Download Blood Infections

Microbiology: Hemopoietic System Infections (Jackson)
BACTERIAL INFECTIONS OF THE BLOOD STREAM
Basic Definitions:

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 leading to hypotension, diminished organ perfusion and high mortality
Series of enzymatic reactions triggered by microorganisms or microbial products (primarily endotoxin)
Endotoxin activates physiological cascades in a pathological manner:
o Systemic coagulation pathways, leading to disseminated intravascular coagulation (DIC)
o Complement activation
o Inappropriate stimulation of cytokines
o Adult Respiratory Distress Syndrome (ARDS)

Bacterial Endocarditis Involves 3 Processes:
Endothelial damage
Bacterial colonization
Amplification
Viridans Streptococci:

Relevant Virulence Factors: low virulence organisms
Adhesins
Fibronectin-binding protein

Etiology/Pathogenesis:
Basics: normal residents of oral cavity (cause of cavities)
Infection Process:
o Transient bacteremia following dental procedure or periodontal disease
o Colonization of damaged heart valves that have fibrin-platelet vegetations, which result from:

Congenital defect in heart valve

Damage due to rheumatic fever

Prosthetic valve

Atherosclerotic heat disease
o Inflammatory response to vegetation damages heart tissue

ID:
Blood culture
Not classified under Lancefield groups
No specific cell wall Ags (no serological testing)
Staphylococcus Aureus:

Relevant Virulence Factors:
Alpha toxin
Adherence factors
Antiphagocytic components

Etiology/Pathogenesis:
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:
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

ID:
Gram positive cocci
Catalase negative
Group D antigen identified serologically
Enterococci grow in 6.5% NaCl

Pathogenic Species:
E.faecalis and E.faecium most common in humans; Group D strep include S.bovis and S.equinus
FUNGAL INFECTIONS OF THE BLOOD STREAM:
Candida:

Relevant Virulence Factors:
Adhesins
Antiphagocytic components

Etiology/Pathogenesis:
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 yeast endocarditis

ID:
Blood culture to reveal systemic infection
KOH or Gram stain (yeast/hyphae)
Aspergillus:

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 shoes branched, septate hyphae
PARASITIC INFECTIONS OF THE BLOODSTREAM:
Plasmodium spp:

Four Species: P.falciparum (most severe), P.malariae, P.vivx, P.ovale

Relevant Virulence Factors:
Life cycle is the main reason for its pathogenesis:
o Sexual Cycle takes place in mosquito gut
o Sporozoites: injected into human host from mosquito; travel to liver
o Schizonts: intracellular stage in liver parenchymal cells
o Merozoites: released from ruptured liver cells into the blood stream
o Hypnozoites: dormant liver stage (responsible for long-term relapses; only occurs with P.vivax/ovale)
o Asexual Cycle takes place in RBC:

Trophozoite, Schizont in RBCs

Merozoites released from RBC
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

Etiology/Pathogenesis:
Epidemiology:
o Leading cause of death due to infectious disease
o Endemic in tropical areas (Africa, Far East, South America); where Anopheles mosquito thrives
o Cases in the US brought in by travelers; onset can be delayed up to 6 months in people taking antimalarial prophylaxis
Symptoms:
o 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)
o Anemia: primary complication (lysis/phagocytosis of RBCs)
o
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-
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Cerebral Malaria: can occur with P.falciparum

Occlusion of small blood vessels with plasmodium filled RBCs causes recrosis (in the brain)

TNF alpha upregulates ICAM (which it can bind) and more adherence occurs
o Hypotension and Shock: related to cytokine production during release or merozoite
o Blackwater Fever: black urine caused by massive hemolysis; autoimmune reaction in patients with
history of infection may contribute to this symptom
o Ag-Ab Complex Deposition: renal tubular necrosis
Relapses: can occur with P.vivax/ovale due to liver hypnozoites
Natural Resistance:
o Lack of Duffy R
o Altered Hb cannot be used by parasite:

HbS

Beta-thalassemia

G6P dehydrogenase deficiency
Immunity to Infection:
o Ab mediated: blood stream stages (merozoite and sporozoite)
o Cell-mediated and intracellular killing mechanisms: intracellular schizont stage
o 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
ID:
Blood Smears: show intraerythrocytic stages
o Thick Films: rapid diagnosis of parasitemia
o Thin Films (one cell thick): for speciating Plasmodia
ELISA: Ab detection
Molecular Techniques: PCR, gene probes have been developed

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:

Relevant to Virulence Factors:
Similar Life Cycle to Plasmodia:
o 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
o Sexual stage in ticks (Ixodes)

Etiology/Pathogenesis:
Transmission via ticks: same ticks that transmit Lyme disease (simultaneous infections possible)
o Also some instances of transmission by blood transfusion or organ transplantation
Babesiosis: typically mild or subclinical
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