overview to enteric G- bacteria Flashcards

1
Q

what are the Enterobacteriaceae?

A

A family of gram-negative bacteria that includes Klebsiella, E. coli, Enterobacter, Salmonella, Shigella, and other species. Members possess intrinsic resistance against bile salts, which allows the bacteria to proliferate in the gastrointestinal tract.

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2
Q

in alcoholics and patients with DM, Enterobacteriaceae have a tendency to colonize??

A

Oropharyngeal colonization in alcoholics & patients with diabetes mellitus

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3
Q

how Enterobacteriaceae are classified?

A

1) Selective Media: All Enterobacteriaceae usually grow well on MacConkey Agar which inhibits the growth of gram-positive bacteria
2) Lactose Fermentation: Enterobacteriaceae are often sub-classified by their capacity to ferment lactose which can be visualized rapidly on EMB medium by the development of pigmented colonies when fermentation is positive. Consequently, organisms can be categorized as lactose fermenters and lactose non-fermenters
3) Indole Production: Enterobacteriaceae are often sub-classified by their capacity to produce indole from tryptophan leading to categorization as indole positive and indole negative organisms.

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4
Q

what are the most notable organisms in Enterobacteriaceae?

A
Escherichia coli
Klebsiella pneumoniae
Proteus mirabilis
Enterobacter
Serratia
Salmonella
Shigella
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5
Q

how Enterobacteriaceae proliferate in the GI tract?

A

Possess an intrinsic resistance against bile salts, which allows the bacteria to proliferate in the gastrointestinal tract

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6
Q

what is the O-antigen (also called a somatic antigen)

A

it is the exposed part of Lipopolysaccharide, which contributes to the variation of the Gram-negative bacterial cell wall.

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7
Q

what is the H-antigen?

A

any of various antigens associated with the flagella of motile bacteria and used in serological identification of various bacteria
— called also flagellar antigen

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8
Q

what is the bacterial K antigen?

A

The K antigen repeat units form a high molecular weight structure called ‘capsule’.

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9
Q

which is external K or O antigen?

A

K, capsular antigen

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10
Q

what is the bacterial capsule?

A

an envelope that surrounds some bacterial cells. Usually composed of polysaccharide. B. anthracis has a polypeptide capsule. Acts as a virulence factor that facilitates adherence to host cells and protection against phagocytosis, lysozymes, reactive oxygen species, and complement-mediated lysis.

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11
Q

what important bacteria produce tick capsule and appear with mucoid colonies on MacConkey agar?

A

Klebsiella pneumonia

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12
Q

what are the virulence factors of Enterobacteriaceae?

A
  • -Adhesins – aid in binding to host cells, e.g. fimbriae
  • -Lipopolysaccharide – potent inducer of host immune response via endotoxin release (lipid A)
  • -Capsules – help avoid phagocytosis but poor immunogens
  • -Toxins – e.g. hemolysins of E. coli
  • -Antimicrobial resistance – e.g. via plasmid exchange
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13
Q

what are the virulence factors that allow colonization? (overall, not only for Enterobacteriaceae)

A

1)Lipoteichoic acid: primarily in gram-positive organisms
Bacterial adhesins: colonizing factors
–Pertussis toxin
–Hemagglutinins
2)Biofilms: adherence to foreign material (e.g., Staphylococcus epidermidis, Staphylococcus mutans, Pseudomonas aeruginosa)
3)Flagella: filamentous organelles that aid in the movement of bacteria
–Peritrichous flagella: flagella around the bacterium (e.g., Escherichia coli)
–Lophotrichous flagella: several flagella at one pole (e.g., Pseudomonas)
–Polar flagella: one flagellum at one of the bacterial poles (e.g., Vibrio cholerae)

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14
Q

what are the virulence factors that allow avoidance of the immune system? (overall, not only for Enterobacteriaceae)

A

1) Capsule
- -Streptococcus pyogenes (M protein)
- -Neisseria gonorrhoeae (pili)
- -Staphylococcus aureus (protein A)
2) IgA protease: cleaves mucosal IgA
- -Neisseria spp.
- -Haemophilus influenzae
- -Streptococcus pneumonia
3) Protein A: binds to Fc region of IgG (e.g., Staphylococcus aureus)

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15
Q

how Enterobacteriaceae are laboratory diagnosed?

