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  • 1. Outside the enteric tract Klebsiella-Enterobacter-Serratia group
  • 2. Klebsiella-Enterobacter-Serratia group Organisms in this group are opportunistic pathogens causing nosochomial infections, especially pneumonia and UTI. K.pneumonia is an important respiratory pathogen outside hospitals, as well.
  • 3. • K.pneumoniae, Enterobacter cloacae and Serratia marcescens are most involved in human infections. • Have similar properties, and distinguished on basis of biochemical tests and motility. • K.pneumonia has a very large polysaccharide capsule, giving its colonies a striking mucoid appearance. • S.marcescens produce red-pigmented colonies.
  • 4. • Pathogenesis: • K.pneumoniae is a primary, non-opportunistic pathogen related • • • • to its antiphagocytic capsule. Nevertheless, patients having predisposing conditions such as advanced age, chronic respiratory disease, diabetes are more susceptible. Enterobacter and Serratia cause nosochomial infections , especially to invasive procedures like intravenous catheterization, respiratory intubation and Urinary Tract manipulations. Outbreaks of Serratia associated with contamination of water in respiratory therapy devices. Serratia can also cause endocarditis in Injection drug users. The pathogenesis of septic shock related to the endotoxins, as in other gm neg rods.
  • 5. • Clinical findings: • UTI and Pneumonia are usual clinical conditions associated, but bacteremia and secondary spread to other areas such as liver and meninges can occur. • Difficult to distinguish infections caused by these orgs. Pnemonia caused by Klebsiella produces a thick, bloody sputum and can progress to necrosis and abscess formation.
  • 6. Lab diagnosis: Lactose fermenting colonies on McConkeys and EMB agar. Serratia is a late lactose fermenter. Organisms differentiated using biochemical tests.
  • 7. • Treatment: • As the antibiotic resistance can vary greatly, antibiotic sensitivity tests decides the choice of the effective drug. • Carbapenem resistant strains are an important cause of nosocomial infections and are resistant to almost all known antibiotics. • An aminoglycoside like Gentamicin and a Cephalosporin like Cefotaxime used until the sensitivity results are known. • In severe Enterobacter infections, a combination of Imipenem and gentamicin is often administered.
  • 8. Prevention by changing the site of intravenous catheters, removing urinary catheters when not required and proper care of respiratory devices are some of the generalized measures taken.
  • 9. Proteus-Providencia-Morganella group • Cause UTI, both hospital and community acquired. • They are gm neg rods . • Distinguished from other enterobacteriaceae by producing enzyme Phenylalanine deaminase. • Produce Urease, that cleaves urea to ammonia and carbon dioxide. • Certain species have a swarming effect on blood agar due to being very motile. • Proteus morganii is now Morganella morganii and Proteus rettgeri is now Providencia rettgeri, based on molecular studies of DNA relatedness, they were found to be significantly different.
  • 10. Certain cell wall O antigens of Proteus cross react with antigens of several species of Rickettsias. These proteus antigens used to detect antibodies against certain rickettsiae in patients serum. This test was called as Weil-Felix test, now used less frequently as more specific procedures made available.
  • 11. • Pathogenesis: • Orgs. Present in colon and soil and water. • Produce UTI due to their presence in colon and to colonize the • • • • urethra, especially in women. The vigorous motility of Proteus contribute to their ability to invade the urinary tract. Production of urease is an important feature , as it produces ammonia from the urea in urine creating alkaline conditions. This encourages formation of magnesium ammonium phosphate stones called Stuvite. Stones in the urinary tract obstruct flow of urine, damages urinary epithelium, and serve as a node for recurrent infection by trapping the bacteria within the stone. Treatment, thus generally involves keeping the urine at low pH, as alkaline conditions also favor the growth of orgs.
  • 12. • Clinical findings: • UTI symptoms similar to those caused by other orgs. • Proteus can also cause pneumonia, wound infections and septicemia. • P.mirabilis causes most community and hospital borne infections. • Providencia rettgeri important agent for nosocomial infections.
