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MSII Micro Unit 2 > Parasites of the Blood > Flashcards

Parasites of the Blood Flashcards

1
Q

global impact of malaria

A
  • 207 million new cases a year
  • 473,000-789,000 million deaths per year
  • increased global tracel
  • drug resistance
  • plasmodium falciparium replaced vivax as the main type of malaria in much of africa
  • control efforts have decayed-india
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2
Q

cause of malaria

A
  • plasmodium-have different geographic distributions
  • falciparum
  • most lethal, majority of 1-3 million deaths
  • vivax common-cases in US
  • transmitted through infected female in genus anopheles
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3
Q

malaria endemic countries

A
  • 104
  • half world at risk
  • africa, asia, south america
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4
Q

genetic and immunological protection

A
  • absence of duffy antigen prevents vivax
  • hereditary elliptocytosis, glycophorin C deficiency and heterozygotes for sickle are less susceptible
  • thalassemias or G6PD deficiency offer degree of protection
  • untreated infectious patients eventually develop curative immunity against the parasitizing strain
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5
Q

life cycle of malarial parasite

A
  1. sporozoites in salivary glands
  2. oocytes in stomach wall
  3. male and female gametocytes
  4. liver phase (human)
  5. release of merozoites from liver
  6. enter red blood cells and burst and spread to new red blood cells causing a cycle of symptoms
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6
Q

symptoms of malaria

A
  • incubation period is 9-14 for falciparum and 12-18 for vivax, 18-40 for malariae, 11-12 for knowlesi
  • appear in 7 days, can be as lone as 8-10 months
  • fever chills, headache, sweats, fatigue, nausea, vomiting
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7
Q

malaria paroxysm

A
  • 4-8 hours begins with sudden onset of chills and intense cold despite temp
  • then hot stage-heat and headache. fatigue, dizziness, anorexia, myalgia, nausea
  • then sweating stage and fever declines then sleep
  • then feels fine until next paroxysm
  • cold is in RBCs
  • hot is burst
  • sweating is in new RBCs
  • synchronous replication of parasite accounts for this-and can tell which species it is
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8
Q

plasmodium falciparum

A
  • much more acute and sever than malaria caused by others
  • almost all deaths directly from malaria are this
  • cerebral malaria, severe anemia, resp failure, renal failure, severe malaria of pregnancy
  • sequesters in deep venous microvasculature
  • invades young RBCs
  • kidneys, liver, brain, GI
  • parasitemia low due to adherence of RBCs to capillary walls
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9
Q

PfEMP-1

A
  • P falciparum erythrocyte membrane protein 1
  • binds to CD36
  • 60 different variants in parasite
  • switches b/n them per generation
  • antigenic variation
  • causes adhesion to endothelium and vasooclusion
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10
Q

cerebral malaria

A
  • sequestration of parasites in the cerebral microvasculature (due to CD36 and PfEMP1)
  • ring hemorrhages, perivascular leukocyte infiltrates, immunohistochemical evidence of endo activation
  • sequestration leads to IF cytokines which leads to reduced local delivery of oxygen and glucose
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11
Q

malaria of pregnancy

A
  • placental colonization by infected RBCs results in maternal morbidity and mortality, IUGR, premies, LBW, increased newborn mortality
  • selective accumulation of mature parasites in placenta due to CSA, hyaluronic acid and Ig
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12
Q

vaccine for malaria

A
  • only 30% effecting
  • targets outer membrane protein of early blood phase (circumsporozoite) of P. falciparum
  • doesnt work as they get older
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13
Q

new diagnostic test for malaria

A
  • now available in the US
  • detects different types of parasites
  • rapid test to detect P. falciparum and P vivax
  • good when microscopy is not available
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14
Q

babesia

A
  • world wide
  • multiple species
  • transmitted by ticks
  • B microti in US
  • infections in NE similar to p vivax
  • midwest and west have fulminate febrile hemolytic disease
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15
Q

life cycle of babesia

A
  • complicated
  • involves mouse intermediate
  • sporozoites infect us
  • goes through trophozoite and metozoite
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16
Q