A
•	Gram-negative bacilli
•	Grow on non-selective & selective media
–	35-37OC, aerobic/ anaerobic, air/CO2
–	MacConkey selective agar
…..lactose versus non-lactose fermenters

• Further identification:
– Biochemical testing or
– Mass Spectrometry: MALDI-TOF
– Antimicrobial susceptibility testing

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16
Q

what is the selective agar for Enterobacteriaceae?

A

MacConkey
A growth medium containing a neutral red pH indicator that turns pink when culturing bacteria that can ferment the lactose (e.g., Klebsiella pneumoniae, Enterobacter, Serratia), which results in the production of acid.

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17
Q

Enterobacteriaceae are anaerobe or aerobe?

A

Facultative anaerobe
Bacterial species that are capable of aerobic respiration but can switch to anaerobic respiration if no oxygen is available.

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18
Q

what is the clinical significance of Enterobacteriaceae?

A
  • Wide range of infections in the community & in healthcare facilities, affecting normal & immunocompromised patients
  • Isolated in microbiology laboratories from urine, blood, abdominal specimens, respiratory tract
  • Resistance to multiple antibiotics - an increasing problem
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19
Q

describe the general features of E. coli

A

• Part of the normal flora especially in the colon (‘coliforms’)
• Most strains nonpathogenic in the GIT but some cause intestinal infection & infection elsewhere
• Pathogenic strains usually produce common virulence factors
- Adhesins – various pili
- Exotoxins – e.g. Shiga toxin, heat-labile toxin

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20
Q

what is the bacterial pilus?

A

A bacterial appendage found on the surface of gram-negative bacteria. Facilitates adhesion of bacteria to specific surfaces. Sex pili are used to exchange genes with other bacteria during conjugation.

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21
Q

what is the labile toxin?

A

A virulence factor that is destroyed at high temperatures and produced by certain bacteria, including enterotoxigenic E. coli (ETEC), Clostridium perfringens, and Bacillus cereus. Heat-labile enterotoxin over-activates adenylate cyclase, increasing the production of cyclic adenosine monophosphate (cAMP). This causes increased secretion of chloride and water efflux into the intestinal lumen, which results in watery diarrhea.

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22
Q

what infections commonly cause E. Coli

A
  1. Urinary tract infection (UTI)
  2. Intra-abdominal infections – cholecystitis, peritonitis, cholangitis
  3. Neonatal meningitis
  4. Bloodstream infection (BSI)
  5. Gastroenteritis
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23
Q

what is the most common cause of UTI?

A

E. Coli

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24
Q

why does E. Coli cause more UTI in females than males?

A

1)Shorter in females hence why UTI more common)
2)Originates from the perianal area & travels along the urethra to the bladder
3)Strains often have pili/fimbriae that aid attachment to epithelial cells – Type 1 fimbriae
4)Certain serotypes more commonly
associated with UTI - 01, 02, 04

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25
Q

what are the symptoms of UTI?

A
  • Suprapubic pain (cystitis – inflamed bladder)
  • Flank pain (pyelonephritis – inflamed kidney)
  • Dysuria = pain when passing urine
  • Frequency* = passing urine every 1-2 hours
  • Urgency* = The urge to pass urine, must pass urine NOW!
  • Nocturia* = passing of urine during the night which is out of usual habit
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26
Q

what are the P fimbriae?

A

virulence factor of uropathogenic E. coli that promotes adherence to urothelial cells via cellular projections composed of glycoproteins. Involved in the pathogenesis of cystitis and pyelonephritis.

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27
Q

what intra-abdominal infections can be caused by E. Coli?

A
–	appendicitis
–	acute cholecystitis
–	peritonitis  
–	sub-phrenic abscess
–	liver abscess
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28
Q

E. Coli can cause meningitis. True/False

A

True
– Neonate – early after delivery, acquired during birth
– Post-traumatic/post-operative, e.g. major road traffic accident

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29
Q

what age group is particularly at risk of meningitis caused by E. Coli

A

neonates

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30
Q

what are the common sources of E. Coli sepsis?

