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Infectious Disease > Week 5: Parasitology Part I > Flashcards

Week 5: Parasitology Part I Flashcards

1
Q

learning objectives

A

For the parasitic organisms identify

  • the geographic region of risk
  • mode of transmission
  • Life cycle
  • Clinical symptoms
  • Clinical complications of infection
  • Laboratory diagnostic tests
  • Appropriate treatment
  • side effects of treatment
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2
Q

Case 1

A
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3
Q

Describe the distribution of Malaria

A
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4
Q

Question

A

Malaria is transmitted by the bite of the female Anopheles mosquito

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5
Q

Describe the mechanism of transmission of Malaria

A
  • Malaria is transmitted by the bite of the female Anopheles Mosquito
  • Sporozoites in the mosquito’s saliva are injected into the human bloodstream
  • Vector-borne infection
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6
Q

Question

A

Merozoites

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7
Q

Describe the life-cycle of Malaria

A
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8
Q

Malaria is caused by?

A

Plasmodium species

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9
Q

Plasmodium characteristics

A
  • Obligate intracellular protozoa
  • Single-celled Eukaryotic
  • The zygote is the only diploid stage in Plasmodium life-cycle
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10
Q

Tropism of Plasmodium

A

Blood protozoa with hepatic stage

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11
Q

Diploid stages of Plasmodium

A

The zygote is the only diploid stage in life-cycle

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12
Q

Definitive host of Plasmodium

A

Mosquito (sexual reproduction in the gut of the mosquito)

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13
Q

Intermediate host of Plasmodium

A

Human

(Asexual reproduction in liver and blood stages)

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14
Q

Plasmodium type and location of reproduction in definitive host

A

Mosquito (Sexual reproduction in the gut of the mosquito)

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15
Q

Plasmodium type and location of reproduction in intermediate host

A

Human (Asexual reproduction in liver and blood stages)

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16
Q

Factors associated with the pathogenicity of Plasmodium

4 listed

A
  • Penetration of anatomic barrier via mosquito bite
  • Avoidance of immune detection
    • Antigenic variation, molecular mimicry, intracellular location, suppression of parasite-specific B & T-cell responses
  • Replication in the host
  • Endotoxin in P. falciparum
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17
Q

How do Plasmodium avoid immune detection

A
  • Antigenic variation
  • molecular mimicry
  • Intracellular location
  • suppression of parasite-specific B & T-cell responses
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18
Q

Question

A

D. Thick & thin peripheral blood smear

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19
Q

Thick and thin peripheral blood smear

A
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20
Q

Clinical symptoms of Malaria are caused by?

A

blood-stage parasites and the host immune response

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21
Q

Pathophysiology of Malaria infection

A
  • RBC destruction
    • Intravascular hemolysis -> severe microcytic, hypochromic anemia
  • Cytokine release
    • Schizont rupture -> macrophage stimulated to release TNF and IL-1 cytokines
  • Sequestration of infected RBCs
    • Adhere to capillary endothelial cells -> impair blood flow
    • Splenomegaly
  • Biochemical & electrolyte changes
    • Hypoglycemia due to parasite glucose consumption, decreased hepatic gluconeogenesis, quinine causing pancreatic insulin release
    • Metabolic acidosis from microvascular ischemia, parasite lactate production
    • Hyponatremia
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22
Q

Pathophysiology of Malaria as a result of RBC destruction

A

Intravascular hemolysis -> severe microcytic hypochromic anemia

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23
Q

Pathophysiology of Malaria as a result of cytokine release

A

Schizont rupture -> macrophage stimulated to release TNF and IL-1 (cytokines)

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24
Q

Pathophysiology of Malaria as a result of sequestration of infected RBCs

A
  • adhere to capillary endothelial cells -> impair blood flow
  • Splenomegaly
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25
Q

Pathophysiology of Malaria as a result of biochemical & electrolyte changes

A
  • Hypoglycemia due to parasite glucose consumption, decreased hepatic gluconeogenesis, quinine causing pancreatic insulin release
  • Metabolic acidosis from microvascular ischemia, parasite lactate production
  • Hyponatremia (SIADH)
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26
Q

What is SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body makes too much antidiuretic hormone (ADH). … ADH is a substance produced naturally in an area of the brain called the hypothalamus. It is then released by the pituitary gland at the base of the brain.

