Parasite Blood Infections (10) Flashcards
Why is Africa most effected by malaria?
- A mosquito that s a very effective vector
- P. falciparum is the predominant species
- Local weather conditions
- Scarce resources/ socioeconomic factors
Vector for malaria?
Anophels mosquito
What are the plasmodium species that cause malaria in humans?
P. falciparum
P, vivax
P. malariae
P. ovale
P. knowlesi (but predominantly in monkeys)
Most deadly plasmodium species?
P. falciparum
Name the genetic/ immunologic factors that offer protection against malaria?
1- Duffy Antigen Negative
2- HE
3- Sickle Cell Trait
4- Thalassemias
5- G6PD deficiency
T/F: The lifecycle of plasmodium requires specialozed protein expression in the verebrate host only
False…specialized protein expression is required in both the vertebrate and invertebrate host
What are the 2 reproductive phases of plasmodium in human hosts?
Pre-erythrocytic/ tissue
Erythrocytic
After the bite of an infected mosquito, what happens in humans to establish a malarial infection?
Within 1 hour the sporozotes enter hepaocytes and begin to divide into exoerythrocytic merozoites.
When merozoites leave the lover they infect erythrocytes and develop into trophozoites
What are parasites called when they start to divide in the RBCs?
Schizonts (and they consist of many daughter merozoites)
The pathology of malaria are mostly due to….
hemolytic anemia and impaired microcirculation
What causes the anemia in malaria?
Rupture of parasitized eythrocytes
Removal of parasitized and unparasitized RBCs by the spleen
Capillary sequestration
Incubation period of the following..
P. falciparumP. falciparum P, vivax P. malariae P. ovale P. knowlesi
P. falciparum–> 9-14 days
P, vivax–> 12-18 days
P. malariae–can be months
P. ovale–> 12-18 days
P. knowlesi–> 11-12 days
Prodrome of malaria?
Fever, HA, diaphoresis, N/V
Length of malarial paroxysm of vivax, ovale, and falciparum?
48 Hours
Length of malarial paroxysm of malariae?
72 hours
How long does it take to establish malarial paroxysm?
About 1 week
What are the 3 stages of malarial paroxysm?
Cold stage: RBC rupture
Host stage: Cytokine response
Sweating stage: Parasite in new RBC
Is relapse seen in all types of malaria?
Not in falciparum and malariae
What causes relapse malaria?
Reactivation of infection via hyponozoites (which can last for 30 years)–> the sporozoites invade hepatocytes and over time the hepatocytes rupture
Is recrudescence seen in all types of malaria?
Yes
What is recruidescence?
Parasitemia falls below detectable levels, later to increase to a detectable parasitemia
What are the major complications of P. falciparum infection?
1-Metabolic acidosis
2- Pulmonary edema/ respiratory distress
3- Hypoglucemia
4- Anemia
What causes pulmonary edema in P. falciparum infections?
Sequestration of infected RBCs in the lungs leads to inflammaotry cytokines and increased capillary permeabilit
What is PfEMP-1?
An antigen of P. falciparum that covers infected RBCs.
It is recognized by CD36 and condroitin sulfate A.
What does PfEMP-1 do?
Mediates sequestration by microvascular endothelial cells and placenta
What 2 conditions can PfEMP-1 lead to?
Cerebral malaria–> cytoadherarence of infected RBCs and sequestration of infected RBCs in the brain, which leads to the breakdown of the BBB
Placental malaria–> accumulation of infected RBCs and monocytes in the placenta which leads to a imune response and early labor
What is specific to P. vivax and P. ovale infections?
They prefer reticulocytes and there is no RBC sequestration
What is specific to P. malariae infections?
Prefer older RBCs and patients present with proteinuria or nephrotic syndrome
Vector for Babesia?
Ixodid ticks
Clinical presentation of babesia?
NorthEastern US: similar to P. vivax
Midwest/ Western US: fulminate, febrile, hemolytic disease
Describe the life cycle of babesia?
Requires a biological stage in a rodent or deer host:
Ticks introduce sporozoites into rodent when taking a blood meal
Sporozoites enter RBC and begin cyclical development between trophozoites and merozoites
Some merozoites produce gametocytes which ticks take up when attache for blood meal
Gametocytes fertilize gut of the tick and develop into sporozoites in the salivary glands
What is the distribution of babesia?
Same as lyme
How is babesia treated?
Clindamycin if it doesnt resolve on its own
What do erhlicia and anaplasma infect? What transmits them?
Tick transmits them and they infect WBCs
Symptoms of anaplamsa?
Fever, chills, HA, myalgia, Add pain, cough, myalgia
Serious: difficulty breathing, renal failure, neuro problems
Symptoms of erhlichia?
Neuro manifestations possible, pancytopenia
Which parasite causes Chagas disease?
Trypanosoma cruzi
What transmits chagas disease?
Reduviid bug (kissing bud) or tsetse fly
What is a typical presenting sign of chagas?
Roman’s sign–> swelling of the eyelid near bite or where bug feces was rubbed into eye
Clinical features of acute chagas?
lasts 4-8 weeks
asymptomatic or self limiting febrile illness
IgM and IgG present
Clinical features of chronic chagas?
10-30 years after initial infection
involvement of heart (chagas heart disease), esophagus (megaesophagus), colon (megacolon), or a combo
IgG only is present (no IgM)
What is chagas heart disease?
insidious myocarditis
impairment of contractile function and deletion of the chambes
sudden death posible
What causes toxoplasmosis?
Toxoplasma gondii
How is toxoplasmosis contracted?
Foodborne illness–> consumption of infected tissue or fecal matter by naive feline–> they then shed infected ooytes–>people then become infected by eating food/ water contaminated with feline fecal matter
Toxoplasmosis symptoms in healthy, nonpregnant people?
No symptoms b/c immune response
Flu like symptoms
Parasite can remain in inactive state and be reactivated if immunosuppressed
Symptoms of congenital toxoplasmosis?
Results from a primary infection of the mother during pregnancy
symptoms depend on the trimester
Can have sequele later in life (developmental issues)
Symptoms of toxoplasmosis in the immunosuppressed?
Neuro symtoms, fever, N/V, HA
** leading cause of focal CNA diseae in AIDS
What speads leishmania?
Sand flies
What are the 3 manifestations of leishmania?
Cutaneous: skin ulcers
Mucocutaneous: destruction of mucosa of mouth, nose, pharynx
Visceral: fever, weightloss, hepatosplenomegaly
What causes lymphatic flariasis?
Several different agents
Clinical features of lymphatic flariasis?
Lymphatic destruction
Elephantitis of lower extremities
