47 Infectious Agents

Michelle To and Valentin Villatoro

Malarial Infection

Causative Agent:1,2

Malaria is transmitted by the female Anopheles mosquito.

 

There are five species of malaria:

Plasmodium falciparum – Most severe

Plasmodium vivax – Most common

Plasmodium ovale – Less common

Plasmodium malariae – Less common

Plasmodium knowlesi

 

Geographic Distribution:1

Tropical and subtropical areas

 

Clinical Features:1,2

Fever, headache, chills, sweating, splenomegaly. Patients can show cyclical patterns of fever and chills being present then absent. In severe malaria, jaundice, shock, bleeding, seizures, or coma may occur. Thrombocytopenia commonly occurs with malarial infections, and may lead to bleeding tendencies.

 

Hemolysis is mostly intravascular and occurs through a number of different mechanisms:1,2

  1. Direct damage to the red blood cells

  2. Immune activation of macrophage activity (Increased extravascular hemolysis)

  3. Release of cytokines that inhibit erythropoiesis (inhibit erythropoietin)

  4. Increased oxidative stress on RBCs during infection

  5. Induction of apoptosis in red blood cell precursors

 

Laboratory Results for Malarial Infections:1,2

CBC:

RBC: Decreased

WBC: Normal to Slightly Increased (neutropenia during chills)

PLT: Decreased

Hct: Decreased

RETIC: Decreased

PBS:

Normochromic

Normocytic

Intracellular Malarial parasite forms (forms and stages of development seen differ by species)

BM:

Erythroid Hypoplasia

Other Tests:

Giemsa stain

Thin Smears: Morphology and parasitemia calculation

Thick Smears: Presence or absence of malaria

Immunoassays

Flow Cytometry

Molecular Testing (PCR)

 

Note: See “Malaria” under RBC inclusions for additional information.


Babesiosis

Causative agents:1,3

Babesia microti is carried by the Ixodes scapularis ticks. Babesia can also be transmitted by blood transfusions.

 

Geographical Distribution:3

Northeast and Midwest United States

 

Clinical Features:3

Clinical symptoms include: flu-like symptoms ranging from fever, headache, anorexia, fatigue. Some patients may be asymptomatic. Hepatosplenomegaly may or may not be present.

 

Laboratory Results for Babesiosis:1,3

CBC:

WBC: Decreased

PLT: Decreased

Hb: Decreased

RETIC: Increased

PBS:

RBCs shows tetrads of merozoites (Maltese cross)

Other Tests:

Hemoglobinuria

Proteinuria

Immunoassays

Molecular testing (PCR)

 

Note: See “Babesia” under Abnormal RBC inclusions for additional information.


Clostridial Sepsis

Causative agent:1,3

Clostridium perfringens is an anaerobic, gram-positive spore-forming bacilli that can infect tissues after events involving trauma to the body. The bacteria releases enzymes and toxins that damage the surrounding tissue and can allow the bacteria to reach the bloodstream.

Blood infection is often fatal and can lead to massive hemolysis and the activation of DIC.

 

Mechanism of RBC Destruction:1,3

Hemolysis by C. perfringens is intravascular and can occur due to direct effects of alpha-toxin that it releases on the red blood cell membrane. Cell becomes spherical and subject to osmotic lysis. Significant intravascular hemolysis ensues, leading to a marked decrease in hematocrit, and dark red/brown plasma and urine.

 

Laboratory Results for Clostridia Infections:1,3

CBC:

RBC: Decreased

PLT: Decreased

Hct: Very Decreased

PBS:

Spherocytes

Microcytes

Ghost cells

Toxic changes with a left shift

+/- ingested bacteria within neutrophils

Other Tests:

Hemoglobinemia

Hemoglobinuria


References:

1. Harmening DM, Yang D, Zeringer H. Hemolytic anemias: extracorpuscular defects. 5th ed. Philadelphia: F.A. Davis Company; 2009. p. 250-79).

2. Akinosoglou KS, Solomou EE, Gogos CA. Malaria: a haematological disease. Hematology [Internet]. 2012 Mar 1 [cited 2018 Jul 9];17(2):106–14. Available from: http://www.tandfonline.com/doi/full/10.1179/102453312X13221316477336

3. Keohane EM. Extrinsic defects leading to increased erythrocyte destruction – nonimmune causes. In: Rodak’s hematology clinical applications and principles. 5th ed. St. Louis, Missouri: Saunders; 2015. p. 394-410.

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