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27
Q

Clinical findings & complications of Malaria

A
  • General
    • Periodic every 48 to 72 hours (q48 or g72 hr) paroxysmal fever, chills and rigors caused by immune reaction from lysis of RBCs
    • Muscle aches, malaise, nausea, vomiting
  • Cerebral Malaria
    • Symptoms: impaired consciousness, delirium, seizures
    • Capillary plugging due to accumulation of malarial pigment and P. falciparum schizont sequestration
    • Mortality 15-25%
  • Blackwater fever
    • Intravascular hemolysis with rapid destruction of RBC infected with P. falciparum causing hemoglobinuria and acute renal failure
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28
Q

List of Plasmodium species

A
  • P. falciparum
  • P. malariae
  • P. ovale
  • P. vivax
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29
Q

P. falciparum region

A

Global

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30
Q

P. falciparum incubation period

A

short 7-10 days

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31
Q

P. falciparum RBC infected

A

All

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32
Q

P. falciparum latent liver phase

A

No

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33
Q

P. falciparum Fever

A

Malignant tertian

*Most severe presentation*

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34
Q

P. malariae region

A
  • Africa
  • Haiti
  • DR
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35
Q

P. malariae incubation period

A

Long 18-40 days

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36
Q

P. malariae RBC infected

A

old

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37
Q

P. malariae latent liver phase

A

No

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38
Q

P. malariae fever

A

Quartan

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39
Q

P. ovale region

A
  • Africa
  • Asia
  • SA
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40
Q

P. ovale incubation period

A

10-17 days

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41
Q

P. ovale RBC infected

A

Young

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42
Q

P. ovale latent liver phase

A

Yes

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43
Q

P. ovale fever

A

Benign tertian

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44
Q

P. vivax region

A

Global; NOT Africa

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45
Q

P. vivax incubation period

A

10-17 days

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46
Q

P. vivax RBC infected

A
  • Young
  • Duffy Ag
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47
Q

P. vivax latent liver phase

A

Yes

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48
Q

P. vivax fever

A

Benign tertian

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49
Q

Question

A

E. All of the above

because they all cause chronic low-grade anemia so there are less cells for the plasmodium to infect and reproduce in

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50
Q

Treatment of Malaria

A
  • Blood schizonticide
  • Tissue schizonticide
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51
Q

Blood schizonticides kill Plasmodium in what stage?

A

Trophozoite in RBC

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52
Q

Tissue schizonticide kill Plasmodium in what stage

A

Dormant hypnozoites in the liver (prevents relapse of OVALE and VIVAX)

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53
Q

Blood schizonticides

A
  • Chloroquine
  • Quinine
  • Mefloquine
  • Artemesins
  • Atovaquone-proguanil
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54
Q

Tissue schizonticides

A
  • Primaquine
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55
Q

Quinine indications

A

Treatment for severe malaria

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56
Q

Quinine MOA

A
  • facilitates the aggregation of cytotoxic heme. Free cytotoxic heme accumulates in the parasites, causing their deaths.
  • (toxic heme buildup and cell lysis)
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57
Q

Quinine side-effects

A
  • arrhythmia
  • Hemolysis in G6PD deficiency
  • Cinchonism
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58
Q

Chloroquine indications

A

Many areas with resistant P. falcuparum and P. vivax

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59
Q

Chloroquine MOA

A

Blocks detox of heme buildup from parasite blood meal -> disrupts parasite membrane function -> lysis of parasite

60
Q

Chloroquine side effects

A
  • GI toxicity
  • itching
  • retinal toxicity
61
Q

Examples of Artemesinin group antimalarials

A

Artesunate

62
Q

Artemesinin group indications

A
  • first-line treatment for P. falciparum in combination with another blood schizonticide
63
Q

Artemesinin group MOA

A

Inhibits P. falciparum EXP1 membrane glutathione S-transferase

64
Q

Artemesinin group side effects

A

no significant side effects

65
Q

Mefloquine indications

A

Second-line for P. falciparum and P. vivax

66
Q

Mefloquine MOA

A

inhibition of heme polymerase

67
Q

Mefloquine side effects

A

neuropsych

68
Q

Atovaquone-Proguanil MOA

A

Inhibits parasitic electron transport chain

69
Q

Atovaquone-Proguanil Side effects

A

GI toxicity

70
Q

Blood schizonticides overview

A
71
Q

Question

A

American trypanosomiasis

72
Q

American trypanosomiasis AKA

A

Chagas Disease

73
Q

How is Chagas Disease transmitted?

A

Bite from reduviid bug (Triatomines) which transmits typomastigote

74
Q

Chagas Disease Region

A

Endemic in Mexico, Central America and South America

75
Q

What is Trypanosoma cruzi?

