2. • Species from genera Pseudomonas, Burkholderia and
Stenotrophomonas were all previously classified in the Pseudomonas
genus.
• P.aeruginosa also known as Burkhoderia aeruginosa
• P. cepacia renamed Burkhoderia cepacia
• P. maltophilia renamed Xanthomonas maltophilia, now named
Stenotrophomonas maltophilia
• P. pseudomallei also known as Burkhoderia pseudomallei
3. Epidemiology & Transmission
• Found mainly in soil and water
• Present as normal flora of colon in 10% of people
• Can colonize upper respiratory tract of hospitalized patients
• Contaminating respiratory therapy and anaesthesia equipment, intravenous fluid,
distilled water due to its ability to grow in simple aqueous solution
• Primarily an opportunistic pathogen causing infection:
o In hospitalized patient (e.g. in burn patient), in whom skin host defense destroyed
o In chronic respiratory disease patient (e.g. cystic fibrosis), in whom normal clearance
mechanism impaired
o In immunosuppressed patient
o In patient with neutrophil count <500/uL
o In patient with indwelling catheter
4. Properties
• Gram negative rod
• Strict aerobe
• Non-fermenters (derived energy only by oxidation of sugar rather by
fermentation)
• Oxidase-positive (oxidation involves electron transport by cytochrome c)
• Able to grow in water containing traces of nutrients (e.g. tap water) –
favors their persistence in hospital environment
• Remarkable ability to withstand disinfectant hospital acquired infection
• Found growing in hexachlorophene-containing soap solution, in antiseptic
and in detergent
5. • Produces 2 pigments
1. Pyocyanin – color the pus in a wound blue
2. Pyoverdin (fluorescein) – a yellow-green pigment that fluoresces
under UV light – can be used in early detection of skin infection in
burn patient
• P aeruginosa the only Pseudomonas species synthesizes pyocyanin
• P aeruginosa isolated from cystic fibrosis patient have a prominent
slime layer (glycocalyx) , giving colonies a very mucoid appearance
• Slime layer mediates adherence of the organism to mucous
membranes of respiratory tract and prevents antibody from binding
to the organism
6. Virulence Factor
• Endotoxin
- Causes symptoms of sepsis and septic shock
• Exotoxin
- Exotoxin A causes tissue necrosis
- Inhibits eukaryotic protein synthesis by ADP ribosylation of elongation
factor-2 (same mechanism as diphteria exotoxin)
• Enzymes
- Elastase and proteases – histotoxic and facilitates invasion of organism into
bloodstream
- Pyocyanin – damages the cilia and mucosal cells of the respiratory tract
7. • “Type III secretion system”
- Significantly more virulent than those that do not
- Transfer the exotoxin grom the bacterium directly into adjacent
human cell, which allows toxin to avoid neutralizing antibody
- The secretion system mediated by transport pump in bacterial cell
membrane
- 4 exoenzyme known to be transported
- Exo S most clearly associated with virulence, most important mode of
action is ADP-ribosylation of a Ras protein -> damage to cytoskeleton
8. Clinical Picture
• Urinary tract infection
• Pneumonia especially in cystic fibrosis patient
• Wound infection especially in burn patient
• Hospital acquired pneumonia – especially ventilator-associated pneumonia
• Sepsis
• Ecthyma gangrenosum – spread to skin causing black, necrotic lesion
• Endocarditis in IVDU
• Severe otitis media (malignant otitis media) and skin lesion (e.g. folliculitis) – in
users of swimming pool and hot tub with inadequate chlorination
• Osteomyelitis of the foot – most common organism, occurs in those who sustain
puncture wounds through soles of gym shoes
• Corneal infection – in contact lenses users
9. Laboratory Diagnosis
• MacConkey’s, EMB agar: non-lactose-fermenting (colorless) colonies
• Oxidase positive
• TSI agar: typical metallic shine
• Nutrient agar: blue-green and a fruity aroma
• Identification for epidemiologic purpose: bacteriophage, pyocin
typing
10. Treatment
• Resistant to many antibiotics
• Antipseudomonal penicillin (piperacillin/tazobactam ,
ticarcillin/clavunate) + aminoglycoside (gentamicin or amikacin)
• Ceftazidime – also effective
• Colistin (polymyxin E) – highly resistant stains
• Ciprofloxacin – drug of choice for UTI
• Trimethoprim-sulfamethoxazole (co-trimoxazole) – infections caused
by B.cepacian, S.maltophilia
12. Epidemiology & Transmission
• Causes meliodosis
• Rare disease found primarily in Southeast Asia
• Found in soil
• Transmission
1. Inhalation of contaminated dust particles (increased cases during rainy
season)
2. Direct contact with contaminated soil and water through penetrating
wounds, existing skin abrasions, burns
3. Aspiration of contaminated water
4. Ingestion of contaminated water
13. Clinical Features
• Incubation period 1-21 days (mean 9 days) but can be as long as
months and even years
• Present acutely with rapid progression and death or run a chronic and
relapsing course
14. Common Presentation
• Pneumonia
- Most common presentation + multiple abcesses in liver, spleen and
prostate
• Septicaemia
⁻ Metastatic foci of infection are established rapidly during
bacteraemia, particularly in the lungs (multifocal pneumonia, which
may cavitate), liver, spleen and kidneys (multiple abscesses), skin and
soft tissues (cellulitis, pustules), bones and joints, lymph nodes and
prostate, although any site may be affected.
15. Other presentations
• Soft tissue infection: cellulitis, fasciitis, skin abscess/ulcer
• Intra abdominal: single or multiple abscesses in the liver, spleen, kidney or
pancreas
• Bone and joint infection: osteomyelitis, septic arthritis (musculoskeletal
meliodosis)
• Genitourinary: prostatic abscess
• CNS infection: cerebral abscess, meningoencephalitis, encephalomyelitis
• Facial: suppurative parotitis
• Ocular infection: conjunctival ulcer, hypopyon, orbital cellulitis
16. • Asymptomatic infection (positive serology up to 50% of healthy adults
in endemic countries)
• Overall mortality of bacteraemic meliodosis approaches 100% if
untreated, reduced to 37-54% with optimal management and
aggressive intensive care
• Localised meliodosis – lower mortality rate (4-5%)
18. • Gram negative rod
• Safety pin appearance on M/E
• Obligate aerobe
19. Treatment
• General treatment include I&D of abscess
• Antibiotics
INTENSIVE THERAPY
Life threatening melioidosis
• IV Meropenem 1g TDS, OR IV Imipenem 1g TDS x 2 weeks (4-8 weeks for deep infection)
• May add adjunct abx; co-trimoxazole (Trimethoprim-Sulphamethoxazole) 3-4 tab BD (for severe infection
and for deep focal infection: bone, joint, prostate and neurological involvement) + Folic acid 5 mg OD
Other melioidosis
• IV Ceftazidime 2g TDS
Localized superficial melioidosis
• T. Augmentin (500mg/125mg) TDS x 12-20 weeks
20. ERADICATION THERAPY
• Oral Co-trimoxazole (Trimethoprim-Sulfamethoxazole) 2-4 tab BD and
Doxycycline 100mg BD x 20 weeks (standard oral combination
regime); OR
• T Augmentin 2 tab TDS x 20 weeks - in pregnant women, allergic to
co-trimoxazole
