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Micro Exam 1 > Jackson: Bloodstream Infections > Flashcards

Jackson: Bloodstream Infections Flashcards

1
Q

Bacteremia:

Septicemia:

A

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

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2
Q

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

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

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3
Q

Bacterial Endocarditis Involves 3 Processes:

A
  • Endothelial damage
  • Bacterial colonization
  • Amplification
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4
Q

Endotoxin in septic shock: (4)

A

Endotoxin activates a series of physiological cascades in a pathological manner

  1. Systemic coagulation pathways –> Disseminated Intravascular Coagulation (DIC)
  2. Complement activation
  3. Inappropriate stimulation of cytokines
  4. Adult Respiratory Distress Syndrome (ARDS)
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5
Q

Viridans Streptococci

Relevant Virulence Factors (2):

A

Relevant Virulence Factors: low virulence organisms

  • Adhesins
  • Fibronectin-binding protein
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6
Q

Viridans Streptococci

Etiology / Pathogenesis:

Location:
Transient bacteremia when?
Inflammatory response to:

A

Viridans streptococci are normal residents of oral cavity

Transient bacteremia following dental procedure or periodontal disease

Inflammatory response to vegetation damages heart tissue

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7
Q

What is the etiologic agent in infective endocarditis cases?

A

Viridans streptococci etiologic agent in infective endocarditis cases

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8
Q

Viridans Streptococci

Colonization of damaged heart valves that have fibrin-platelet vegetations which result from:

A

a. Congenital defect in heart valve
b. Damage due to rheumatic fever (rare in US)
c. Prosthetic valve
d. Atherosclerotic heart disease

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9
Q

Viridans Streptococci

ID (4):

A
  • Blood culture
  • Not classified under Lancefield groups
  • No specific cell wall Ags (no serological testing)
  • Identification using biochemical tests
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10
Q

Staphylococcus Aureus

Relevant Virulence Factors (3):

A
  • Alpha toxin
  • Adherence factors
  • Antiphagocytic components
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11
Q

Staphylococcus Aureus:

Responsible for:
Most virulent cause of:

A

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)

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12
Q

Group D Streptococcus and Enterococcus
Relevant Virulence Factors:

Etiology/Pathogenesis:
Normally inhabits:
Introduced into the bloodstream via:
Frequent cause of:

A

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

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13
Q

Group D Streptococcus and Enterococcus

ID (4):

A
  • Gram positive cocci
  • Catalase negative
  • Group D antigen identified serologically
  • Enterococci grow in 6.5% NaCl
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14
Q

Group D Streptococcus and Enterococcus

Pathogenic Species:

A

E.faecalis and E.faecium most common in humans;

(nonenterococcal) Group D strep include S.bovis and S.equinus

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15
Q

Candida

Relevant Virulence Factors (2):

A
  • Adhesins

- Antiphagocytic components

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16
Q

SPECIAL CASE BACTERIAL HEMOPOIETIC SYSTEM INFECTIONS

Pseudomonas aeruginosa

Classification:
Syndrome:

A

Classification: Gram negative rod
Syndrome: Intravenous drug abuse

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17
Q

SPECIAL CASE BACTERIAL HEMOPOIETIC SYSTEM INFECTIONS

Staphylococcus epidermidis

Classification:
Syndrome:

A

Classification: Gram positive cocci
Syndrome: Prosthetic heart valves, indolent infections

18
Q

Candida
Etiology/Pathogenesis

C. albicans:
commonly inhabits:
can be introduced via:

C. parapsilosis:
often seen in:
causes:

A

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

19
Q

Candida

ID (2):

A
  • Blood culture to reveal systemic infection

- KOH or Gram stain (yeast/hyphae)

20
Q

Aspergillus
Relevant Virulence Factors:
Etiology/Pathogenesis:
ID:

A 
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
21
Q

Plasmodium spp

Four Species:

A

P.falciparum (most severe), P.malariae, P.vivx, P.ovale

22
Q

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
A

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
23
Q

Plasmodium spp

RBC Receptors (2):

Adhesins:
P.falcifarum can bind:

Antigenic variation:
Genetic hypervariability of antigenic surface proteins in what stage?

A

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

24
Q

Plasmodium spp
Etiology/Pathogenesis
Epidemiology:

A

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

25
Q

Plasmodium spp

Symptoms (6):

A

Fever

Anemia

Cerebral Malaria

Hypotension and Shock

Blackwater Fever

Ag-Ab Complex Deposition

26
Q

Plasmodium spp
Fever:

Induced by?
What are both antigenic and pyrogenic?
What cytokines contribute?

A

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

27
Q

Plasmodium spp

Anemia: due to

A

Anemia: primary complication (lysis/phagocytosis of RBCs)

28
Q

Plasmodium spp
Cerebral Malaria:

Can occur with?
What happens with plasmodium filled RBCs?
TNF alpha upregulates:

A

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

29
Q

Plasmodium spp

Hypotension and Shock:

A

Hypotension and Shock: related to cytokine production during release or merozoite

30
Q

Plasmodium spp

Blackwater Fever:

A

Blackwater Fever: black urine caused by massive hemolysis (hemoglobinuria); autoimmune reaction in patients with history of infection may contribute to this symptom

31
Q

Plasmodium spp

Ag-Ab Complex Deposition:

A

Ag-Ab Complex Deposition: renal tubular necrosis

32
Q

Plasmodium spp
Relapses can occur with:

Natural Resistance (3):

A

Natural resistance to infection

  1. Lack of Duffy red blood cell antigen receptor
  2. Altered hemoglobin that cannot be utilized by parasite
  3. HbS and HbC mutations
33
Q

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:

A

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
34
Q

Plasmodium spp

Altered hemoglobin that cannot be utilized by parasite (4)

A

a. Heterozygous for sickle cell (hemoglobin S)
b. Hemoglobin C is another mutation
c. beta-thalassemia
d. Glucose-6-phosphate dehydrogenase deficiency

35
Q

Plasmodium spp
HbS and HbC mutations

Prevents parasite from:

A

a. Prevent parasite from rearranging actin to form cell-surface adhesin
b. Reduced cell-surface adhesin –> reduced stickiness of infected erythrocyte

36
Q

Plasmodium spp

ID (3):

A

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

37
Q

Plasmodium spp

Prophylaxis:

A

CDC recommendations: always changing

Mosquito control and bed nets

Vaccine Development: difficult due to Ag variation; acellular vaccine to surface Ags under development

38
Q

Babesia Microti

Similar Life Cycle to:
Asexual stage in:
Sporozoites transmitted from:
Trophozoite formed in:
Merozoites:
Sexual stage in:
A

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)

39
Q

Babesia Microti

Transmission via:
Also some instances of transmission by:
Babesiosis:
Incubation period:
Symptoms:
A

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

40
Q

Babesia Microti

Clinical identification of organism (2):

A

Giemsa-stained blood film shows ring forms similar to P. falciparum

Serology may be used; Babesia antigens cross-react with Plasmodium

Micro Exam 1 (18 decks)

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