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Hematology Block 1 > Bugs > Flashcards

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1
Q

Ehrlichia chareensis infects ____ and causes a disease called _______

A

Ehrlichia chareensis infects monocytes and causes a disease called Human Monocytic Ehrlichiosis (HME)

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2
Q

Anaplasma phagocytophilum infects _____ and causes a disease called _____

A

Anaplasma phagocytophilum infects granulocytes (specifically neutrophils) and causes a disease called Human granulocytic anaplasmosis (HGA)

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3
Q

Malaria specied infect ____ cells and ____ cells

A

red blood cells and liver cells

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4
Q

Babesia microti infects ____ cells

A

red blood cells

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5
Q

Trypanosoma species infects ____ and _____

A

monocytes and macrophages

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6
Q

Leishmania species infect _____ and _____

A

macrophages and reticuloendothelial cells

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7
Q

Describe the characteristics of Ehrliciha:

A

obligate intracellular gram-negative bacteria

tick borne

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8
Q

Describe the characteristics of Anaplasma:

A

obligate intracellular gram-negative bacteria

tick borne

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9
Q

Where/when are cases of Ehrlichia most common?

A

Southeast to south central US

Most cases occur in the spring and summer

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10
Q

How is Ehrlichiosis transmitted?

A

Vector:

  • Lone star tick (Amblyomma americanum)
  • Has been described in other ticks as well

Animal reservoir:

  • White tail deer
  • Dogs
  • Coyotes

Other routes:

  • Maternal-child
  • Blood transfusion
  • Direct contact with slaughtered deer
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11
Q

Morulae:

A

Seen in monocytes with Ehrlichiosis infection and granulocytes with Anaplasmosis infection.

Vacuoles containing bacteria in infected cells.

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12
Q

How is Ehrlichoisis diagnosed?

A

Indirect fluorescent antibody (IFA) - Acute and convalescent serology

Examination of peripheral blood

PCR

Immunochemical staining in tissue

Clinical diagnosis

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13
Q

When/where are cases of Anaplasmosis most common?

A

Upper midwest and northeast US (some in Europe)

Spring/summer

[high seroprevalence, so likely lots of asymptomatic transmission]

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14
Q

How is anaplasmosis transmitted?

A

Vector:

  • Deer tick or black legged tick (Ixodes scapularis)
  • –Tick may be co-infected with Borrelia or Babesia (a few % of ticks)

Animal reservoir:

  • White-tailed deer
  • Also rodents/small mammals

Other routes:

  • Person-person (cluster in China)
  • Blood transfusion
  • Nosocomial
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15
Q

How is anaplasmosis diagnosed?

A

Smear (Detects morulae in 20-75% of cases)

PCR

Serology

Clinical diagnosis

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16
Q

Compare/contrast clinical signs and symptoms of Ehrlichosis and Anaplasmosis

A

Incubation period 1-2 weeks after bite of infected tick

May cause asymptomatic to chronic infection

Typically an acute febrile illness (most cases). Infections more severe in immunocompromised

Rash and GI symptoms more common in Ehrlichosis

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17
Q

____% of confirmed cases of Ehrlichiosis are hospitalized. Explain.

A

62% of confirmed cases are hospitalized

Delay in antibiotic therapy is associated with an increased risk of mechanical ventilation and prolonged hospital stay.

Estimated mortality rate 2-5% (likely over estimated)

Multiorgan involvement in fatal cases with most bacteria in spleen, LN and BM

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18
Q

What is the appropriate treatment for Ehrlichiosis and Anaplasmosis?

A

Doxycycline (or tetracycline) because it can get into the cells

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19
Q

Trophozoites:

A

Form of parasite that is motile, feeding, reproducing

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20
Q

-mastigotes:

A

Flagellated form/stage of parasite

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21
Q

Sexual stages of parasites:

A

merozoites, schizonts, gametes, oocysts

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22
Q

What disease is suggested by this peripheral blood smear?

A

Babesiosis (Babesia microti)

Characteristic tetrad and ring stage

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23
Q

How is Babesia transmitted?

A

Vector:

  • Nymphal stage of the Deer tick or black legged tick (Ixodes scapularis)
  • Ticks can also have Lyme, Anaplasma
  • Few patients recall tick exposure

Animal reservoir:

  • White-footed mice

Other routes:

  • Blood transfusion
  • Rarely, congenital
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24
Q

Where is Babesia most common?

