Jackson: Bloodstream Infections Flashcards
Bacteremia:
Septicemia:
Bacteremia: viable bacteria in the blood as demonstrated by positive blood culture; causative agent depends on the age of the patient and the route of infection
Septicemia: bacteremia with symptoms suggesting bacteria are multiplying in the bloodstream
Septic Shock:
Septicemia may lead to:
What is triggered by microorganisms or microbial products?
What is the primary microbial product in the bloodstream?
Endotoxin activates?
A. Septicemia may lead to hypotension, diminished organ perfusion, high mortality
B. Complex series of enzymatic reactions triggered by microorganisms or microbial products
C. Primary microbial product is endotoxin in the bloodstream.
D. Endotoxin activates a series of physiological cascades in a pathological manner
Bacterial Endocarditis Involves 3 Processes:
- Endothelial damage
- Bacterial colonization
- Amplification
Endotoxin in septic shock: (4)
Endotoxin activates a series of physiological cascades in a pathological manner
- Systemic coagulation pathways –> Disseminated Intravascular Coagulation (DIC)
- Complement activation
- Inappropriate stimulation of cytokines
- Adult Respiratory Distress Syndrome (ARDS)
Viridans Streptococci
Relevant Virulence Factors (2):
Relevant Virulence Factors: low virulence organisms
- Adhesins
- Fibronectin-binding protein
Viridans Streptococci
Etiology / Pathogenesis:
Location:
Transient bacteremia when?
Inflammatory response to:
Viridans streptococci are normal residents of oral cavity
Transient bacteremia following dental procedure or periodontal disease
Inflammatory response to vegetation damages heart tissue
What is the etiologic agent in infective endocarditis cases?
Viridans streptococci etiologic agent in infective endocarditis cases
Viridans Streptococci
Colonization of damaged heart valves that have fibrin-platelet vegetations which result from:
a. Congenital defect in heart valve
b. Damage due to rheumatic fever (rare in US)
c. Prosthetic valve
d. Atherosclerotic heart disease
Viridans Streptococci
ID (4):
- Blood culture
- Not classified under Lancefield groups
- No specific cell wall Ags (no serological testing)
- Identification using biochemical tests
Staphylococcus Aureus
Relevant Virulence Factors (3):
- Alpha toxin
- Adherence factors
- Antiphagocytic components
Staphylococcus Aureus:
Responsible for:
Most virulent cause of:
Basics: responsible for native valve infections; bacteria introduced in the bloodstream from skin colonization sites (ie. IV drug users)
Most virulent cause of endocarditis (highest mortality)
Group D Streptococcus and Enterococcus
Relevant Virulence Factors:
Etiology/Pathogenesis:
Normally inhabits:
Introduced into the bloodstream via:
Frequent cause of:
High level resistance to a wide variety of antibiotics (VRE a great concern)
Etiology/Pathogenesis:
Basics: normal inhabitants of intestine and vagina; introduced into the blood stream after surgical procedure
Frequent cause of nosocomial infections
Group D Streptococcus and Enterococcus
ID (4):
- Gram positive cocci
- Catalase negative
- Group D antigen identified serologically
- Enterococci grow in 6.5% NaCl
Group D Streptococcus and Enterococcus
Pathogenic Species:
E.faecalis and E.faecium most common in humans;
(nonenterococcal) Group D strep include S.bovis and S.equinus
Candida
Relevant Virulence Factors (2):
- Adhesins
- Antiphagocytic components
SPECIAL CASE BACTERIAL HEMOPOIETIC SYSTEM INFECTIONS
Pseudomonas aeruginosa
Classification:
Syndrome:
Classification: Gram negative rod
Syndrome: Intravenous drug abuse
SPECIAL CASE BACTERIAL HEMOPOIETIC SYSTEM INFECTIONS
Staphylococcus epidermidis
Classification:
Syndrome:
Classification: Gram positive cocci
Syndrome: Prosthetic heart valves, indolent infections
Candida
Etiology/Pathogenesis
C. albicans:
commonly inhabits:
can be introduced via:
C. parapsilosis:
often seen in:
causes:
C. albicans: commonly inhabits skin; can be introduced via IV drug use to cause prosthetic valve infections (systemic infections seen in immunocompromised)
C. parapsilosis: also often seen in IV drug users; causes 25% of yeast endocarditis
Candida
ID (2):
- Blood culture to reveal systemic infection
- KOH or Gram stain (yeast/hyphae)
Aspergillus
Relevant Virulence Factors:
Etiology/Pathogenesis:
ID:
Relevant Virulence Factors: Infectious spores (ubiquitous; common cause of mold allergies)
Etiology/Pathogenesis:
- Can cause prosthetic valve infections in the immunsuppressed (poor prognosis)
ID:
- Blood cultures will be negative; need a biopsy of infected tissue
- Culture shows branched, septate hyphae
Plasmodium spp
Four Species:
P.falciparum (most severe), P.malariae, P.vivx, P.ovale
Plasmodium spp
Life cycle is the main reason for its pathogenesis:
Sexual Cycle takes place in: Sporozoites: Schizonts: Merozoites: - P.falciparum vs others Hypnozoites: Asexual Cycle takes place in: - Trophozoite vs Merozoites
Sexual Cycle takes place in mosquito gut
Sporozoites: injected into human host from mosquito; travel to liver
Schizonts: intracellular stage in liver parenchymal cells
Merozoites: released from ruptured liver cells into the blood stream
- P.falciparum releases 40,000 merozoites
- P.vivax releases 10,000
Hypnozoites: dormant liver stage (responsible for long-term relapses; only occurs with P.vivax/ovale)
Asexual Cycle takes place in RBC:
- Trophozoite, Schizont in RBCs
- Merozoites released from RBC
Plasmodium spp
RBC Receptors (2):
Adhesins:
P.falcifarum can bind:
Antigenic variation:
Genetic hypervariability of antigenic surface proteins in what stage?
