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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
Pathophysiology of Malaria as a result of 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 (SIADH)
26
What is SIADH
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.
27
Clinical findings & complications of Malaria
* 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
28
List of Plasmodium species
* P. falciparum * P. malariae * P. ovale * P. vivax
29
P. falciparum region
Global
30
P. falciparum incubation period
short 7-10 days
31
P. falciparum RBC infected
All
32
P. falciparum latent liver phase
No
33
P. falciparum Fever
Malignant tertian \*Most severe presentation\*
34
P. malariae region
* Africa * Haiti * DR
35
P. malariae incubation period
Long 18-40 days
36
P. malariae RBC infected
old
37
P. malariae latent liver phase
No
38
P. malariae fever
Quartan
39
P. ovale region
* Africa * Asia * SA
40
P. ovale incubation period
10-17 days
41
P. ovale RBC infected
Young
42
P. ovale latent liver phase
Yes
43
P. ovale fever
Benign tertian
44
P. vivax region
Global; NOT Africa
45
P. vivax incubation period
10-17 days
46
P. vivax RBC infected
* Young * Duffy Ag
47
P. vivax latent liver phase
Yes
48
P. vivax fever
Benign tertian
49
Question
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
50
Treatment of Malaria
* Blood schizonticide * Tissue schizonticide
51
Blood schizonticides kill Plasmodium in what stage?
Trophozoite in RBC
52
Tissue schizonticide kill Plasmodium in what stage
Dormant hypnozoites in the liver (prevents relapse of OVALE and VIVAX)
53
Blood schizonticides
* Chloroquine * Quinine * Mefloquine * Artemesins * Atovaquone-proguanil
54
Tissue schizonticides
* Primaquine
55
Quinine indications
Treatment for severe malaria
56
Quinine MOA
* facilitates the aggregation of cytotoxic heme. Free cytotoxic heme accumulates in the parasites, causing their deaths. * (toxic heme buildup and cell lysis)
57
Quinine side-effects
* arrhythmia * Hemolysis in G6PD deficiency * Cinchonism
58
Chloroquine indications
Many areas with resistant P. falcuparum and P. vivax
59
Chloroquine MOA
Blocks detox of heme buildup from parasite blood meal -\> disrupts parasite membrane function -\> lysis of parasite
60
Chloroquine side effects
* GI toxicity * itching * retinal toxicity
61
Examples of Artemesinin group antimalarials
Artesunate
62
Artemesinin group indications
* first-line treatment for P. falciparum in combination with another blood schizonticide
63
Artemesinin group MOA
Inhibits P. falciparum EXP1 membrane glutathione S-transferase
64
Artemesinin group side effects
no significant side effects
65
Mefloquine indications
Second-line for P. falciparum and P. vivax
66
Mefloquine MOA
inhibition of heme polymerase
67
Mefloquine side effects
neuropsych
68
Atovaquone-Proguanil MOA
Inhibits parasitic electron transport chain
69
Atovaquone-Proguanil Side effects
GI toxicity
70
Blood schizonticides overview
71
Question
American trypanosomiasis
72
American trypanosomiasis AKA
Chagas Disease
73
How is Chagas Disease transmitted?
Bite from reduviid bug (Triatomines) which transmits typomastigote
74
Chagas Disease Region
Endemic in Mexico, Central America and South America
75
What is Trypanosoma cruzi?
Flagellated protozoa
76
Describe the life-cycle of Trypanosoma cruzi
* 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
Trpanosoma cruzi vector
Reduviid bug
78
Describe Trypanosoma cruzi stage in reduviid bug
metacytic trypomastigotes
79
Describe thick and thin smear
* 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
Describe Trypanosoma cruzi stage in humans
in humans trypomatigotes in blood and Amastigotes in tissue
81
Reduviid bug AKA
Kissing bug
82
Definitive host of Trypansoma cruzi
wild-animal reservoir
83
Signs & symptoms of Acute Chagas Disease
* Chagoma at the inoculation site * Fever, chills, malaise, myalgias, lymphadenopathy * Rarely: arrhythmia, meningoencephalitis * Romaña's Sign
84
Prognosis of Chagas disease
Most recover & then remain in asymptomatic indeterminate phase w/ persistent low-level parasitemia unless immunosuppressed then chronic Chagas Disease
85
Signs & symptoms of Chronic Chagas Disease
* 20-30% of people infected progress to chronic disease with significant manifestations * Destruction of nerve cells (Auerbach plexus) * Dilated cardiomyopathy * Megacolon * Megaesophagus
86
Diagnosis of Acute Chagas Disease
Peripheral blood smear, culture or xenodiagnosis
87
Diagnosis of Chronic Chagas Disease
* Serology: antibody titer * Biopsy of infected organ * Peripheral blood-smear * Xenodiagnosis
88
Acute Chagas disease treatment
Drugs available are not FDA approved and need to be obtained with special permission from the CDC (Benznidazole, Nifurtimox)
89
Chronic Chagas Disease Treatment
Drugs available are not FDA approved and need to be obtained with special permission from the CDC (Benznidazole, Nifurtimox)
90
When to treat Acute Chagas Disease?
