Parasites of Blood and Lymphatics (Buxton) Flashcards

1
Q

Name the 3 protozoans discussed in this lecture.

A

Plasmodium sp.

Babesia sp.

Trypanosoma sp.

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2
Q

Name the Trematode infection of the blood discussed in this lecture.

A

Schistosomes

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3
Q

Name the 4 filarial Nematodes discussed in this lecture.

A

Wuchereria bancrofti

Brugia malayai

Onchocerca volvulus

Loa loa

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4
Q

Why learn about parasites not found in the US?

A

Immigration

Travel

Military

Medical missions

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5
Q

What is the etiology of malaria?

A

Plasmodium sp.

P. vivax

P. ovale

P. malariae

P. falciparum

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6
Q

Protozoa that replicate in hepatocytes and RBCs are what species?

A

Plasmodium

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7
Q

Where is malaria most endemic?

A

Africa, parts of Central & South America, SE Asia

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8
Q

What percent of deaths of children per year from malaria are due to P. falciparum?

A

95%

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9
Q

Describe life cycle of mosquitos.

What are the most important stages?

A

Sporozoites enter and grow in hepatocytes (liver schizonts)

Merozoites - infectious form for RBC

Gametes are sucked up by another mosquito getting blood

Gamates become zygote, becomes oocyte - sporozoites burst out of cyst and move into salivary gland of mosquito

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10
Q

Patient presents with cyclic episodes of high fever, chills, rigors. Prior to this, he complained of experiencing a flu-like illness with headache, loss of appetite, and general malaise about 2 weeks ago.

A

Malaria

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11
Q

What are the classic signs of malaria?

Explain the pattern of these symptoms.

A

Cyclic episodes of high fever, chills, rigors.

Due to host cell reaction to rupture of RBC, with release of hemoglobin and other cellular debris, and the release of the parasite antigen, which leads to host secretion of TNF & IL-1.

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12
Q

Do all species of Plasmodium have the same cyclical response to malaria?

A

No - P. falciparum does not have any periodicity to the classical signs of infection.

P. vivax & P. ovale do - every 48 hours

P. malariae - every 72 hours

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13
Q

______ or ______ involvement can in occur in P. falciparum infections with increased fatality rates.

A

CNS…renal…

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14
Q

Which species of Plasmodium is the most prevalent, geographically widespread species infecting humans?

A

P. vivax

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15
Q

Which species of Plasmodium replicates in young RBCs?

A

P. vivax & P. ovale

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16
Q

Which species of Plasmodium form hypnozoites (dormant form), which are found in the liver?

A

P. vivax & P. ovale

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17
Q

Which species of Plasmodium replicates in mature RBCs?

A

P. malariae

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18
Q

What additional drug is needed to treat hypnozoites?

A

Primaquine

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19
Q

Which species of Plasmodium causes the most severe infection?

A

P. falciparum

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20
Q

This species of Plasmodium has many strains that are resistant to chloroquine. It replicates in erythrocytes of any age and has more parasite replication and RBC lysis compared to any other Plasmodium species.

A

P. falciparum

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21
Q

What does P. falciparum do to blood that makes it so dangerous?

A

Infected RBCs express a protein, pfEMP-1, on their membranes that binds to ICAM-1, an adhesion molecule, on endothelial cells. This leads to RBC blockage of small vessels. This is particularly bad when blood gets blocked from reaching the CNS, kidneys, and placenta.

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22
Q

Cerebral malaria, Blackwater fever, and maternal & fetal death in pregnancy are all severe manifestions of complications due to which species of Plasmodium? What causes these complications?

A

P. falciparum

Blood blockage

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23
Q

You obtain lab results that show parasites in Giemsa-stained blood smears. You see ring forms, gametocytes, trophozoites, and schizonts. What’s your diagnosis?

A

Malaria

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24
Q

What is your diagnosis based off of this slide?

A

Malaria

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25
Q
A

Ring forms - P. falciparum in RBC

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26
Q
A

Schizont - P. falciparum in RBC

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27
Q
A

Gametocyte - P. falciparum in RBC

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28
Q
A

Ring forms - P. ovale in RBC

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29
Q
A

Schizont - P. ovale in RBC

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30
Q
A

Gametocyte - P. ovale in RBC

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31
Q

What can you use to treat chloroquine-resistant P. falciparum?

A

Mefloquine

Quinine + doxycycline or clindamycin

Atovaquone + proguanil (combo = Malarone)

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32
Q

What can you use to treat chloroquine-sensitive P. falciparum and P. malariae?

A

Chloroquine

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33
Q

What can you use to treat P. vivax and P. ovale?

A

Chloroquine + primaquine (for hypnozoites)

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34
Q

What are some methods for control/prevention of malaria?

A

Insecticides - mosquitos

Repellents, bed nets - mosquito bites

Chemoprophylaxis - best for travelers

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35
Q

What is the best method of prevention for malaria? Why?

A

Bed nets - biting cycles are worse at night and nets have proven to be extremely effective at protecting people from bites. They’re alse extremely affordable.

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36
Q

What would you use as chemoprophylaxis for malaria?

A

Areas with P. vivax & P. ovale - same as treatment; chlorquine + primaquine

Areas with chloroquine-sensitive P. falciparum - chloroquine

Areas with choloroquine-resistant P. falciparum - similar to treatment; mefloquine, doxycycline, atovaquone + proguanil (combo = malarone)

37
Q

Out of Uganda, Thailand, Haiti, and Peru, which country(ies) is(are) at high risk for malaria? Which strain is most prevelant? Is there any drug resistance?

