Vector Born Apicomplexans Flashcards
(22 cards)
What are vector born apicomplexans?
They are sporozoans that have an apical complex that lets them get into host cells and they are vector born because they start in a tick or mosquito or other ‘vector’ and end in the host human
Two diseases they cause that we will talk about are Malaria and Babesiosis
Malaria
5 Plasmodium apicomplexans that cause malaria (5 strains).
- Plasmodium falciparum
- Plasmodium Vivax
- Plasmodium Ovale
- Plasmodium Malariae
- Plasmodium Knowlesi
Hosts: The human is the intermediate host the Anopheles Mosquito is the DEFINITIVE host
Transmission Vector-borne (Anopheles Mosquito) Transfusions IV drug use (mainlining malaria) Congenital (rare)
Shizogony
Asexual reproduction. The Malaria causing Plasmodium does its asexual reproduction in the human
Asexual repro in HUMAN
Pigment (Hemozoin)
is produced in the infected RBC, a source of toxicity when the RBCs lyse
Malaria Parasite life cycle in humans
- Mosquito takes a blood meal & injects sporozoites
- Sporozoites travel to liver cells and invade/infect
- Schizogony occurs in the liver cells (asexual reproductions) parasite/cell is schizont
- Schizont Ruptures! and Merozoites are released
- Merozoites infect Red Blood Cells (RBCs) and do 2 things
A. Undergo more Schizogonty, make more Schizonts and rupture more merozoites.
B. Merozoite infects RBC, is an Immature Trophozoite (Ring stage) then develops into Gametocytes - Gametocytes become banana shapes and wait to be eat by another mosquito
Plasmodium Falciparum
Africa, 80-90% cases in Africa
Incubation 7-10 day incubation
Infects all RBC types
Drug resistant
Paroxysms initially quotidian (every 24 hours), then tertian (every 48 hours)
Malignant disease and causes severe malaria
Plasmodium Vivax
Uncommon in Africa, 70-90% of cases in Southeast Asia and South America
Incubation 10 -17 days
Infects, Reticulocytes
Drug Resistant
Paroxysms Tertian (every 48 hours)
Disease benign
Can establish a persistent infection as Hypnozoites (so can Plasmodium Ovale)
Malaria observed caused from P. Vivax only in immuno compromised patients
Pathology related to Immune status
The species of Plasmodium and immune status dictate outcome (i.e. children, pregnancy, elderly, immune status).
Infections caused by P. Falciparum (i.e. high parasitemia with all RBCs infected) are the most likely to progress to severe, potentially fatal forms (severe malaria)
Malaria (signs and symptoms)
Fever, the regular fever pattern does not occur until synchronized schizogony is established after 1 week
Splenomegaly, acute malaria enlarges spleen
Jaundice, a mild jaundice due to hemolysis may occur in malaria.
Severe jaundice occurs in P. Falciparum and is due to liver involvement
Anemia, b/c RBC destruction
Common symptoms include fever, chills, sweats, nausea and vomiting, body aches and general malaise
Severe Malaria
Nearly all deaths are from Malaria from Plasmodium Falciparum
Vital Organ dysfunction, abnormalities in the blood (clotting) or metabolic complications (hypoglycemia, acidosis)
3 most common,
Cerebral Malaria
Acute Respiratory Distress Syndrome
Severe Anemia
Cerebral Malaria
Unarousable coma after ruling everything else out.
CM observed in 1% of P. falciparum infections (20% mortality)
Children older than 2 years old at risk because maternal immunity waynes
Causes
Infected RBCs adhere to the vascular endothelium of the blood vessels in the brain
this is called plugging
This is Cytoadherence, to avoid getting cleaned out by the spleen
Acute Respiratory Distress
Pulmonary Capillaries and venules are packed with parasitized Red Blood Cells and Inflammatory Cells (mononuclear cells).
Pro-Inflammatory processes increase vascular permeability, leading to severe edema
Cyto Adherence in respiratory tract, promotes inflammatory response with mononuclear cells, edema, lose oxygen exchange
Severe Anemia
Microbe-mediated hemolysis of parasitized RBCs
Antibody-mediated destruction of non parasitized RBCs
the Parasitic proteins coat the healthy RBCs and antibodies opsonize even health RBCs and destroy them
Decrease in erythropoiesis
Anemia
Diagnosis
Microscopy, it’s cheap and it works, Gold standard
Visualize the parasite in thick (is it there) and thin smear (level of parasitemia and type)
You can visualize the multiple rings from the trophozoite near the edge
Microscopy of Plasmodium Falciparum (distinguishing features)
Distinguishing features
- multiple rings (immature trophozoite stage)
- crescent shaped gametocytes
- infected RBCs not larger than normal
- high parasitemia (greater that 10%)
Malaria Immune Response
Immune Evasion
Anatomical Seclusion, RBC lack the MHC class I proteins, Antigenic variation of surface antigens on infected RBC (Recrudescence)
Immunity
Short lived and incomplete, but may be enough to render the host asymptomatic (not sufficient for preggy women, children with loss of maternal IgG, returning to endemic area after being gone)
Prevention
Avoidance, bed nets
Drug prophylaxis (Doxycycline)
No vaccine
Genetic Resistance
Inheritable anemia
Sickle cell anemia
Thalassemia
Duffy blood group negative phenotype
-receptor for P. Vivax and P. Knowlesi absent
Babesiosis
Cause Babesia Microti
Cells infect RBC only
Hosts
Definitive host is Loxdes scapularis (deer tick)
Intermediate host is mouse
Accidental host is humans
Transmission
Nymph stage of tick
Blood transfusions
Congenitally (during pregnancy and delivery)
Babesiosis Epidemiology
70% of Babesia Microti in Africa, Asiam Europe and North America
Tick-Borne infections in the US occur in New England, New Jersey, Wisconsin and Minnesota
Babesia Mircroti Life Stage
Incubation Phase 1 -9 weeks
Asymptomatic or flu-like symptoms, anemia, mild jaundice
Severe complications and death in immunocompromised b/c severe anemia, vital organ dysfunction
Chloroquine
Raises the pH inside the cells to combat Malaria causing Plasmodium etc.
Falciparum has become resistant to Choloroquine
Diagnosis/Prevention Babesiosis
Blood smears
False-Negative Blood smears due to low parasitemia
Prevention
Avoidance, insecticides, repellants
there is no vaccine
