HRR: gram negative rods Flashcards
What are the three species of Bordetella that infect humans?
- Pertussis: causes whooping cough
- Parapertussis: milder pertussis-like illness
- Bronchiseptica: kennel cough in canines and sometimes chronic respiratory tract infection in humans
What are some clinical manifestations of Bordetella pertussis?
Black eyes, whooping cough, dehydration, exhaustion
Describe culture of Bordetella pertussis.
It requires a special medium and grows slow; antibiotics are needed. It is too late to culture once the cough starts as the bacteria is usually cleared.
Describe the 3 stages of Bordetella pertussis.
- Catarrhal: 1-2 weeks and causes fever, malaise, profuse rhinorrhea
- Paroxysmal: 2-4 weeks and causes coughing, lymphocytosis, and whoop (audible gasps for breath)
- Convalescent: symptoms fade
Describe clinical presentation of Bordetella.
Bacteremia does not occur. Infants have a high mortality rate. Adult disease is atypical. Bacterial replication is localized to respiratory epithelium. Can cause rib fracture.
What are the virulence factors of B. pertussis?
Adhesins (pili and FHA) and exotoxins (pertussis toxin, AC, and TCT)
Describe the pathogenesis of B. pertussis.
- It adheres to cilia via FHA
- PT and pore-forming AC injure cells
- TCT damages ciliated epithelium
- PT absorbed into bloodstream and causes immune dysregulation
Describe PT toxin.
An AB toxin that ADP-ribosylates G proteins that regulate adenylate cyclase; the effect is tissue specific.
What are systemic effects of PT and AC?
Lymphocytosis, inactivation of neutrophils/macrophages/lymphocytes, histamine sensitization, insulin secretion
How do we prevent B. pertussis?
Acellular pertussis vaccines DTaP and Tdap booster
What can be found in Tdap boosters?
Inactivated PT, FHA, and other virulence factors
What are the two human pathogens of Haemophilus?
H. influenza and H. ducreyi
What do the Haemophilus require for growth?
H. influenza requires hematin and NAD, while H. ducreyi only needs hematin. Blood must be lysed for them to get these.
How is H. influenza typed?
If they are encapsulated, they are typed by antibodies specific for the capsular material.
What is the worst strain of H. influenzae? What is the capsule made of?
Type B; polyribitol phosphate
What are some common characteristics of encapsulated and non-encapsulated H. influenzae that help cause disease?
Adhesins (pili and outer membrane proteins) and endotoxins (LOS and LPS)
What are the virulence factors of Haemophilus?
Attachment via pili and HMWs and anti-phagocytic capsules if they are encapsulated. This allows them to enter the bloodstream.
What are clinical manifestations of encapsulated H. influenza?
Cellulitis, purulent meningitis, acute epiglottis, pneumonia and septic arthritis, bacteremia
What are clinical manifestations of non-encapsulated H. influenza?
Chronic sinusitis, otitis media, chronic bronchitis, pneumonia
How does H. influenzae spread?
Through respiratory droplets; only spread person to person.
Describe immunity to H. influenzae.
At 0-6 months you’re protected by maternal antibodies. 6-18 months there is a lack of T-independent immune response. Over 18 months there is increasing immunity.
What confers protection against H. influenzae?
Anti-PRP antibodies
How do we diagnose H. influenzae?
Clinical presentation, gram stain, growth on chocolate agar.
How do we treat H. influenzae?
Empiric therapy, beta lactams with beta lactamase inhibition, rifampin prophylaxis.
Describe H. ducreyi.
It is an STI that causes soft and painful ulcers. You can be infected over and over again, and the ulcers increase HIV transmission.
Describe the growth of Pseudomonas.
Very minimal growth requirements; can grow in wide temperature range, is salt tolerant, grows readily on common media, and is hemolytic on blood agar.
Describe Pseudomonas.
Motile, pale-staining, aerobic gram-negative rod.
What is the relation between Pseudomonas and lactose?
It fails to ferment it.
What are distinctive features of Pseudomonas aeruginosa?
Colorful water-soluble pigment, strong odor, oxidase positive, and mucoid colonies.
What are infection sites for Pseudomonas?
Eyes, ears, burns, wounds, catheters (UTI), and in cystic fibrosis.
What are the virulence factors of Pseudomonas aeruginosa?
- LPS
- Pili
- Flagella
- Slime made of secretion of alginate polymer
- Exotoxin A that inactivates EF2
- Elastase that cleaves elastin, IgA/G, and complement components
- Exotoxin S that acts on protein G to affect the cytoskeleton and induce apoptosis.
What injection system does exotoxin S use?
Type III.
What does elastase do?
Disrupts blood vessels and lung structures.
Which species survives in tap water?
Pseudomonas aeruginosa.
What are modes of transmission of Pseudomonas aeruginosa?
Sinks, nebulizers, humidifiers, contact lens solution, pools.
What is the most significant pathogen in cystic fibrosis patients?
Pseudomonas aeruginosa.
What are clinical presentations of Pseudomonas aeruginosa?
Infections of burns and wounds, pneumonia with necrosis/infarct/vascular invasion, otitis externa, folliculitis, eye infection.
What temperature does Pseudomonas grow at?
42 Celsius.
How do we diagnose Pseudomonas?
Growth at 42 degrees on almost any media showing pigment production and positive oxidase.
How do we treat Pseudomonas aeruginosa?
It is pretty resistant to antibiotics, and the only effective agents are given IV. CF patients can be given cipro and aztreonam.
Which gram-negative species do not ferment lactose?
Pseudomonas and Burkholderia.
What are the virulence factors of Burkholderia?
Elastase, adhesins, and LPS.
Describe Burkholderia cepacia.
An opportunistic pathogen found in aquatic environments that colonizes in CF patients and causes rapidly fatal cepacia syndrome with respiratory distress and septicemia.
How is Burkholderia cepacia transmitted?
Contaminated IV solutions, nebulizers, disinfectant, urinary catheters.
How do we treat Burkholderia?
It is resistant to many antibiotics, so TMP-SMX is first line.
Where do we find Burkholderia pseudomallei?
Southeast Asia and aquatic environments.
How is Burkholderia transmitted?
Inhaled, ingested, traumatic inoculation.
What is the clinical presentation of Burkholderia pseudomallei?
Melliodosis, acute pneumonia, cutaneous melliodosis.
What population might we see Burkholderia pseudomallei in?
Vietnam veterans.
Describe Burkholderia mallei.
Causes glanders in horses and sometimes humans; presents with ulcerative lesions in nasal mucosa and lung nodules.