RBC Receptors:
o Duffy Antigen: receptor for vivax on reticulocytes
o Glycophorin A: receptor for falciparum on all RBC types
Adhesins:
o P.falcifarum: can bind ICAM-1 on vascular wall
- Keeps infected RBCs out of peripheral circulation (prevents detection)
- Contributes to pathogenesis by occluding small vessels
Antigenic variation: confounds antibody response
o Genetic hypervariability of antigenic surface proteins in schizont stage; due to genetic recombination during sexual stage
Plasmodium spp
Etiology/Pathogenesis
Epidemiology:
Leading cause of death due to infectious disease
Endemic in tropical areas (Africa, Far East, South America); where Anopheles mosquito thrives
Cases in the US brought in by travelers; onset can be delayed up to 6 months in people taking anti-malarial prophylaxis
Plasmodium spp
Symptoms (6):
Fever
Anemia
Cerebral Malaria
Hypotension and Shock
Blackwater Fever
Ag-Ab Complex Deposition
Plasmodium spp
Fever:
Induced by?
What are both antigenic and pyrogenic?
What cytokines contribute?
Fever: induced by asexual blood stage and release of merozoites into the bloodstream
Malarial metabolites and hemozoin (from Hb) that are released are both antigenic and pyrogenic
Cytokines (IL-1, TNF) contribute
Bouts of fever/chills are sporadic and then cyclical (parasite growth eventually becomes cyclical); due to Ag variation (parasite load goes up and down)
- Parasite growth eventually becomes synchronized
Plasmodium spp
Anemia: due to
Anemia: primary complication (lysis/phagocytosis of RBCs)
Plasmodium spp
Cerebral Malaria:
Can occur with?
What happens with plasmodium filled RBCs?
TNF alpha upregulates:
Cerebral Malaria: can occur with P.falciparum
Occlusion of small blood vessels with plasmodium filled RBCs causes necrosis (in the brain)
TNF alpha upregulates ICAM (which it can bind) and more adherence occurs
Plasmodium spp
Hypotension and Shock:
Hypotension and Shock: related to cytokine production during release or merozoite
Plasmodium spp
Blackwater Fever:
Blackwater Fever: black urine caused by massive hemolysis (hemoglobinuria); autoimmune reaction in patients with history of infection may contribute to this symptom
Plasmodium spp
Ag-Ab Complex Deposition:
Ag-Ab Complex Deposition: renal tubular necrosis
Plasmodium spp
Relapses can occur with:
Natural Resistance (3):
Natural resistance to infection
- Lack of Duffy red blood cell antigen receptor
- Altered hemoglobin that cannot be utilized by parasite
- HbS and HbC mutations
Plasmodium spp
Immunity to Infection:
Ab mediated:
Cell-mediated and intracellular killing mechansims:
Natural cure due to:
Time for P.falciparum:
P.falciparum:
P.vivax and ovale hypnozoite hepatic infections:
Ab mediated: blood stream stages (merozoite and sporozoite)
Cell-mediated and intracellular killing mechanisms: intracellular schizont stage
Eventual natural cure from adequate antibody response:
- P.falciparum takes up to a year
- P.malariae is more persistent
- P.vivax and ovale hypnozoite hepatic infections can relapse in 5 year periods
Plasmodium spp
Altered hemoglobin that cannot be utilized by parasite (4)
a. Heterozygous for sickle cell (hemoglobin S)
b. Hemoglobin C is another mutation
c. beta-thalassemia
d. Glucose-6-phosphate dehydrogenase deficiency
Plasmodium spp
HbS and HbC mutations
Prevents parasite from:
a. Prevent parasite from rearranging actin to form cell-surface adhesin
b. Reduced cell-surface adhesin –> reduced stickiness of infected erythrocyte
Plasmodium spp
ID (3):
Blood Smears: show intraerythrocytic stages
- Thick Films: rapid diagnosis of parasitemia
- Thin Films (one cell thick): for speciating Plasmodia
ELISA: Ab detection
Molecular Techniques: PCR, gene probes have been developed
Plasmodium spp
Prophylaxis:
CDC recommendations: always changing
Mosquito control and bed nets
Vaccine Development: difficult due to Ag variation; acellular vaccine to surface Ags under development
Babesia Microti
Similar Life Cycle to: Asexual stage in: Sporozoites transmitted from: Trophozoite formed in: Merozoites: Sexual stage in:
Relevant Virulence Factors to bloodstream infections:
Similar Life Cycle to Plasmodia:
Asexual stage in human RBCs:
Sporozoites: transmitted from salivary glands of the tick
Trophozoite: formed in cytoplasm of infected RBC
Merozoites: asexual division in RBC produces 4 of these; ring forms can be seen in RBCs
Sexual stage in ticks (Ixodes)
Babesia Microti
Transmission via: Also some instances of transmission by: Babesiosis: Incubation period: Symptoms:
Transmission via ticks: same ticks that transmit Lyme disease (simultaneous infections possible)
Also some instances of transmission by blood transfusion or organ transplantation
Babesiosis: typically mild or subclinical
1-4 week incubation period
Symptoms
o Fever: periodic febrile paroxysms seen in malaria not seen here
o Other: myalgia, hepatosplenomegaly, hemolytic anemia, renal dysfunction
o Spontaneous resolution in a few weeks
Babesia Microti
Clinical identification of organism (2):
Giemsa-stained blood film shows ring forms similar to P. falciparum
Serology may be used; Babesia antigens cross-react with Plasmodium
