Bloodstream Infections Flashcards

1
Q

What is bacteremia vs septicemia?

A

Bacteremia - Viable bacteria in blood as seen by culture

Septicemia - Bacteremia with signs of multiplication

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2
Q

What facilitates decompensation during septic shock?

A

Bacterial endotoxins cause:

  1. Systemic coagulation pathways -> disseminated intravascular coagulation
  2. Complement activation
  3. Inappropriate cytokines
  4. Adult Respiratory Distress Syndrome
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3
Q

What are virulence factors used by Viridans Streptococci to cause blood stream infections?

A
  1. Adhesins

2. Fibronectin-binding protein

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4
Q

When do Viridians streptococci enter the bloodstream? How are they identified in the lab?

A

Normal inhabit the oral cavity, enter during dental procedure or periodontal disease

Lab: No specific cell wall antigens, identified using biochemical tests

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5
Q

What types of heart valves do Viridians streptococci colonize?

A

Ones with fibrin-platelet vegetations, including congenital heart defect, rheumatic fever, prosthetic valve, or atherosclerotic heart disease

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6
Q

What is the primary virulence factor of Group D Streptococcus / Enterococcus?

A

Multiple, high-level resistances to a wide variety of antibiotics

Includes VRE

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7
Q

Where do GDS and enterococcus normally live and how are they introduced? How are they identified?

A

In the intestine or vagina, introduced into bloodstream via surgical procedures, frequent nosocomial infection

Identified as gram + cocci, with Group D antigen

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8
Q

What two fungi can cause endocarditis, especially among immunosuppressed?

A
  1. Candida - IV drug users

2. Aspergillus - environmental mold

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9
Q

How is Aspergillus identified in culture?

A

Branched, septate hyphae (mold form). Blood cultures will be negative, biopsy of infected tissue is necessary (unlike Candida).

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10
Q

What are the four forms of malaria and which is most virulent?

A
  1. P. falciparum - most virulent
  2. P. malariae
  3. P. vivax
  4. P. ovale
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11
Q

What is the life cycle of malaria in the human host?

A
  1. Sporozoites injected by female Anopheles mosquito into human host
  2. Parasites travel to liver, form schizonts (dividing merozoite vesicles) in the liver
  3. Merozoites are released from ruptured liver cells, with P. falciparum being the most
  4. Merozoites invade RBCs, digest hemoglobin to form trophozoite, schizont, and again merozoites are released
  5. Gametocytes will differentiate during some cycles to be taken up by mosquitos
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12
Q

What malaria strains can go through hypnozoite stage?

A

P. vivax and P. ovale can lay dormant in the liver for many years to come and release more parasites from schizonts in liver cells

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13
Q

What is the receptor for P. vivax and P. falciparum on RBCs?

A

P. vivax - Duffy antigen

P. falciparum - Glycophorin A

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14
Q

Why are P. falciparum adhesions problematic?

A
  1. Used to help RBCs adhere (via ICAM-1) to vascular wall to prevent splenic clearance and peripheral detection

Problematic because they can cause occlusion of small vessels (brain aneurysms) - cerebral malaria

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15
Q

What is the mechanism of malaria antigen variation?

A
  1. Hypervariability of surface proteins in the schizont stage
  2. Recombination during sexual reproduction
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16
Q

Why does fever occur in malaria?

A

When merozoites leaves RBCs in the bloodstream, the released metabolites including hemozoin (broken down heme crystals) are antigenic / pyrogenic, causing IL-1 / TNFa release

Can lead to hypotension / shock

17
Q

How do bouts of fever become sporadic then cyclical?

A

Parasite begins to time release of merozoites to invade immune response.

Some species have tertian (48 hour) and quartan (72 hour) cycles

18
Q

What is the major complication of all malaria?

A

Anemia

19
Q

What is Blackwater fever?

A

Black urine, caused by massive intravascular hemolysis and subsequent hemoglobinuria in malaria

20
Q

What are a few resistance mechanisms to malaria?

A
  1. Lack of Duffy RBC antigen - no P. vivax infection
  2. Sickle cell -> prevents parasite from using actin to form cell-surface adhesion, and increases splenic clearance this way
  3. Glucose-6-phosphate dehydrogenase deficiency -> increase free radical killing of parasite
21
Q

What is ultimately needed to clear the malaria infection? What had the longest infection?

A

Cell-mediate immunity / intracellular killing mechanisms to kill schizonts, and antibody to bloodstream stages (merozoite, sporozoite)

Natural cure once adequate antibody response, with P. vivax & P. ovale relapsing over 5 year periods.

P. malariae is most persistant (53 year infection)

22
Q

What is used for malaria prophylaxis?

A

Atovaquone / Proguanil = Malarone

23
Q

What are the definitive and intermediate hosts of Babesia microti?

A

Definitive - Ticks (same tick transmitting Lyme disease, Ixodes)

Intermediate - humans

24
Q

What are the symptoms of babesiosis? How does it resolve?

A

Fever, not periodic
Myalgia, anemia, hepatosplenomegaly, renal dysfunction

Resolves spontaneously within a few week

25
Q

Who is Babesiosis very dangerous in?

A

Asplenic individuals, causing hemolytic anemia, jaundice, and renal failure

26
Q

How is babesia identified?

A

Stained blood film (like malaria) - thin for identification

Antigens will cross-react with plasmodium