  • 13. • Lab diagnosis: • Swarming growth on blood agar, can frustrate isolation of • • • • • pure cultures of other orgs. Phenyethyl alcohol inhibits the swarming, allowing isolated colonies of Proteus and other orgs. Lactose non-fermenting colonies on McConkeys agar. P.vulgaris and mirabilis produce hydrogen sulfide thet blackens the TSI slant, but M.morganii and Pr. Rettgeri does not. P.mirabilis is indole negative unlike other species in the group. A distinction to guide the choice of antibiotics. All the species are Urease positive.
  • 14. • Treatment: • Strains are sensitive to trimethoprim sulfamethoxazole and aminoglycosides. • P.mirabilis most sensitive to Ampicillin. • The indole positive species are most resistant to antibiotics. Antibiotic of choice for them is a cephalosporin like Cefotaxime. • Providencia rettgeri is frequently resistant to multiple antibiotics. • Prevention involves prompt removal of urinary catheters to avoid nosocomial UTI.
  • 15. Pseudomonas • P.aeruginosa (Burkholderia aeruginosa) causes infections • • • • • like sepsis, UTI and pneumonia, primarily in patients with lowered immunity and host defenses. Causes chronic lower respiratory tract infections in Cystic fibrosis patients, Causes wound infections (cellulitis) in burn cases, and Causes malignant otitis externa in diabetic patients. It is an imp cause of ventilator associated pneumonia. P.pseudomallei causes Melioidosis (high fever with bloody, purulent sputum and in chronic form, the infection resembles TB or appear as pneumonia or with lung abscess)
  • 16. • Pseudomonas are gm neg rods resemble other • • • • enterobacteriaceae. They differ in being strict aerobes (derive energy by oxidation of sugars rather than fermentation) As theydo not ferment Glucose, they are known as nonfermenters, in contrast to other enterobacteriaceae who are glucose fermenters. They are oxidase positive (oxidation involves electron transport by cytochrome c). Pseudomonas are able to grow in water with minimum nutrients, hence their persistence in hospital surroundings. P.aeruginosa and P. cepacia have remarkable ability to withstand disinfectants and detergents.
  • 17. • Pseudomonas produce 2 pigments: • Pyocyanin, which colors the pus in the wound blue. It is a • • • • bacteriocin. Pyoverdin (Fluorescein), a yellow green pigment that fluoresces under UV light, a property used to detect early infection in burn patients. In the lab. These pigments diffuse imparting a blue-green color. P.aeruginosa alone produces pyocyanin. Strains of P.aeruginosa isolated from Cystic fibrosis patients have a prominent slime layer (glycocalyx), giving the colonies a mucoid appearance. The slime layer mediates adherence to respiratory mucous membranes and prevents antibody from binding, thus protecting the org.
  • 18. • Pathogenesis: • It is primarily an opportunistic pathogen (after burn or cystic fibrosis or immunocompromised individuals or patients with indwelling catheters). • It colonizes the upper respiratory tract of hospital patients. • Causes 10-20% of nosocomial infections and most common cause of nosocomial pneumonia. • Pathogenesis on multiple virulent factors like endotoxin, exotoxin and enzymes.
  • 19. • Endotoxin produces symptoms of sepsis and septic shock like other gm neg.bacteria. • Exotoxin A causes tissue necrosis. It prevents protein synthesis by ADP-ribosylating EF-2 like diphtheria toxin. • Enzymes such as elastase and proteases produced are histotoxic and facilitate invasion of the org into the blood stream. • Pyocyanin damages the cilia and mucosal cells of the respiratory tract.
  • 20. • Strains of P.aeruginosa have a “TypeIII secretion system”. • These are significantly more virulent than those who don’t • • • • have it. This secretion system transfers the exotoxin from the bacterium directly into the adjacent human cell, thereby avoiding the neutralizing antibody of the host. Type III secreting systems are mediated by transport pumps in the bacterial cell membrane. Of the 4 exoenzymes(exotoxins) known to be transported thus, Exo S is the most clearly associated with virulence. Exo S has several modes of action, the most imp. Is the ADP-ribosylation of a Ras protein, leading to the damage to the cytoskeleton.
