Bloodstream Infections

Question 1

What is bacteremia vs septicemia?

Answer 1

Bacteremia - Viable bacteria in blood as seen by culture

Septicemia - Bacteremia with signs of multiplication

Question 2

What facilitates decompensation during septic shock?

Answer 2

Bacterial endotoxins cause:

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

Question 3

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

Answer 3

1. Adhesins

2. Fibronectin-binding protein

Question 4

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

Answer 4

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

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

Question 5

What types of heart valves do Viridians streptococci colonize?

Answer 5

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

Question 6

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

Answer 6

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

Includes VRE

Question 7

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

Answer 7

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

Identified as gram + cocci, with Group D antigen

Question 8

What two fungi can cause endocarditis, especially among immunosuppressed?

Answer 8

1. Candida - IV drug users

2. Aspergillus - environmental mold

Question 9

How is Aspergillus identified in culture?

Answer 9

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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

What malaria strains can go through hypnozoite stage?

Answer 12

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

Question 13

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

Answer 13

P. vivax - Duffy antigen

P. falciparum - Glycophorin A

Question 14

Why are P. falciparum adhesions problematic?

Answer 14

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

Question 15

What is the mechanism of malaria antigen variation?

Answer 15

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

Question 16

Why does fever occur in malaria?

Answer 16

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

Question 17

How do bouts of fever become sporadic then cyclical?

Answer 17

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

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

Question 18

What is the major complication of all malaria?

Answer 18

Anemia

Question 19

What is Blackwater fever?

Answer 19

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

Question 20

What are a few resistance mechanisms to malaria?

Answer 20

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

Question 21

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

Answer 21

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)

Question 22

What is used for malaria prophylaxis?

Answer 22

Atovaquone / Proguanil = Malarone

Question 23

What are the definitive and intermediate hosts of Babesia microti?

Answer 23

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

Intermediate - humans

Question 24

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

Answer 24

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

Resolves spontaneously within a few week

Question 25

Who is Babesiosis very dangerous in?

Answer 25

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

Question 26

How is babesia identified?

Answer 26

Stained blood film (like malaria) - thin for identification Antigens will cross-react with plasmodium