1. Introduction

Entry and multipliation require a breach in immunity
Very poor or no horizontal spread
Found in AIDS patients, immunosuppressed cancer patients, burn victims, smokers or drinkers with transient suppression of the mucociliary elevator, transplant recipients, and patients with diabetes

2. Pseudomonas aeruginosa

Introduction
1. Gram-negative bacillus with motility
2. Requires only carbon and nitrogen for growth therefore ubiquitous in soil and water
3. Oxidase-positive
4. Fruity odor
Encounter
1. Asymptomatic carriage rate approximately 2%
2. Tap water, contaminated vegetables, or hot tubs
3. Causes 11% of hospital-acquired infections
Entry
1. Enter through burn, cut, puncture, or abrasion
2. Pili adhere to epithelium a. binds respiratory cells more facilely in cystic fibrosis patients
3. In normal patients, does not adhere well to our surfaces, but can stick to underlying tissue where organisms are killed by PMNs
Spread/Multiplication
1. If it multiplies successfully, can spread to neighboring tissues
2. Dissemination aided by flagella, elastase, toxin A, and exoenzyme S
3. Multiply extracellularly in patients with decreased neutrophil count
4. In CF patients, alginate shields organism from immune system
Damage
1. Infection in skin leads to cellulitis
2. Infection in urinary tract leads to UTIs
3. Infection in the airways leads to pneumonia
4. Infection in the eye causes corneal infection
5. Invasion of the bloodstream can result in endocarditis, septic arthritis, or osteomyelitis
Diagnosis and Identification
1. Clinical presentation of ecthyma gangrenosum
2. Easy to culture
Virulence Factors
1. Pili: attach to sites of epithelial damage
2. Elastases: cleave transferrin for iron, ECM to facilitate dissemination, or antibodies to evade host immune response
3. Alkaline phosphatase: interferes with gamma-interferon activity
4. Phospholipase C: phosphate acquisition
5. LPS: anti-phagocytic and anti-complement
6. Exotoxin A: inhibits host protein synthesis by blocking elongation of amino acid chain a. kills PMNs
7. Exotoxin S: ADP-ribosylates small G-proteins such as Ras
8. Mucoid capsule: anchors bacteria to host, blocks clearance by mucociliary action, blocks phagocytosis, blocks antibody- and complement-mediated lysis
9. Flagellum: motility
Treatment
1. Late-generation beta-lactams, fluoroquinolones and aminoglycosides
2. Highly-resistant organism therefore treat with multiple antibiotics
Outcome
1. Endocarditis carries 50% mortality rate
2. High-grade bacteremia in neutropenic patient carries 50-70% mortality rate

3. Legionella pneumophila

Introduction
1. Aerobic gram-negative bacillus with motility
2. Intracellular pathogen of amoebae
Encounter
1. Found in ponds, lakes, hot springs, tap water, shower heads, humidifiers, and hot water tanks
Entry
1. Inhaled into lungs through aerosols from showers, air conditioners or humidifiers, or microaspirated while drinking infected water
2. Coiling phagocytosis in alveolar macrophages
Spread/Multiplication
1. Associates with mitochondria and ribosomes in macrophage and mutliplies intracellularly
2. Hematogenous dissemination leads to multiple organ dysfunction
Damage
1. Most of the damage is caused by host inflammatory response
2. Legionnaire’s disease
  1. mild-severe pneomonia and fever, diarrhea, and vomiting
  2. possible mental status changes
  3. risk factors: cancer, diabetes, emphysema, immunosuppressive therapy, renal dialysis, and alcohol consumption
3. Pontiac fever
  1. mild, self-limiting infection
  2. fevers, chills, headaches and malaise
Diagnosis and Identification
1. Clinical diagnosis based on history and pneumonia unresponse to normal treatment
2. Culture on charcoal yeast extract agar
3. Urine antigen test
Treatment
1. Erythomycin or tetracycline
Outcome
1. 15% fatality rate for Legionnaire’s disease

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