A

Flagellated protozoa

76
Q

Describe the life-cycle of Trypanosoma cruzi

A
  • Bugs bite humans and infect humans by defecating on humans and the wound is rubbed causing infection
  • In humans, trypomastigotes lose flagellum and undulating membrane and become smaller oval intracellular amastigotes which multiply via binary fission and transform into trypomastigotes and burst out of the cell into the blood
  • Triatomine bug takes a blood meal from infected human and epimastigotes use asexual reproduction and can infect another human via bite and defacation
77
Q

Trpanosoma cruzi vector

A

Reduviid bug

78
Q

Describe Trypanosoma cruzi stage in reduviid bug

A

metacytic trypomastigotes

79
Q

Describe thick and thin smear

A
  • thin smear - see the red cells and see the organism in its phase that is inside RBCs
  • thick smear - to catch the gametocytes
  • Get 3 thick and thin smears because this test is 100% operator dependent
80
Q

Describe Trypanosoma cruzi stage in humans

A

in humans

trypomatigotes in blood and Amastigotes in tissue

81
Q

Reduviid bug AKA

A

Kissing bug

82
Q

Definitive host of Trypansoma cruzi

A

wild-animal reservoir

83
Q

Signs & symptoms of Acute Chagas Disease

A
  • Chagoma at the inoculation site
  • Fever, chills, malaise, myalgias, lymphadenopathy
  • Rarely: arrhythmia, meningoencephalitis
  • Romaña’s Sign
84
Q

Prognosis of Chagas disease

A

Most recover & then remain in asymptomatic indeterminate phase w/ persistent low-level parasitemia unless immunosuppressed then chronic Chagas Disease

85
Q

Signs & symptoms of Chronic Chagas Disease

A
  • 20-30% of people infected progress to chronic disease with significant manifestations
  • Destruction of nerve cells (Auerbach plexus)
  • Dilated cardiomyopathy
  • Megacolon
  • Megaesophagus
86
Q

Diagnosis of Acute Chagas Disease

A

Peripheral blood smear, culture or xenodiagnosis

87
Q

Diagnosis of Chronic Chagas Disease

A
  • Serology: antibody titer
  • Biopsy of infected organ
  • Peripheral blood-smear
  • Xenodiagnosis
88
Q

Acute Chagas disease treatment

A

Drugs available are not FDA approved and need to be obtained with special permission from the CDC

(Benznidazole, Nifurtimox)

89
Q

Chronic Chagas Disease Treatment

A

Drugs available are not FDA approved and need to be obtained with special permission from the CDC

(Benznidazole, Nifurtimox)

90
Q

When to treat Acute Chagas Disease?

A

All acute and congenital cases should be treated

91
Q

When to treat Chronic Chagas Disease?

A
  • Only immunosuppressed patients and children
  • Symptomatic treatment of GI and cardiac issues
92
Q

Question

A

D. Tsetse fly

93
Q

Vector of African Sleeping Sickness

A

Tsetse fly

94
Q

Reduviid bug bite pain level

A

painful

95
Q

Tsetse fly bite pain level

A

painful

96
Q

African Sleeping Sickness pathogen

A

Trypanosoma brucei

97
Q

Describe the life-cycle of Trypanosoma brucei

A
  • Tsetse flys take a blood meal from infected animal or human, trypomastigotes perform Asexual reproduction in Tsetse fly.
  • Tsetse fly bites human and trypomastigotes enters bloodstream and does asexual reproduction in body fluids (blood, lymph and spinal fluid) and are not intracellular
  • Tsetse fly bites infected human and trypomastigotes continue infection
98
Q

Infective stage of Trypanosoma brucei

A

trypomastigotes injected into human by Tsetse fly

99
Q

Diagnostic stage of Trypanosoma brucei

A

Trypomastigotes in human bloodstream

100
Q

Trypanosoma brucei causes

A

African Sleeping Sickness

101
Q

Trypanosoma brucei type

A
  • Flagellated blood protozoa
102
Q

Trypanosoma brucei vector

A

Tsetse fly

103
Q

Trypanosoma brucei reservoirs

A

Humans and game

104
Q

African Sleeping sickness diagnosis

A

Trypanosoma brucei trypomastigote in blood smear

105
Q

Trypanosoma brucei rhodesiense region

A

East Africa

106
Q

Trypanosoma brucei gambiense region

A

West Africa

107
Q

Signs & symptoms of African Sleeping sickness

A

Days to weeks after infection

  • Recurring fever (due to antigenic variation), headache and joint pain

Several months after infection

  • Parasitemia -> fever, diffuse lymphadenopathy, confusion, numbness and trouble sleeping

