotics ).

16. sources 1.Lippincot – chapter 13. third ed. 2. Jawetz -chapter 15. 28 th ed. 3. Levinson chapter-18. 14 th ed.

17. Thank you