A

Northeast and upper midwest

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25
What are the clinical manifestations of Babesia?
Can be asymptomatic or present w/flu-like symptoms Can cause hemolytic anemia w/dark urine due to lysed RBCs Severe, life-threatenting disease in: * patients without a spleen * immunocompromized * advanced age
26
How is Babesia diagnosed?
Smear: * Detects infected RBCs * Can be difficult to distinguish Babesia from Plasmodium Serology: * IFA detects antibody in ~88-96% of infected patients PCR Clinical diagnosis, malaria-like illness in Babesia endemic region.
27
It can be difficult to distinguish Babesia from _____ on a peripheral smear
Plasmodium
28
How is Babesia treated?
Most asymptomatic persons do not require treatment. For ill patients, 7-10 days of * atovaquone PLUS azithromycin; OR * clindamycin PLUS quinine
29
Leshmaniasis infects what cells?
Intracellular pathogen of **macrophages**
30
How is Leshmaniasis transmitted to humans?
Vector: * Female Sand flies Animal reservoir * small rodents & other mammals * Anthroponotic (human reservoir) in some regions Other routes: * Blood transfusion * IV Drug use, needle sharing * Congenital Congenital
31
Kala-azar is another name for \_\_\_\_\_
Leshmaniasis
32
What are the clinical manifestations of Leshmaniasis:
Irregular bouts of fever Substantial weight loss Swelling of spleen and liver Serious anemia Untreated, fatality rate in developing countries 100% within 2 years. Post-kala-azar dermal manifestations * hypopigmented maculopapular and nodular rash * usually \> 6months after cure, but may be concurrent with visceral leishmaniasis, esp. in Sudan
33
How is Leshmaniasis diagnosed?
**Bone marrow** or splenic aspirate (detects **amastigotes** in macrophages) **Serology** (may be useful as supportive evidence of diagnosis)
34
What is shown in this image?
This is an image of a macrophage infected with **Leshmaniasis**, containing **amastigotes**. Note that each amastigote has a **nucleus** (red arrow) and a rod-shaped **kinetoplast** (black arrow). Visualization of the kinetoplast is important for diagnostic purposes, to be confident the patient has leishmaniasis.
35
What is the treatment for Leshmaniasis?
**Amphotericin B** - antifungal agent **Pentavalent antimony** * Antimony is a chemical element with symbol Sb and atomic number 51. * not licensed for commercial use in the US * CDC has IND protocol **Paromomycin** * aminoglycoside, binds parasite ribosomes **Miltefosine** * FDA-approved in 2014 * membrane-active synthetic ether-lipid analogue originally developed for the treatment of cutaneous metastasis from mammary carcinomas
36
T. brucei:
Causes African trypanosomiasis aka sleeping sickness
37
T. cruzi:
Causes American trypanosomiasis aka Chagas disease
38
How is Chagas disease transmitted?
Vector: * reduviid bug * **bites then poops**, parasites are in the bug’s GI tract Animal reservoir: * armadillos, raccoons * also dogs, guinea pigs and rats Other routes: * Blood transfusion * Congenital
39
Describe the clinical manifestations of Chagas Disease:
**Acute** and **chronic** stages. Acute may be asymptomatic or nonspecific flu-like symptoms, last ~2 months **Classic Romana’s sign**, swelling of the eyelids near the bite or where the feces was rubbed into the eye Chronic infection is usually asymptomatic but some patients develop **myocarditis**. Death from Chagas is usually due to cardiac pathology.
40
How is Chagas Disease diagnosed?
41
How is Chagas Disease Treated?
Antiparasitics thought to **increase oxygen radicals** and damage parasite DNA * **nifurtimox** * **benznidazole** These drugs are not FDA approved and are available in the US only from CDC under investigational protocols.
42
What is Malaria?
Obligate intracellular eukaryotic parasite Infects liver cells and red blood cells at different stages of the life cycle
43
The ____ stage occurs in humans and the ____ stage occurs in mosquitos
The **asexual** stage occurs in humans and the **sexual** stage occurs in mosquitos
44
What is the vector for Malaria?
The female Anopheles mosquito
45
Describe the Malaria lifecycle in humans:
**Sporozites** are injected into the body by the mosquito. These travel to the **liver**, which is the first site of infection/the parasite replicates here. During this initial period, don't know you're infected (**asymptomatic**). Merozites burst from the liver and begins replicating in **RBCs** - this is the stage associated with **symptoms**. See characteristic **ring stage** --\> **trophozite** --\> **Schizont**. Some emerge as male and female **gametocytes**, which recombine in the malaria midgut. These can then travel to salivary gland of a new mosquito for uptake.
46