A
  • intra-abdominal pathology
  • urinary tract sepsis
  • neonatal meningitis
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31
Q

list the serotypes of E.Coli that cause gastroenteritis?

A
A.	Enterotoxigenic E. coli (ETEC)
B.     Enterohaemmorhagic (EHEC)
C.	Enteropathogenic E.coli (EPEC)
D.	EnteroinvasiveE. coli (EIEC)
E.	Enteroaggregative E. coli (EAEC)
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32
Q

which bacteria is the most common cause of Traveller’s diarrhea?

A

ETEC

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33
Q

what is the traveler’s diarrhea?

A

Infectious diarrhea caused by a variety of bacterial, viral, and parasitic organisms. Typically acquired during travel to resource-limited regions, most commonly through the ingestion of contaminated food or water. Causative pathogens include enterotoxigenic E. coli (most common), enterohemorrhagic E. coli, Campylobacter, Salmonella, Entamoeba histolytica, Norovirus, and Rotavirus.

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34
Q

ETEC prodduce diarrhea by ivasion into intestinal wall. True/False

A

False

It is non-invasive (vs shigella, salmonella, EHEC). Diarrhea is due to enterotoxins

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35
Q

how toxins produced by ETEC cause diarrhea?

A

1) Heat-labile enterotoxin (AB toxin; two-component protein, similar to cholera toxin): activation of adenylate cyclase → ↑ cAMP-level → increased chloride secretion → water efflux into the intestinal lumen (secretory diarrhea)
2) Heat-stable enterotoxin: activation of guanylate cyclase → ↑ cGMP-level → decreased NaCl reabsorption → water efflux into the intestinal lumen (secretory diarrhea)

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36
Q

what are the clinical features of the traveler’s diarrhea?

A
  • -Watery diarrhea
  • -Abdominal cramping
  • -Nausea and possibly vomiting
  • -Fever
  • -Decreased appetite
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37
Q

ETEC causes bloody diarrhea. True/False

A

False

Secretory not inflammatory

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38
Q

which one is the most significant serotype of EHEC?

A

Serotype O + H antigens: E. coli O157:H7 =most common isolate, common cause HUS

39
Q

how EHEC produce bloody diarrhea?

A

Adherence is rapidly followed by the invasion of the intestinal epithelial cells
–Shiga toxin (verotoxins) = acute inflammatory response and tissue destruction……bloody diarrhea
Adhesion to receptors of gut cells → Shiga-like toxin secretion → toxin cleaves adenine from the rRNA → inactivation of the 60S subunit → protein synthesis inhibited → cell death → necrosis and inflammation of the GI mucosa → watery-bloody diarrhea with mucus (otherwise known as dysentery)

40
Q

how EHEC acquires Shiga toxin?

A

EHEC bacteria are infected by bacteriophages that integrate their genes into the bacteria’s genome; these genes then code for toxins (verotoxin/Shiga toxin 1 and 2).

41
Q

how EHEC is acquired by humans (transmitted)

A

– Consumption of contaminated food, water, minced beef products, such as burgers
– Exposure to a contaminated environment involving direct or indirect contact with animals or their feces

42
Q

what are the features of EHEC diarrhea?

A
  • Bloody diarrhea +/- vomiting
  • More severe disease in extremes of age
  • Complications: Haemolytic uremic syndrome (10% children < 10 yrs): acute renal failure, thrombocytopenia, hemolytic anemia.
  • Antibiotics NOT INDICATEDas associated with increased toxin production which can lead to further cell death and worsening of symptoms …rehydration NNB
43
Q

what is the HUS (Hemolytic-Uremic-Syndrome)

A

A condition in which microthrombi occlude the arterioles and capillaries, which results in microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Predominantly affects children and most commonly occurs following dysentery due to Shiga toxin-producing enterohemorrhagic Escherichia coli (EHEC), typically serotype O157: H7.

44
Q

why antibiotics should be used very carefully and only in severe cases of EHEC infection?

