Pseudomonas and Legion ella • Pin Lin ( 凌 凌 ), Ph.D. Departg ment of Microbiology & Immunology, NCKU ext 5632 [email protected]• References: 1. Chapter 34 & 38 in Medical Microbiology (Murray, P. R. et al; 5 th edition) 2. 凌凌凌凌凌凌 ( 凌凌凌 凌凌凌 , 4th edition)
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Pseudomonas and Legionella Pin Lin ( 凌 斌 ), Ph.D. Departg ment of Microbiology & Immunology, NCKU ext 5632 [email protected] References: 1. Chapter.
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Acinetobacter baumannii: opportunistic infections of RT
Moraxella catarrhalis: RT infections
P. Aeruginosa (refer to green pigment)
Forms round colonies with a fluorescent greenish color, sweet odor, and -hemolysis.
Pyocyanin- nonfluorescent bluish pigment;
pyoverdin- fluorescent greenish pigment;
pyorubin, and pyomelanin
Some strains have a polysaccharide capsule.
Identification of P. aeruginosa is usually based on colonial m
orphology (flat colonies w/ spreading border), -hemolysis, o
xidase positive, the presence of characteristic pigments and
sweet odor, and growth at 42 oC.
Outline
1. Physiology & Structure
2. Pathogenesis & Immunity
3. Lab Diagnosis, Treatment, & Prevention
P. aeruginosaPathogenesis and Immunity
1. This organism is widely distributed in nature and is commonly present in moist environments in hospitals. It is pathogenic only when introduced into areas devoid of normal defenses, e.g.,
1. Disruption of mucous membrane and skin.
2. Usage of intravenous or urinary catheters.
3. Neutropenia (as in cancer therapy).
2. P. aeruginosa can infect almost any external site or organ.
3. P. aeruginosa is invasive and toxigenic. It attaches to and colonizes the mucous membrane or skin, invade locally, and produces systemic diseases and septicemia.
4. P. aeruginosa is resistant to many antibiotics. It becomes dominant when more susceptible bacteria of the normal flora are suppressed.
Virulence Factors of P. aeruginosa-I
Structural Components
1. Pili and nonpilus adhesins.
2. Polysaccharide capsules (seen in cultures from patients
catalyzes production of toxic forms of oxygen that cause
tissue damage.
Toxins & Enzymes
Elastases: LasA (serine protease) & LasB (zinc metalloprotease); destruct elastin-containing tissues and the lung parenchymal damage and hemorrhagic lesions
(Ecthyma Gangrenosum); help bacteria spread and inhibit neutrophil chemotaxis; induces antibodies in chronic infections.
Hemolysins:Phospholipase C (Heat-sensitve): breaks down lipid & lecithin Rhamnolipid (Heat-stable): inhibits ciliary activity.
Exotoxin A: blocks protein synthesis; immunosuppressive; causes dermal tissue necrosis.
Exoenzyme S and T: ADP-ribosyltransferase activity, cytotoxic to host cells.
Virulence Factors of P. aeruginosa-II
Primary Skin infections: The most common is infection of wounds and burns (blue-green pus). *Fluorescent pigment detected in wounds, burns, or urine by UV fluorescence.
Pulmonary infections: P. aeruginosa infections of lower respiratory tract. Tracheobronchitis to severe Necrotizing pneumonia. Colonization seen in CF patients (diffuse, bilateral bronchopneumonia with necrosis).
Meningitis (when introduced by lumbar puncture).Eye infections: corneal ulcer.
Clinical Diseases of P. aeruginosa-I
Ear infections:External Otitis => Often seen in “Swimmer’s ear”
mild in swimmers; malignant (invasive) in diabetic patients. Chronic otitis media
Endocarditis seen in intravenous drug abusers.
Urinary tract infection
Sepsis: most cases originate from infections of lower RT, UT, and skin and soft tissue.*Ecthyma gangrenosum in sepsis: hemorrhagic necrosis of skin, often do not contain pus.
2. Culture: blood agar plate and differential media. Identification
of P. aeruginosa is described above.
3. Identification of P. aeruginosa is usually based on colonial morphology, b-hemolysis, oxidase positive, the presence of characteristic pigments and sweet odor, and growth 42 C
4. Several subtyping methods, including phage typing and molecular typing, are available for epidemiologic purposes.
Treatment
Combined antibiotic therapy is generally required because the bacteria develop resistance rapidly when single drugs are employed.
Laboratory Diagnosis of P. aeruginosa
Prevention and Control-I1. Pseudomonas spp. normally inhabit soil, water, and vegetation and can be isolated from the skin, throat, and stool of healthy persons.2. Spread is from patient to patient via contact with fomites or by ingestion of contaminated food and water.3. Methods for control of infection are similar to those for other nosocomial pathogens.4. Special attention should be paid to sinks, water baths, showers, hot tubs, and other wet areas.5. High risk population: patients with leukemia, burns, cystic fibrosis, and immunosuppression.
