Outside the enteric tract
Organisms in this group are opportunistic pathogens
causing nosochomial infections, especially pneumonia
K.pneumonia is an important respiratory pathogen
outside hospitals, as well.
• 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.
• 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
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.
• 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
Lactose fermenting colonies on McConkeys and EMB
agar. Serratia is a late lactose fermenter.
Organisms differentiated using biochemical tests.
• 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
• An aminoglycoside like Gentamicin and a Cephalosporin
like Cefotaxime used until the sensitivity results are
• In severe Enterobacter infections, a combination of
Imipenem and gentamicin is often administered.
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.
• 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
• 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
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.
• 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.
• Clinical findings:
• UTI symptoms similar to those caused by other orgs.
• Proteus can also cause pneumonia, wound infections
• P.mirabilis causes most community and hospital
• Providencia rettgeri important agent for nosocomial
• 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
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.
• Strains are sensitive to trimethoprim sulfamethoxazole
• 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
• Prevention involves prompt removal of urinary catheters
to avoid nosocomial UTI.
• 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
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
• Pseudomonas are gm neg rods resemble other
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
• Pseudomonas produce 2 pigments:
• Pyocyanin, which colors the pus in the wound blue. It is a
Pyoverdin (Fluorescein), a yellow green pigment that fluoresces
under UV light, a property used to detect early infection in burn
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.
• 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
• Causes 10-20% of nosocomial infections and most
common cause of nosocomial pneumonia.
• Pathogenesis on multiple virulent factors like
endotoxin, exotoxin and enzymes.
• 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
• Enzymes such as elastase and proteases produced are
histotoxic and facilitate invasion of the org into the
• Pyocyanin damages the cilia and mucosal cells of the
• Strains of P.aeruginosa have a “TypeIII secretion system”.
• These are significantly more virulent than those who don’t
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.
• Clinical findings:
• P.aeruginosa can cause infection virtually anywhere in the body.
• Pneumonia (Cystic fibrosis cases), wound infections(burn cases) and
Imp cause of HA-pneumonia, especially in those undergoing
Once they enter blood stream, mcause sepsis. Can spread to the skin,
where thwy cause black, necrotic lesions called ecthyma
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.
• 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.
• 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
• 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
• For UTI : Ciprofloxacin is the drug of choice.
Prevention is to keeping Neutrophil counts high,
removing indwelling catheters promptly and special
care of burns.
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
• Bacteroides and Prevotella are anaerobes, non-spore
forming gm neg rods.
Bact. fragilis and Bact.corrodens are human
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.
• 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
Predisposing factrs such as surgery, trauma and chronic
disease play an imp role in pathogenesis.
Polysaccharide capsule of Bact. Fragilis imp virulence
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.
Bact. Fragilis group most frequently associated with
intra-abdominal infections, either peritonitis or
Bact.fragilis causes disease below the diaphragm and
Pre.melaninogenica above the diaphragm.
• 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
• Pre.melaninogenica produces characteristic black
colonies on blood agar.
• 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
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
Prevention involves perioperative administration of cephalosporin like
Cefoxitin, dor abdominal or pelvic surgery.