A

due to increased risk of HUS (not 100 percent proved)

45
Q

what is the significance of EPEC?

A

• A major cause of Infantile gastroenteritis especially in developing countries – infants < 6 months
• The high mortality rate due to severe dehydration
After rotavirus infections, EPEC is one of the leading causes of death in children in developing countries

46
Q

how EPEC cause diarrhea?

A

EPEC blocks absorption by attaching to the apical surfaces of the intestinal epithelium, causing the villi to flatten–malabsorption. No toxin production is involved.

47
Q

does EPEC produce toxins?

A

no

48
Q

does EIEC cause bloody diarrhea?

A

Yes.

The invasion of gut epithelium leads to inflammation and necrosis. Fever, cramps similar to shigellosis

49
Q

what is the clinical significance of EAEC?

A
  • -Persistent diarrhea in young children.

- -Important virulence factor: the ability to aggregate with one another

50
Q

what are the laboratory aspects of E. Coli?

A

• Specimens depend on the infection
–Urine /Blood /CSF etc
• Grows on a wide variety of media
• Facultative anaerobe / 37° C / 24-48 hrs
• MacConkey – lactose fermenting pink colonies

51
Q

how E. Coli infections are treated?

A
  • Depends on source/patient factors
  • NB: Gastroenteritis – no treatment (supportive)
  • Approx 70% E. coli are amoxicillin resistant
  • Co-amoxiclav or cefuroxime reasonable empiric agent for community-acquired/post-operative infections
  • Trimethoprim/nitrofurantoin for lower UTI
  • Antibiotic resistance increasing e.g. extended-spectrum β-lactamases (ESBL)
52
Q

what is ESBL?

A

group of bacteria that produce beta-lactamases capable of inactivating penicillins, cephalosporins, and carbapenems in isolated cases. Common pathogens include gram-negative bacteria (e.g., Klebsiella, E. coli).

53
Q

how ESBL is treated?

A

1) carbapenems

2) If the MDRGN is resistant to all four antibiotic groups: colistin, linezolid, tigecycline (last resort antibiotics)

54
Q

what is the Friedlander pneumonia?

A

Atypical pneumonia that is caused by Klebsiella. The disease is named after Carl Friedlander, a German microbiologist, who discovered that pneumonia was caused by bacteria in 1883.

55
Q

who is at risk for having pneumonia caused by Klebsiella?

A

– In alcoholics, compromised respiratory function

56
Q

what are the clinical features of Klbesiellal pneumonia?

A

– Necrotizing pneumonia, “red currant jelly” sputum
– Often affects upper lobes; may cause abscesses
– Also causes VAP

57
Q

describe the sputum seen with Klebsiellal pneumonia?

A

red currant jelly” sputum

rusty sputum in streptococcal lobar pneumonia

58
Q

what is the VAP?

A

A hospital-acquired infection that develops 48 hours after the initiation of mechanical ventilation via either tracheostomy or intubation. Approx. 5–10% of patients on mechanical ventilation develop VAP.

59
Q

how Klebsiella is diagnosed?

A
Specimens depend on the infection
-	Urine
-	Blood
-	Sputum
Grows on a wide variety of media
Facultative anaerobe / 37° C / 24-48 hrs
MacConkey – (mucoid) lactose fermenting pink colonies
60
Q

what is the characteristic feature of Klebsiella colonies/

A

large, mucoid colonies

61
Q

how Klebsiella is treated?

A
  • Depends on the isolate so you need to perform antimicrobial susceptibility testing
  • Beta lactams (e.g. co-amoxicillin/cefuroxime), quinolones, aminoglycosides usually effective empiric agents
62
Q

what are the mechanisms of resistance to multiple antibiotics of Klebsiella?

A
  1. β lactamase producer (e.g., ESBL) with a 2nd resistance mechanism e.g. impermeability due to reduced porin expression (so antibiotic is unable to penetrate bacteria)
  2. Plasmid-mediated acquisition of a β lactamase which preferentially hydrolyzes carbapenems, i.e. a carbapenemase
    - Also resistant to a range of other antibiotics due to different mechanisms and have very limited, if any, treatment options
63
Q

what are the carbapenems?

