15 - Multisystem Infections Flashcards
(39 cards)
What is a multisystem infection?
An infection caused by an agent that can:
1: Disseminate (spread) to infect multiple tissues, usally via blood or lymphatics
2. Replicate and/or persist in mult. tissues.
3. Cause disease (symptoms/pathology) in multiple tissues.
What are opportunistic bacteria that cause multisystem infections?
Bugs that are artifically introduced into places where they don’t normally go (eg CSF a normally sterile site), spread and survive, often in compromised hosts.
Often are commensal flora or environmental bacteria.
MAY disseminate and cause multisystem infections if the host is compromised.
What is the role of “professional” multisystem pathogens?
All disseminate and cause multisystem infections in immunocompetent hosts.
This ability is often a key feature of the lifestyle (some are transmitted by an arthropod vector).
What are the routes of entry that opportunistic multi-system bacterial pathogens can use?
Disruptions to physical barriers: constituting a first line of host defense (indwelling lines, IV drug use, surgery, ventilators).
Systemic disruptions to host defenses: may be due to chemotherapy, irradiation, immunosuppressive therapies.
Not essential to lifestyle of these bacteria.
Describe the routes of entry and disruptions to host defenses that can lead to multi-system bacterial infections by “professional” multi-system pathogens?
Overcoming physical barriers and dissemination are often ESSENTIAL to the biology of the organism.
Multi-system infections in previously healthy people are usually caused by bacteria that by nature evade defenses and disseminate.
What are some mechanisms used by professional multisystem bacteria that contribute to its virulence?
Immune evasion or disruption: antigenic variation or absence, serum resistance (resist complement), cloaking themselves with host protein to avoid recognition.
Invasiveness: cell invasion and dissemination/tissue invasion
What are the vector-borne PROFESSIONAL multi-system bacterial infections frequently seen in the US? What about non-vector-borne?
Vector borne:
- Anaplasmosis (human granulocytic anaplasmosis)
- Ehrlichiosis (human monocytic ehrlichiosis)
- Rocky mountain spotted fever
- Lyme disease
Non-vector-borne: syphilis
Where can vector-borne infections occur?
Pretty much everywhere; BUT specific vectors and therefore diseases vary with geographic location.
What is biological transmission? What is vector competence?
When a pathogen has a specific life stage in a vector (ie colonizes a specific site and alters its gene expression in the vector).
The ability of a vector to transmit a pathogen: reflects ability to acquire, maintain, and transmit a pathogen which are three distinct processes.
What is transstadial transmission? What are examples of disease in which this occurs?
When a pathogen is transmitted or maintained in the different life stages of the same individual vector
Lyme disease, anaplasmosis, ehrlichiosis
What is transovarial transmission? What are examples of diseases in which this occurs?
When a pathogen is transmitted from one vector generation to the next
Rocky mountain spotted fever rickettsiosis.
What agent causes Rocky Mountain Spotted Fever? What are its characteristics? What is the vector and reservoir?
Rickettsia ricketsii -
Ticks are the vector and reservoir
Tiny gram-negative intracellular coccobacilli - replicates in the cytoplasm.
What is the agent that causes anaplasmosis? What are its characteristics? What are the endemic regions for this disease? What is the vector?
Anaplasmosis caused by anaplasma phagocytophilum - gram negative intracellular bacilli.
Endemic in north america, europe, and asia.
Ixodes ticks
What is the classic presentation of anaplasmosis? What is the treatment?
Fever, chills, headache, myalgias, malaise.
Treat with doxycycline (even kids).
What are the key virulence factors associated with anaplasmosis?
Cell invasion and absence of PAMPS recognized by TLRs.
Type IV secretion system, intracellular replication in vacuole in PMNs, no LPS or peptidoglycan.
How would you diagnose anaplasmosis in the lab?
Thick or thin blood smear, serology.
Culture is difficult so it’s not done in clinical labs.
What is the agent that causes Ehrlichiosis? What are its characteristics? Where is this diseases endemic? What are the vectors?
Several Ehrlichia species: tiny gram negative intracellular coccobacilli.
Endemic in north america, europe, and asia.
Vectors: dermacentor, amblyomma, and ixodes ticks.
What is the classic presentation of Ehrlichiosis? How is it treated?
Fever, chills, headache, myalgias, and malaise.
Treat with doxycycline (even kids or pregnant).
What are the key virulence determinants of Ehrlichiosis? How is it tested in lab?
Type IV secretion system, obligate intracellular bacteria that replicate in vacuoles in monocytes; no LPS or peptidoglycan.
Cell invasion and absence of PAMPS recognized by TLRs.
Thick or thin blood smear in which you see morulae (intracell colonies) in PMNs or monocytes. Serology. Culture is difficult so not done.
What is the agent responsible for Lyme disease? Where is this disease endemic? What is the vector?
Borrelia burgdorferi, B. garinii, B. afzelii - gram negative extracellular spirochetes that replicate outside of the host cell.
Endemic in north america, europe, and asia.
Vector are ticks.
What is the classic presentation of Lyme disease? What can this sometimes be confused with?
Non-itchy, non-tender erythema migrans lesion (usually bullseye but not always), facial palsy, oligoarticular arthritis, heart block.
This contrasts from STARI (Southern Tick Associated Rash Illness) which may be a borrelia infection that cannot disseminate in humans.
What are key virulence factors associated with lyme disease (borrelia)?
Antigenic variation, tissue invasion, complement resistance, adhesions, do NOT reach high titers in blood, no LPS.
Absence of PAMP recognized by TLR. Flagella hidden.
What is the treatment for lyme disease?
Doxycycline, amoxicillin, ceftriaxone if CNS involvement is suspected.
How would you diagnose Lyme disease in lab?
Clear erythema migrans and history of likely or known tick attachment.
Lesion, can be confirmed by serology with two steps:
- ELISA screen followed by immunoblot confirmation of positive ELISA
- IgM should be positive within 2-3 weeks, IgG within 3-4 weeks.
Culture difficult so not done.
