Recurrent/Opportunistic Infections Flashcards Preview

Infection & Immunity Block > Recurrent/Opportunistic Infections > Flashcards

Flashcards in Recurrent/Opportunistic Infections Deck (16):

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
Use of certain medications: prescription or OTC
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:
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

Microaerophilic (5% Oxygen); grows best in low O2

Pathogenesis not completely understood
Cytotoxin (VacA)

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

1. Inactivate drug

2. Modify Target

3. Reduce Concentration

4. Metabolic Bypass

5. 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
1. Express alternative PBP - mecA in staph aureus (metabolic bypass)
2. Express Beta-lactamase - degrade antibiotic (inactivation of drug)
3. Express altered Porin - spits antibiotic out (reduce drug concentration)



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



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)


Non-Genetic Mechanisms of Resistance

Failure of the drug to reach the bacteria:
Bacteria within abscess structure
Intracellular bacteria

Presence of a foreign body

Apparent resistance:
Wrong drug and/or dose
Non-compliance by patient