A

A class of broad-spectrum, β-lactam antibiotics that are resistant to β-lactamase. Effective against gram-positive and gram-negative aerobes and anaerobes. Administered intravenously due to poor enteric absorption. Examples include imipenem, meropenem, ertapenem, and doripenem.

64
Q

what is the Proteus mirabilis?

A

A gram-negative, urease-positive, rod-shaped bacterium that is part of the natural flora of the gastrointestinal tract. It can cause urinary tract infections and lead to the development of kidney stones (struvite stones).

65
Q

what infections commonly cause proteus?

A

– Urinary tract infection (UTI)
– Intraabdominal infections
– Bloodstream infection (usually in hospitalized patients)

66
Q

why proteus can cause struvite kidney stones?

A

These bacteria convert urea to ammonia. Elevated ammonia causes alkaline urine and precipitates the ammonium magnesium phosphate salt, causing stone formation ( Proteus mirabilis, Klebsiella, and Pseudomonas)

67
Q

how proteus ascends through the urinary tract?

A

• Common in patients with urinary catheters
• Infection mainly via ascending route from the perineum
– It has multiple flagella and fimbriae to facilitate movement and attachment to the urinary tract epithelium, respectively.

68
Q

how proteus is diagnosed?

A

Characteristic ‘swarming’ appearance on blood but not on MacConkey agar where they form NON- lactose fermenting colonies
Swarming due to peritrichous flagella
Cultures have a characteristic fishy smell

69
Q

what are the characteristic features of proteus colonies/

A

swarming’ appearance on blood but not on MacConkey agar where they form NON- lactose fermenting colonies
Swarming due to peritrichous flagella
Cultures have a characteristic fishy smell

70
Q

what smell is characteristic to proteus colonies?

A

fishy smell

a fishy odor is also characteristic of vaginitis caused by Gardnerella vaginalis

71
Q

what is the oxidase test?

A

A test used to identify bacteria that produce cytochrome c oxidase, an enzyme that converts oxygen to H₂O₂ and H₂O to produce energy. Oxidase-positive bacteria include Pseudomonas, Campylobacter jejuni, Vibrio cholerae, and Helicobacter pylori. Oxidase-negative bacteria include E. coli, Salmonella, Shigella, and Klebsiella.

72
Q

proteus is oxidase positive or negative?

A

It is oxidase-negative but catalase- and nitrate-positive. Specific tests include positive urease (which is the fundamental test to differentiate Proteus from Salmonella)

73
Q

how proteus is treated?

A

Fluoroquinolones (e.g., ciprofloxacin), cephalosporins, or TMP/SMX

74
Q

describe the Enterobacter, Citrobacter, and Serratia

A
  • Act as opportunistic pathogens
  • Produce infections in “at-risk” hospitalized patients – healthcare-associated infections eg pneumonia, intravascular catheter sepsis, UTI, GI infections eg wound infection/abscess
  • Often resistant to multiple antibiotics such as cephalosporins and aminoglycosides
75
Q

what is the characteristic feature of Serratia?

A

A catalase-positive, gram-negative bacillus in the family Enterobacteriaceae. It causes nosocomial pneumonia and urinary tract infections. Some strains produce red pigment-red colonies

76
Q

define pseudomonas aeruginosa

A

A gram-negative rod that grows in water and humid conditions (e.g., hot tubs, lakes, or contaminated contact lens solution). Causes nosocomial infections (e.g., urinary tract infections or pneumonia), pneumonia in adult patients with cystic fibrosis, external otitis (“swimmer’s ear”), and endocarditis in intravenous drug users.

77
Q

pseudomonas is only pathogenic. True/False

A

False

• Normal flora of the gastrointestinal tract

78
Q

where pseudomonas grows easily

A

– Widespread in moist areas in the environment e.g. sinks, drains, water etc.
– Also soil, plants

79
Q

what are the virulence factors of pseudomonas?

A

1) Lophotrichous flagella
2) Aerobic
3) Special macroscopic characteristics
- -A typical blue‑green pus may form in infection
- -Sweet odor, if grown in culture
4) Produces exotoxin A, which inhibits protein synthesis by inactivating elongation factor 2
5) Produces phospholipase C, which degrades cell membranes
6) Produces pyoverdin and pyocyanin

80
Q

what is the pyocyanin?