babesia infection

A
  • more than 100 species infect vertebrates
  • obligate erythrocyte parasite-modification and rupture
  • asynchronous-lack of periodicity
  • erythropoiesis increased- anemia and low level parasitemia explained by clearing not sick RBCs
  • hemolytic anemia and non-specific flu like symptoms
  • splenomegaly, hepatomegaly, jaundice
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17
Q

anaplasma phagocytophilum

A
  • NE
  • tick vector
  • have more than anaplasmosis- usually Lyme and/or Babesia
  • white footed mouse and squirrels
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18
Q

anaplasmosis

A
  • first symptoms in 1-2 weeks- fever, headache, muscle pain, malaise, cough, confusion
  • fatal if not treated correctly
  • difficulty breathing, hemorrhage, renal failure, neurological problems
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19
Q

chagas disease

A
  • american trypanosomiasis
  • trypanosoma cruzi
  • insect vectors
  • only in americas and australia (another species elsewhere- T brucei and tsetse fly)
  • transmitted by triatomine insects
20
Q

trypanosome infections

A
  • american trypanosomiasis is most frequent in US
  • southern to middle texas region
  • southern cal
  • differences observed in contact of bug-needs and hour
  • acute-death within a few weeks
  • chronic-symptoms may not present for 5-15 years
21
Q

typanosome life cycle

A
  • can infect esophagus, heart, colon
  • bites under eye swell because poop releases irritant-romana sign–other places called chagoma
  • trypmastigotes infect us
22
Q

leishmaniasis

A
  • sandflies
  • obligate intracellular
  • multiplication in histiocytes-diagnose here
  • focal disease
  • can survive for decades in asymptomatic people-important for transmission of visceral disease
  • neutrophils
23
Q

cutaneous lesihmaniasis

A
  • chronic skin ulcers

- may or may not be where bite was

24
Q

mucocutaneous lesihmaniasis

A

-metastatic spread of primary lesions to the mouth, nose, pharynx, destruction of the mucosa and secondary bacterial infection

25
Q

visceral lisihmaniasis

A

-fever weight loss
anorexia
spleno/hepatomegaly

26
Q

What is the importance of vectors in parasitic diseases?

A
  • the geographic distribution and occurrence of many parasitic diseases is directly related to the distribution of various vectors that are responsible for the transmission of the parasite and the distribution of secondary or intermediate hosts
  • mosquito borne diseases
  • sand fly borne diseases
  • tick borne diseases
27
Q

What are the blood borne parasites?

A
  • malaria
  • babesia
  • typanosomes
  • leishmania
  • filarial infections
28
Q

Have there been malaria deaths in the US? If so..when?

A
  • yes in the 19th century malaria was extremely common in the US with over 1 million cases during the Civil War
  • of the 5 species that cause malaria P. falciparum and P. vivax were the most common
29
Q

What are the Plasmodium species?

A
  • Plasmodium falciparum- one of most common and most deadly
  • Plasmodium vivax- the other most common
  • Plasmodium malarie
  • Plasmodium oval
30
Q

What is the incidence of malaria in the US?

A
  • the number of reported cases has been stable for the last 5 years
  • nearly all infections occur in travelers
31
Q

What is the anemia associated with malaria caused by?

A

Due to the rupture of parasitized erythrocytes, removal of parasitized and unparasitized erythrocyes by the spleen, capillary sequestration and bone marrow dyserythropoiesis

32
Q

What is the cyclic pattern associated with malaria?

A
  • symptoms may appear in cycles and may come and go at different intensities and for different lengths of time
  • at the beginning at the illness they might not follow a typical pattern
  • the cyclic pattern of malaria symptoms is due to the life cycle of malaria parasites as they develop, reproduce and are released from the red blood cells and liver cells
  • P falciparum is not very cyclical
33
Q

What is malaria recrudescence?

A

-the situation where parasitemia falls below detectable levels and then later increases to a detectible parasitemia

34
Q

What is a malarial relapse?

A
  • the sporozoites invade heptocytes in which they develop into schizonts and may not be observed in the circulation and the individual may be asymptomatic
  • after a period of time the hepatocyte ruptures. Each infected hepatocyte ruptures liberates 10,000 to 30,000 merozoites that invade circulating erythrocytes
35
Q

What is the pathophysiology of P. falciparum?