All acute and congenital cases should be treated
91
When to treat Chronic Chagas Disease?
* Only immunosuppressed patients and children * Symptomatic treatment of GI and cardiac issues
92
Question
D. Tsetse fly
93
Vector of African Sleeping Sickness
Tsetse fly
94
Reduviid bug bite pain level
painful
95
Tsetse fly bite pain level
painful
96
African Sleeping Sickness pathogen
Trypanosoma brucei
97
Describe the life-cycle of Trypanosoma brucei
* 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
Infective stage of Trypanosoma brucei
trypomastigotes injected into human by Tsetse fly
99
Diagnostic stage of Trypanosoma brucei
Trypomastigotes in human bloodstream
100
Trypanosoma brucei causes
African Sleeping Sickness
101
Trypanosoma brucei type
* Flagellated blood protozoa
102
Trypanosoma brucei vector
Tsetse fly
103
Trypanosoma brucei reservoirs
Humans and game
104
African Sleeping sickness diagnosis
Trypanosoma brucei trypomastigote in blood smear
105
Trypanosoma brucei rhodesiense region
East Africa
106
Trypanosoma brucei gambiense region
West Africa
107
Signs & symptoms of African Sleeping sickness
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
Question
C. Leishmania braziliensis
109
Describe Leishmania life-cycle
* 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
Leishmaniasis pathogen
* Leishmania donovani (old world/Eastern hemisphere) * Leishmania brasiliensis (New world/Western hemisphere)
111
Leishmania donovani or brasiliensis type
Flagellated blood protozoa
112
Vector of Leishmania
Phlebotomine sand flies
113
Leishmania reservoir
* Rodents * dogs * infected humans
114
Leishmania donvani causes
Visceral Leishmaniasis
115
Leishmania brasiliensis causes
Mucosal Leishmaniasis
116
Signs & Symptoms of Mucosal Leishmaniasis
Cutaneous Leishmaniasis with dissemination to naso-oropharyngeal mucosa (nose, mouth, nasal septum)
117
Signs & Symptoms of Visceral Leishmaniasis
* Fever * HSM * Pancytopenia
118
Visceral Leishmaniasis AKA
Kalazar
119
Photos of Leishmaniasis
120
Diagnosis of Cutaneous Leishmania
Skin biopsy for histology \> culture or PCR
121
Diagnosis of Visceral Leishmaniasis
Bone marrow or spleen aspirate for: * Smear: macrophages with intracellular amastigotes * Culture (rarely used) * PCR * Serology
122
Ampho
* Amphotericin B * Miltefosine
123
Treatment of Visceral Leishmaniasis
* Amphotericin B * Miltefosine
124
Question
D. Toxoplasma gondii
125
What is Toxoplasma gondii?
Tissue protozoa
126
Describe the life-cycle of Toxoplasma gondii
* 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
Question
A. Cat
128
Plasmodium species clinical disease
Malaria
129
Plasmodium species vector
Female anopheles mosquito
130
Plasmodium species diagnosis of acute disease
* peripheral thick and thin smear (in febrile phase or will miss because RBCs are not rupturing when afebrile) * Trophozoite in RBCs
131
Trypanosoma cruzi clinical disease
Chagas Disease
132
Trypanosoma cruzi vector
Reduviid bug
133
Trypanosoma cruzi diagnosis of acute disease
* Peripheral smear * trypomastigote
134
Trypanosoma brucei clinical disease
African Sleeping Sickness
135
Trypanosoma brucei vector
Tsetse fly
136
Trypanosoma brucei diagnosis of acute disease
* Peripheral smear * Trypomastigote
137
Leishmania donovani clinical disease
Visceral leishmaniasis (Kala-Azar)
138
Leishmania donovani vector
Sandfly
139
Leishmania donovani diagnosis of acute disease
* Peripheral smear * Amastigotes in macrophages
140
Leishmania brasiliensis clinical disease
Mucosal leishmaniasis
141
Leishmania brasiliensis vector
Sandfly
142
Leishmania brasiliensis diagnosis for acute disease
* Biopsy for histology * Amastigotes
143
Toxoplasma gondii clinical disease
Toxoplasmosis; Acute: mono Reactivation: CNS
144
Toxoplasma gondii vector
* none * Oral-fecal contamination
145
Toxoplasma gondii Diagnosis of acute disease
Serology

Infectious Disease (82 decks)

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