Months to years later

  • Parasites invade the CNS causing symptoms: headache, somnolence, confusion and coma
108
Q

Question

A

C. Leishmania braziliensis

109
Q

Describe Leishmania life-cycle

A
  • Sandfly takes a blood meal from infected human or animal and ingests infected macrophages with amastigotes
  • amastigotes transform into promastigote stage in midgut of Sand fly and do asexual reproduction
  • Sandfly takes a blood meal from human and promastigotes get phagocytosed by human macrophages
  • Promastigotes transform into amastigotes inside macrophages
  • Amastigotes multiply by binary fission invade other cells
110
Q

Leishmaniasis pathogen

A
  • Leishmania donovani (old world/Eastern hemisphere)
  • Leishmania brasiliensis (New world/Western hemisphere)
111
Q

Leishmania donovani or brasiliensis type

A

Flagellated blood protozoa

112
Q

Vector of Leishmania

A

Phlebotomine sand flies

113
Q

Leishmania reservoir

A
  • Rodents
  • dogs
  • infected humans
114
Q

Leishmania donvani causes

A

Visceral Leishmaniasis

115
Q

Leishmania brasiliensis causes

A

Mucosal Leishmaniasis

116
Q

Signs & Symptoms of Mucosal Leishmaniasis

A

Cutaneous Leishmaniasis with dissemination to naso-oropharyngeal mucosa (nose, mouth, nasal septum)

117
Q

Signs & Symptoms of Visceral Leishmaniasis

A
  • Fever
  • HSM
  • Pancytopenia
118
Q

Visceral Leishmaniasis AKA

A

Kalazar

119
Q

Photos of Leishmaniasis

A
120
Q

Diagnosis of Cutaneous Leishmania

A

Skin biopsy for histology > culture or PCR

121
Q

Diagnosis of Visceral Leishmaniasis

A

Bone marrow or spleen aspirate for:

  • Smear: macrophages with intracellular amastigotes
  • Culture (rarely used)
  • PCR
  • Serology
122
Q

Ampho

A
  • Amphotericin B
  • Miltefosine
123
Q

Treatment of Visceral Leishmaniasis

A
  • Amphotericin B
  • Miltefosine
124
Q

Question

A

D. Toxoplasma gondii

125
Q

What is Toxoplasma gondii?

A

Tissue protozoa

126
Q

Describe the life-cycle of Toxoplasma gondii

A
  • Organisms develop in the intestinal cells of cat & during extraintestinal cycle with passage to the tissue via the blood stream
  • Organisms from intestinal cycle are passed in cat feces and mature into infective cysts within 3-4 days in the environment
  • Oocysts (containing sporozoites) are ingested by humans (meat, cat feces) and produce acute and chronic infection
127
Q

Question

A

A. Cat

128
Q

Plasmodium species clinical disease

A

Malaria

129
Q

Plasmodium species vector

A

Female anopheles mosquito

130
Q

Plasmodium species diagnosis of acute disease

A
  • peripheral thick and thin smear (in febrile phase or will miss because RBCs are not rupturing when afebrile)
  • Trophozoite in RBCs
131
Q

Trypanosoma cruzi clinical disease

A

Chagas Disease

132
Q

Trypanosoma cruzi vector

A

Reduviid bug

133
Q

Trypanosoma cruzi diagnosis of acute disease

A
  • Peripheral smear
  • trypomastigote
134
Q

Trypanosoma brucei clinical disease

A

African Sleeping Sickness

135
Q

Trypanosoma brucei vector

A

Tsetse fly

136
Q

Trypanosoma brucei diagnosis of acute disease

A
  • Peripheral smear
  • Trypomastigote
137
Q

Leishmania donovani clinical disease

A

Visceral leishmaniasis (Kala-Azar)

138
Q

Leishmania donovani vector

A

Sandfly

139
Q

Leishmania donovani diagnosis of acute disease

A
  • Peripheral smear
  • Amastigotes in macrophages
140
Q

Leishmania brasiliensis clinical disease

A

Mucosal leishmaniasis

141
Q

Leishmania brasiliensis vector

A

Sandfly

142
Q

Leishmania brasiliensis diagnosis for acute disease

A
  • Biopsy for histology
  • Amastigotes
143
Q

Toxoplasma gondii clinical disease

A

Toxoplasmosis;

Acute: mono

Reactivation: CNS

144
Q

Toxoplasma gondii vector

A
  • none
  • Oral-fecal contamination
145
Q

Toxoplasma gondii Diagnosis of acute disease

A

Serology

Infectious Disease (82 decks)

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