P. aeruginosa
Prevention and Control-IIControl:1. Patients at high risk should not be admitted to a
ward where cases of pseudomonas infection are present.
2. Patients infected with P. aeruginosa should be isolated.
3. Sterilizeall instruments, apparatus, and dressing;antimicrobial and other therapeutic substances.
4. Monitor clinically relevant isolates of P. aeruginosa by a suitable typing system to identify epidemic strains.
P. aeruginosa
Stenotrophomonas maltophilia
1. A common nonfermentative, gram-negative isolate.
2. It infects debilitated or immunocompromised persons, and
causes a wide spectrum of diseases, including wound infectio
ns, UT infections, pneumonia, sepsis, meningitis, etc.
3. It is resistant to many commonly used antibiotics, and patie
nts receiving long-term antibiotic therapy are particularly at ris
k for acquiring infections.
4. Infections may be acquired from contaminated disinfectant
s, respiratory therapy and monitoring equipment, and ice ma
chines.
Burkholderia1.They colonize the moist environmental surfaces and are com
monly associated with nosocomial infections.
2. B. cepacia and B. pseudomalei are important pathogens.
3. B. cepacia causes RT infections (particularly in cystic fibrosis
patients), UT infections and septicemia. Usually non-fatal excep
t for RT infections in CF patients.
4. B. pseudomalei usually causes opportunistic infections, but m
ay sometimes infect previously healthy persons. Infection by thi
s organism may result in asymptomatic infection, acute suppura
tive cutaneous infection that may progress to sepsis, and chroni
c pulmonary infection ranging in severity from mild bronchitis to
Requires L-cysteine for growth; grows slowly on complex media, such as BCYE (buffered charcoal-yeast extract) agar, at pH 6.9, 32 oC, and 90% humidity.
L. pneumophila is nonfermentative, catalase-positive, oxidase-positive, and produces gelatinase and -lactamase.
Morphology and identification
Fastidious aerobic gram-negative bacillus. This organism is not seen in stains of clinical specimens, but gram-stain can be made for those grown on agar media. Basic fuchsin should be used as the counterstain.
Serogroup 1 is the most common isolate from humans.
Produces proteases, phosphatase, lipase, DNase, RNase, hemolysin and cytotoxin.
Antigens and cell products
Legionellae are ubiquitous in warm moist environments, such as air-conditioning systems and washing facilities.
Legionellae can parasitize ameba in water; they are relatively resistant to heat and disinfectants.
Legionellosis, sporadic or epidemic, is distributed worldwide. The elderly are at greatest risk. Person-to-person spread or an animal reservoir has not been demonstrated.
Contact with the organism and acquisition of immunity after an asymptomatic infection are common.
Epidemiology
Legionella spp. Associated with human disease
L. pneumophila Infects mainly debilitated or immunocompromise
d humans following inhalation of the bacteria from aerosols gene
rated from contaminated sources, and causes acute purulent pne
umonia.
L. pneumophila is facultative intracellular parasite, readily enters
(via CR3 complement receptor) macrophages and monocytes; in
hibits phagolysosomal fusion; and multiplies in the vacuole until t
he host cells is lysed. It is not effectively killed by PMNs, also.
Immunity to disease is primarily cell-mediated, with humoral imm
unity playing a minor role.
Pathology and Immunity
Risk factors: compromised pulmonary functions (e.g., smoking, chronic bronchitis and emphysema); decreased cellular immunity (e.g., elderly persons, chemotherapy, steroid and other immunosuppressants, and diabetes mellitus).
Legionair's disease (legionellosis): typically severe, rapidly progressive illness with high fever, chills, malaise, nonproductive cough, hypoxia, diarrhea, and delirium. Multiorgan involvement is common. Primary manifestation: pneumonia with multilobar consolidation and inflammation and microabscesses in lung tissue.
Pontiac fever (influenza-like illness): self-limited; fever and chills, myalgia, malaise, and headache, but no evidence of pneumonia. A hypersensitivity reaction to the organism.
Clinical Diseases
Microscopic examination: direct fluorescent antibody (DFA) test. Specific, but sensitivity is low.
Culture: use BCYE supplemented with antibiotics to suppress rapidly growing contaminating bacteria. Legionellae grow after 3 to 5 days. Identification of Legionella is by the finding of typical morphology and specific growth requirements.
Urinary antigen tests: detection of Legionella-specific LPS antigens secreted in the urine of patients by EIA.
Serology: Detection of antigen requires serogroup-specific reagents, however, only serogroup-1 antibodies is commercially available. Antibodies can be detected by indirect fluorescent antibody test.
Laboratory Diagnosis
Macrolides or fluoroquinolones are used to treat severe
Legionella infections.
Pontiac fever is self-limited and requires no specific ther
apy.
Prevention of legionellosis requires identification of the
environmental source of the organism and reduction of t
he microbial burden. Chlorination and heating of water,
and cleaning of the air-conditioning systems are usually
effective for prevention and control of legionellosis.