Recurrent/Opportunistic Infections Flashcards
Specific Susceptibility
Barrier: damaged integument, loss of normal flora; staphylococcus, streptococcus, enterics, C. difficile
Humoral Function; loss of spleen, IgA deficiency, complement deficiency; extracellular bacteria
Cell Mediated Function: abnormal number or function of T cells or macrophages; intracellular bacteria, viruses, and fungi
Structural Abnormalities
Skin integrity
Incomplete bladder emptying
Sphincter between ureters and bladder
Ear canals
Risk Behaviors
Sexual Activity Smoking Use of certain medications: prescription or OTC Travel Diet Recreational activities
Immune Status
Decreased innate immunity: physical, chemical, cellular
Decreased acquired immunity: humoral and cell-mediated
Recurrent Infections
A re-occurrence of the same illness from which an individual has previously recovered
Not necessarily the same strain of the bacterium
Host factors contributing to recurrent bacterial infections:
Anatomical
Behavioral
Immune status
Persistent Infections
Definition: an infection that persists for a long period of time in a single host which may or may not result in overt symptoms
In the absence of treatment
Different than Normal Flora because…
Whether symptomatic or not, persistent infections represent a burden to the host
Persistency facilitates spread of the pathogen to other individuals.
Bacteria Responsible for Persistent Infections
Mycobacterium tuberculosis Helicobacter pylori Salmonella enterica sv. Typhi Borrelia burgdorferi Treponema pallidum Brucella species
Mechanisms of Bacterial Persistence
Environmental modification
Modulation or avoidance of host immune response
Biofilm formation
Helicobacter pylori
Gram-negative
Microaerophilic (5% Oxygen); grows best in low O2
Pathogenesis not completely understood
Cytotoxin (VacA)
Adhesins
Urease
Persistence Mechanism: environmental modification
Attach with adhesions to stomach and urease breaks down urea to increase pH the microenvironment immediately surrounding the bacteria (not the whole environment)
Also produces toxin to degrade eukaryotic cells = ulcers
Know – mechanism of persistence is via environmental modification by urease
Borrelia burgdorferi
Motile spirochete, gram negative
Causative agent of Lyme disease
Transmitted by tick bite
Virulence Factors: none
Persistence Mechanisms:
Avoidance of Immune response via antigenic variation of surface proteins to avoid Ab-mediated killing
Modulation of host immune defense by binding host factors to bacterial surface (Factor H)
Dental Plaque
Mixed bacterial populations
Mechanisms of Persistence: biofilm
Dental plaque represents the most dense collection of bacteria in the body
General Mechanisms of Resistance
- Inactivate drug
- Modify Target
- Reduce Concentration
- Metabolic Bypass
- Non-genetic Basis of Resistance
Beta Lactams
Mechanism of action: inhibit cell wall synthesis and binds Penicillin Binding Protein (PBP) to prevent cross linking of peptidoglyan
Key feature of Antibiotic: ring structure
Mechanisms of Resistance
- Express alternative PBP - mecA in staph aureus (metabolic bypass)
- Express Beta-lactamase - degrade antibiotic (inactivation of drug)
- Express altered Porin - spits antibiotic out (reduce drug concentration)
Macrolides
Mechanism of Action:
Prevents Protein Synthesis
Binds the 50s Subunit
Resistance: methylating 23s rRNA, once rRNA is methylated it is still functional, but cannot be bound by the drug; this modification importantly doesn’t change the function and is just as effective
Efflux pumps can be expressed to pump drug out
Trimethoprim
Mechanisms of Action:
Prevents Nucleic Acid Synthesis
Inhibits activity of Dihydrofolate reductase
Dihydrofolic acid is converted to tetrahydrofolic acid via dihydrofolate reductase to make purines and pyrimidines
Mechanism of Resistance: different enzyme (plasmid encoded) from bacteria can be used to replace the inhibited enzyme to allow bacterial growth (metabolic bypass)