A

A virulence factor produced by Pseudomonas aeruginosa that generates reactive oxygen species that damage host cells. Contributes to the blue-green color of some Pseudomonas infections.

81
Q

what are the lophotrichous fimbriae?

A

Bacteria with two or more flagella located at one end of the cell

82
Q

what are the clinical presentations of pseudomonas infection?

A

•Community:
– Chronic otitis externa (swimmers, diabetics)
– Wound infections in susceptible patients.
•Hospital:
– Infections in burns (bloodstream infection)
– Pulmonary infections:
•Acute infection in ventilated patients
– Can cause a necrotizing pneumonia
•Chronic infection in cystic fibrosis/bronchiectasis
– Wound infections – especially in the diabetic leg/foot ulcers
– Urinary tract infections (especially if urinary catheter in situ)
– Eye infections: trauma, contaminated fluids e.g. contact lens solutions; can lead to the destruction of eye.

83
Q

what is the malignant otitis externa?

A

A subtype of otitis externa characterized by necrotizing inflammation of the external auditory canal. Most frequently caused by Pseudomonas aeruginosa. Risk factors are poorly controlled diabetes mellitus and immunosuppression.

84
Q

what are the laboratory aspects of pseudomonas?

A

• Grow on & in a wide variety of media
• Mucoid to small colonies, non-lactose fermenting pale colonies on MacConkey
• Oxidase positive
• Strict aerobe
• Produce a variety of pigments
– Pyocyanin (blue), pyoverdin / fluorescein (green), pyorubin (dark red),

85
Q

what is pyoverdin?

A

virulence factor produced by some species of Pseudomonas, including P. aeruginosa. Acts as a siderophore that facilitates bacterial survival in iron-deficient conditions. Contributes to the blue-green color of some Pseudomonas infections.

86
Q

is pseudomonas aerobe or anaerobe?

A

strict aerobe

87
Q

pseudomonas is oxidase positive or oxidase negative

A

Oxidase positive

88
Q

pseudomonas lactose fermenting or non-fermenting?

A

non-fermenting

89
Q

what are the anti-pseudomonal antibiotics?

A
  • Piperacillin-tazobactam
  • Ceftazidime (3rd generation cephalosporin)
  • Ciprofloxacin (quinolone)
  • Aminoglycosides e.g. gentamicin
  • Carbapenems e.g. meropenem (reserved)
90
Q

moxifloxacin is used to treat Pseudomonas?

A

No,

Although it is pseudomonas, it is ineffective against pseudomonas in contrast to ciprofloxacin or levofloxacin

91
Q

what is the Burkholderia cepacia?

A

• Previously known as Pseudomonas cepacia
• A major cause of opportunistic infection in the lungs of patients with cystic fibrosis
• Particular worry in this group of patients as
multi antibiotic resistance, easily transmitted by social contact
• Can cause “cepacia syndrome” with acute fatal necrotizing pneumonia +/- BSI

92
Q

what is the cepacia syndrome

A

In cystic fibrosis, it can cause “cepacia syndrome” which is characterized by a rapidly progressive fever, uncontrolled bronchopneumonia, weight loss, and in some cases, death.

93
Q

what is the Melioidosis

A

An infection caused by Burkholderia pseudomallei endemic primarily to northern Australia and Southeast Asia. Transmitted via environmental contact with the skin, respiratory tract, and gastrointestinal tract. It can cause local skin disease, pneumonia, and/or bacteremia, though most cases are subclinical.

94
Q

Burkholderia mallei cause…

A

Glanders

  • -Signs of glanders include the formation of nodular lesions in the lungs and ulceration of the mucous membranes in the upper respiratory tract. The acute form results in coughing, fever, and the release of an infectious nasal discharge, followed by septicemia and death within days. In the chronic form, nasal and subcutaneous nodules develop, eventually ulcerating; death can occur within months, while survivors act as carriers.
  • -May also get pneumonia from inhalation of the organism