  • 21. • Clinical findings: • P.aeruginosa can cause infection virtually anywhere in the body. • Pneumonia (Cystic fibrosis cases), wound infections(burn cases) and • • • • • UTI predominate. Imp cause of HA-pneumonia, especially in those undergoing mechanical ventilation. Once they enter blood stream, mcause sepsis. Can spread to the skin, where thwy cause black, necrotic lesions called ecthyma gangrenosum. Patients with P.aeruginosa sepsis have >50% mortality rate. Severe external otitis and folliculitis(skin infection) in inadequately chlorinated swimming pools. Osteochondritis of the foot Wounds through the soles of gym shoes) and Corneal infections (contact lens users) can also occur.
  • 22. • Lab diagnosis: • Lactose non-fermenting on McConkeys /EMB agar. • It is Oxidase positive. • On TSI : a typical metallic sheen, coupled with a blue- green pigment on nutrient agar, with a fruity aroma, is sufficient presumptive diagnosis. • Diagnosis confirmed by biochemical tests. • Identification done by bacteriophage typing or Pyocin typing for epidemiological purposes.
  • 23. • Treatment: • P.aeruginosa is notoriously resistant to many antibiotics. • They must be tailored to the sensitivity of each isolate and monitored frequently as resistant strains can emerge during therapy. • Anti-psedomonal penicillin (like piperacillin coupled with tazobactam, or Ticarcillin with Clavulanate ) plus an aminoglycoside (like gentamicin or amikacin) is the treatment of choice. • For highly resistant strains : Colistin (Polymyxin E) is useful. • For UTI : Ciprofloxacin is the drug of choice.
  • 24. Prevention is to keeping Neutrophil counts high, removing indwelling catheters promptly and special care of burns.
  • 25. Bacteroides and Prevotella Bacteroides most common cause of serious anaerobic infections like sepsis. Peritonitis and abscesses. Bacteroides fragilisis the most frequent pathogen. Prevotella melaninogenica, formally known as Bacteroides melaninogenicus is also an important pathogen.
  • 26. • Bacteroides and Prevotella are anaerobes, non-spore • • • • forming gm neg rods. Bact. fragilis and Bact.corrodens are human pathogens. Pathogenesis: These are part of normal flora of colon, oral cavityand the female genital tract. Variety of infections such as local abscess at the site of mucosal break, metastatic abscesses by hematogenous spread to distant organs or lung abscess by aspiration of oral flora.
  • 27. • Local tissue necrosis, impaired blood supply and growth of • • • • facultative anaerobessuch as E.coli, that utilize the oxygen reducing their levels and contributing to anerobic conditions for these orgs. To grow are the contributing factors. Predisposing factrs such as surgery, trauma and chronic disease play an imp role in pathogenesis. Polysaccharide capsule of Bact. Fragilis imp virulence factor. Endotoxin of Bact.fragilis less potent.as it contains a variant of Lipid A. Enzymes such as Hyaluronidase, collagenase and phospholipase contribute to tissue damage.
  • 28. Clinical findings: Bact. Fragilis group most frequently associated with intra-abdominal infections, either peritonitis or localized abscess. Bact.fragilis causes disease below the diaphragm and Pre.melaninogenica above the diaphragm.
  • 29. • Lab diagnosis: • Bacteroides isolated anaerobically on blood agar plates containing kanamycin and vancomycin. • Identified by biochemical reactions such as sugar fermentations and by production of organic acids like formic, acetic and propionic acid detected by gas chromatography. • Pre.melaninogenica produces characteristic black colonies on blood agar.
  • 30. • Treatment: • Members of Bact. Fragilis are resistant to penicillins, first generation • • • • • cephalosporins and aminoglycosides, making them the most resistant among the anaerobic pathogens. Metronidazole is the drug of choice. Cefoxitin, Clindamicin, and Chloramphenicol are alternate drug of choice. Aminoglycosides combined to treat mixed infections with facultative gm neg rods. For Pre. Melaninogenica: Metronidazole or Clindamicin is the drug of choice. Surgical drainage of abscesses usually accompany antibiotic therapy. Prevention involves perioperative administration of cephalosporin like Cefoxitin, dor abdominal or pelvic surgery.