What is shown in this image?
Malaria
47
What are the 5 parasites that cause malaria?
* •Plasmodium falciparum* * •Plasmodium vivax* * •Plasmodium ovale* * •Plasmodium malariae* * •Plasmodium knowlesi*
48
Fill in the table:
49
What is the clinical course of uncomplicated malaria?
_Prepatent period:_ patient is asymptomatic while parasite multiplies in liver (7-14 days) _Paroxysm:_ * shaking chills, then high fever (\<106° F) when infected RBC burst to release new merozoites. May or may not be periodic * Headache, nausea, vomiting, malaise & more
50
What strain of malaria most commonly causes severe malaria? What symptoms are associated with this?
Almost always due to **falciparum malaria** Cerebral malaria (coma, impaired consciousness, seizures) Severe anemia Multi organ failure
51
Describe the pathogenesis of severe malaria:
Parasite exports malaria proteins onto the surface of the RBC, specifically **PfEMP1**. This protein interacts with ligands on human cells, especially **ICAM-1** and **CR-1** (also CSA and CD36), which allows blood cell to stick to endothelial lining, resulting in clogging in microvasculature. Body causes a massive immune response. Many problems arise due to host response to the parasite, such as cerebral malaria, metabolic acidosis, and high mortality.
52
Pregnancy-specific Falciparum:
Falciparum parasites turn on specific genes (**VAR2CSA**) to promote **placental cytoadherence** (only turned on in pregnant hosts) In areas of high transmission, primigravidae not immune to these but multigravidae develop immunity Malaria --\> **low birth weight** (Infections in pregnant women cause 400,000 low birth weight babies annually)
53
What 3 ways does Malaria kill children?
**Infection in pregnancy** - low birth weight, preterm delivery **Acute febrile illness** - Cerebral malaria, respiratory distress, hypoglycemia **Chronic repeated infections** - severe anemia
54
Explain immunity to malaria:
People can develop partial protective immunity but never fully protective immunity to malaria. In areas where patients only get a few bites per year, never see adult immunity. See symptomatic mlaraia in kids and adults. Semi-protective immunity depends on continuously seeing parasites in the immune system. As exposed more (in areas with hundreds of bites/year), have asymptomatic infections as adults. Immunity is fleeting. Need to be continuously exposed to maintain.
55
Explain how certain conditions predispose patients to a genetic resistance to malaria:
Inhospitable erythrocyte: * Sickle cell trait * Thalassemia * G6PDH deficiency Inhibition of invasion: * Ovalocytosis (rigid membrane) * Duffy antigen receptor for chemokines (DARC) absent in African populations
56
Plasmodium falciparum:
Causes the worst, most drug-resistant form of Malaria. Most commonly found in Africa.
57
Plasmodium vivax:
Outside of Africa - doesn't usually kill, but severe symptoms and has **recurrence**.
58
Plasmodium ovale:
Global distribution, causes dormancy and **recurrence**.
59
Plasmodium malariae:
Global distribution - doesn't cause much disease; "silent"
60
Plasmodium knowlesi:
Zoonotic pathogen, associated with monkeys in SE Asia. Not documented a human being bit by mosquito and transmitting to another human. Need monkey involvement.
61
Resistant to vivax malaria is due to the lack of _____ in persons of ____ descent
Duffy antigen African descent
62
Primaquine:
Treats P. vivax and P. ovale malaria (which can become latent) in liver stages Causes hemolytic anemia in G6PD deficient patients
63
What biologic characteristics make Plasmodium falciparum the malaria species most likely to cause severe disease?
The ability to sequester in the microvasculature
64
How is the spread of malaria currently controlled?
Indoor residual spraying Chemotherapy Insecticide treated bed nets
65
Indoor residual spraying (IRS):
•Selectively kills female anophelines, resting on walls or in roofing material after blood meal **•DDT** * Most effective and cheapest * Not introduced into environment * No evidence for human toxicity •Works with organized health infrastructure (S. Africa, Zambian mining communities)
66
Artemisinin combination therapy (ACT) is the global standard for treating which malarial parasite?
Falciparum
67
How is P. vivax treated?
* Chloroquine * ACT where there is chloroquine resistance * Terminal prophylaxis with primaquine for hypnozoites –G6PDH deficiency
68
Artemisnin:
* Artemisinins derived from Chinese herbal remedy * Fast-acting but must be used in combination with long acting drug such as mefloquine

Hematology Block 1 (5 decks)

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