Flashcards in Parasite Infections of the Blood Deck (43):
what is the most common species of malarial infection? which is the most deadly?
p falciparum (both questions)
what genetic predispositions are protective against malaria?
absence of duffy antigen (vivax), hereditary elliptocytosis, heterozygotes for sickle cell disease, thalassaemia and G6PD deficiency
what hemoglobin variants are protective against malaria?
thalassemia, hemoglobin S and HbC
why are people without a duffy antigen less likely to get malarial infections?
because it is the erythrocyte receptor for p vivax
what is the pathogenicity of malarial infections?
produces anemia by hemolysis and impaired microcirculation
what is the range of malarial incubation?
generally around 10-40 days but may take as long as 8-10 months with vivax and ovale
what is the malarial paroxysm? how long does it last?
begins with an intense feeling of cold followed by the feeling of intense heat. the fever will then break and the patient will be sweaty and tired takes 4-8 hrs
what are the causes of the malaria paroxysm stages?
cold stage- lysis of RBC by schizonts
hot stage- cytokine response to parasite in plasma
sweating stage- parasites infect new RBC and are cleared from circulation
when does the malaria cyclic pattern not occur?
it may take time for the schizonts to sync their replication cycle. (beginning of infection).
p falciparum does not exhibit this cycle
what is malaria recrudescence?
parasitemia is undetectable for a period of time and later recurs
why do relapses of malaria occur?
the sporozoites invade hepatocytes and remain latent there until after a period of time when the hepatocyte ruptures
what are the severe manifestations of p falciparum?
cerebral malaria, severe anemia, respiratory failure, renal failure and severe malaria of pregnancy
what is an abnormal feature of the pathogenesis of p falciparum?
ability to sequester in the deep venous microvasculature
what are the metabolic manifestations of p falciparum infection?
lactic acidosis from impaired O2 delivery and hypoglycemia
what causes pulmonary edema and respiratory distress in p falciparum infection?
sequestration of infected erythrocytes in the lungs initiates production of cytokines that increase capillary permeability
what is the significance of PfEMP-1?
a ligand for the receptor CD36 that allows RBC to attach to cells in the vasculature
what is the classic finding in cerebral malaria?
sequestration of parasites in cerebral microvasculature accompanied by ring hemorrhages, perivascular leukocytes and endothelial cell damage
what is the harm of placental malaria?
maternal morbility and mortality, growth retardation, premature delivery, low birth weight and newborn mortality
why do mature parasites accumulate in the placenta?
they interact with syncytiotrophoblastic antigens, hyaluronic acid and immunoglobulins
what are the benefits for rapid diagnostic testing for malaria? what does it test for?
microscopy is not always available and it detects antigens of p falciparum and p vivax
what has been the result of phase three trials for the mosquirix vaccine for malaria?
effectiveness was 35% but stops working after about 6 months in 50% of patients
what clinical features are shared by p vivax and p ovale?
they have low mortality because they do not inhibit sequestration and they favor reticulocytes. they also may recur
what cells does p malariae often infect? what is the incubation period and what is the usual presentation?
infects older RBC with an incubation period of 40 days. patients present with proteinuria or nephrotic syndrome
why has a new species of malaria just recently been found? what does it usually infect?
because p knowlesii is similar to p malariae and is often misdiagnosed. it is primarily a primate parasite
what transmits babesia? what does the presentation resemble?
different types of ticks
in the northeast it resembles p vivax infection. in the rest of the country it presents as a fulminate, febrile hemolytic disease
what does the distribution of babesia resemble?
lyme disease and anaplasmosis (there is a lot of coinfections)
what is a major reservoir for anaplasmosis?
white footed mouse and squirrels
what are the first symptoms of anaplasmosis?
constitutional symptoms, nausea, cough and confusion
what are some serious clinical presentations of anaplasmosis?
difficulty breathing, hemorrhage, renal failure or neurological problems
what disease does trypanosomiasis cause? what is the causative agent?
trypanosoma cruzi causes it in america
what are the two vectors for trypanosomiasis?
the tsetse fly in Africa and the reduvid bug in the americas
where is chagas' disease spread and what are the forms of the disease?
in southern california and texas.
acute form- death in weeks
chronic form- symptoms may not present for years
how does american trypanosomiasis infect humans?
the reduvid bug excretes the parasite in its feces. when the bug bites a human it leaves the feces behind. the feces cause itching and when the person scratches, it produces breaks in the skin
what parasite is a leading cause of foodborne illness death in the US? what is the usual host?
the usual host are cats
how is toxoplasmosis transmitted from cats to humans?
oocysts are shed in the cat's feces (especially in kittens) and they infect people by accidental consumption through food or water contamination
what nonfeline modes may transmit toxoplasmosis?
may be transmitted via the consumption of undercooked meat that contain infective cysts or may transmit transplacentally
what is the progression of toxoplasma infection in healthy people?
most people are asymptomatic or have mild flu like symptoms. the parasite remains in muscle tissue and may reactivate with immunosupression
how is congenital toxoplasmosis acquired? what determines severity?
with an acute primary infection of the mother during pregnancy. severity dictated with the trimester of infection (early has more severe symptoms but is less likely to be transmitted)
what is the most common presentation of congenital toxoplasmosis infection? what are more severe manifestations?
most are aymptomatic but may develop learning, visual and hearing disabilities later.
may cause miscarriage, still born or abnormal head size
what is the manifestation of toxoplasmosis with immunosuppression?
infection will cause severe symptoms with neuro involvement (lesions in brain)
what transmits leishmania?
certain species of blood feeding sand flies
what are the clinical manifestations of leishmaniasis?
cutaneous-chronic skin ulcers
mucocutaneous- spread of lesion to mouth, nose and pharynx with mucosal destruction
visceral- fever, weight loss, anorexia and hepatosplenomegaly