A
  • Metabolic (Lactic) Acidosis- most common feature of severe malaria, caused by reduced delivery of oxygen to tissues
  • Pulmonary edema and respiratory distress- sequestration of infected erythrocytes in the lungs is thought to initiate regional production of inflammatory cytokines that increase capillary permeability
  • Hypoglycemia- can cause coma and convulsions
  • Anemia- excess removal of uninfected erythrocytes may account for the loss
36
Q

What about P vivax and P ovale?

A
  • infections with both are similar clinically
  • although rarely fatal P. vivax can be debilitating with serious complications such as acute lung injury and splenic rupture
  • low mortality rates associated because they favor reticulocytes and they do not exhibit sequestration
37
Q

How does a P malariae infection present?

A
  • infects old RBC, so parasitemia is low
  • incubation period is longest (40 days)
  • parasites may be found several days before symptoms
  • patients present with proteinuria or nephrotic syndrome
  • ring forms look like a large signet ring
  • 72 hour periodity is seen
  • infected RBCs are normal or smaller than normal
  • Merozoites form a daisy head arrangment
38
Q

What is the new malaria?

A
  • P knowlesis is a primate parasite commonly found in south east asia
  • accounts for up to 70% of cases in South East Asia
  • it replicates and completes its blood stage cycle in 24 hour cycles resulting in fairly high loads of parasite densities in a very short period of time
  • the appearance is similar to P malariae
  • monkeys in India!
39
Q

What is the distribution of Lyme Disease and Babesia?

A
  • the prevalence and distribution of Lyme Disease and Babesia are the same
  • the transmission vector is the same
  • Ixodes scapularis in NE, mid-Atlantic and north central US, the Ixodes pacificus in the Pacific coast
40
Q

What is Toxoplasmosis?

A
  • leading cause of death attributed to foodborne illness in the US- more than 60 million carry the parasite but few have symptoms because immune system keeps them in check
  • Toxoplasma gondii has a high prevalence globally and capable of infecting all species of animals and birds
  • definitive hots are the cat family- the only animals capable of shedding oocysts in their feces and transmitting the parasite by this means, oocysts are shed in large numbers by acutely infected cats once for approx 2 weeks
41
Q

How is Toxoplasma gondii transmitted?

A
  • consumption of infected tissue or fecal material by naive or young felines results in their infection and subsequent shedding of infectious oocysts
  • people become infected through the accidental consumption of feline fecal material, through food or water with fecal contamination, through the consumption of undercooked meat containing infective cysts, through transplantation or transplacentally from mother to fetus
42
Q

What is a toxoplasma infection in healthy people?

A
  • often asymptomatic
  • when illness occurs it is flu like for several weeks and then goes away
  • the parasite remains in their body in an inactive state- can become reactivated if the person becomes immunosuppressed
43
Q

What is a congenital toxoplasma infection?

A
  • results from an acute primary infection acquired by the mother during pregnancy
  • the incidence and severity varies with the trimester during which infection was acquired
  • 1/2 of women infected can transmit across the placenta
  • infection early in pregnancy less likely to be transmitted to the baby than infection later in pregnancy
  • could result in miscarriage, stillborn, born with signs of toxoplasmosis (abnormal enlargement or smallness of the head)
  • most babies infected during pregnancies show no signs at birth but may develop learning, visual and hearing disabilities later in life
44
Q

How is toxoplasma expressed in the immunosuppressed?

A
  • person with compromised immune systems may experience severe symptoms if they are infected with Toxoplasma while immune suppressed
  • a person who is HIV infected and who has reactivated can have fever, confusion, headaches, seizures, nausea, and poor coordination
  • leading cause of focal CNS disease in AIDS
45
Q

What is the distribution of Lymphatic Filariasis?

A
  • Wuchereria bancrofti- tropical areas
  • Brugia malayi- Asia
  • Brugia timori- restricted to some islands of Indonesia
  • Oncocerca volvulus (river blindnesses)- Africa and some foci and Latin America and the Middle East
  • Loa Loa and Mansonella Streptocerca- Africa
46
Q

What are the clinical features of Lymphatic Filariasis?

A
  • some patients develop lymphatic dysfunction causing lymphedema and elephantiasis (freq in lower extremities)
  • with Wuchereria bancrofti there is hydrocele and scrotal elephantisis

MSII Micro Unit 2 (7 decks)

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