A

Uganda - P. falciparum accounts for 85% of infections and there is chloroquine-resistance

Haiti - P. falciparum accounts for 99% of infections and there is no resistance

38
Q

Out of Uganda, Thailand, Haiti, and Peru, which country(ies) is(are) at low risk for malaria? Which strain is most prevelant? Is there any drug resistance?

A

Thailand - P. falciparum & P. vivax account for 50% of infections each and there is chloroquine as well as mefloquine resistance

Peru - P. vivax accounts for 85% of infections and there is chloroquine resistance

39
Q

This protozoan-sporozoan is found in the US, especially in the coastal northeastern region. The vector is ticks and the reservoir is mice.

A

Babesia microti

40
Q

What is the pathogenesis of Babesiosis?

A

Bite of infected tick - babesia replicates in erythrocytes - RBC lysis releases merozoites - 1-4 week incubation period - fever, chills, headache, fatigue, weakness - potential for hemolytic anemia or renal failure (rare) - recovery in 2-4 weeks

41
Q

Describe the life cycle of Babesia microti.

A

Similar to that of mosquito, but no hepatocyte involvement.

42
Q

What is on this slide and how is this diagnosis made?

A

Babesiosis

Diagnose via demonstration of parasite in thick and thin blood smears

43
Q

How would you treat Babesiosis?

A

Clindamycin + quinine

or

Atovaquone + azithromycin

44
Q

How can you control Babesiosis?

A

Avoid tick bites

Eliminate reservoir from home sites, work areas

45
Q

This flagellated protozoan causes Chagas’ disease. Its vector is the triatomid bug, and its reservoirs include armadillos, rodents, and dogs. It is endemic in Central and South America.

A

Trypanosoma cruzi

46
Q
A

Trypanosoma cruzi

47
Q

Describe the life cycle of Trypanosoma cruzi.

A

Metacyclic trypomastigotes are produced in vector (infectious in human) - infects intestinal tract of Triatomine bug - bug crawls on you, often around lips - bug feeds on blood while simultaneously pooping infectious trypomastigote into you - trypomastigote travels to muscle cells, where it likes to replicate - replicated trypomastigotes enter bloodstream, where they can be taken up again by Triatomine bug

48
Q
A

Chagas’ Disease acute phase - chagoma & Romana’s (unilateral periocular swelling)

49
Q

Acute phase of this disease is often asymptomatic or present with fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, myocarditis. Patient usually presents with chagoma or Ramana sign. How does this disease resolve?

A

Chagas’ Disease

Most acute cases resolve in weeks ot months into an asymptomatic chronic form of the disease.

50
Q

Symptoms of chronic phase develop after years - decades even. Chronic infection can lead to megaesophagus or megacolon as a result of nerve damage to those areas. Cardiomyopathy can also occur as a result of parasite growth in and damage to cardiac myocytes. Chronic disease and its complications can be fatal.

A

Chronic Chagas Disease

51
Q

Cardiomyopathy appears to be what type of response (in terms of disease, infection, etc.)?

A

Autoimmune - Chagas antigen is similar to naturally occurring antigen found on heart. The immune system attacks microbial antigen, but eventually moves on to attack the heart.

52
Q
A

Blood trypomastigotes - T. cruzi

53
Q
A

Tissue amastigotes - T. cruzi

54
Q

How do you diagnose Chagas Disease?

A

By finding trypomastigotes in blood films or amastigotes in biopsies of lymph nodes, spleen, liver, bone marrow.

55
Q

How do you prevent Chagas from happening?

A

Insect & reservoir control around dwellings

56
Q

What causes African Sleeping Sickness?

What is the reservoir?

What is the vector?

A

Trypanosomas brucei

Reservoir - wild ungulates

Vector - tse tse fly

57
Q

Describe the pathogenesis of African Sleeping Sickness.

A
58
Q
A

T. brucei in blood

59
Q

How do you diagnose T. brucei?

A

Detection of trypomastigotes on blood films, lymph node aspirates, or CSF

60
Q

What is treatment for T. brucei?

A

Suramin for blood and lymphatic stages

Malarsoprol for CNS disease

61
Q

What preventative measures should you take against T. brucei?

A

Vector control

62
Q

What are the 3 blood flukes discussed in this lecture?

A

Schistosoma haematobium

Schistosoma mansoni

Schistosoma japonicum

63
Q

Which Schistosoma can be found in Afria, the Middle East, the Caribbean, Brazil, Venequela, and Suriname?

A

S. mansoni

64
Q

Which Schistosoma can be found in China, Indonesia, and the Philippines?

A

S. japonicum

65
Q

Which Schistosoma can be found in Africa and the Middle East?

A

S. haematobium

66
Q

What is the basic life cycle of Schistosomiasis?

A

Adults found in infected blood vessels of host

  • Lay eggs that will be released in either stool or urine
  • Eggs then HAVE to get into the water
  • Egg hatches, releases miracidium
  • FRESHWATER SNAILS ARE INTERMEDIATE HOST
  • Releases cercaria – infectious for humans
  • Swims in freshwater
  • Burrow through skin of host (bathing in river, collecting water for use, washing clothes)
67
Q

This parasite, when infecting a human, stays in vessels of bladder as an adult. Eggs migrate through bladder wall and are released in urine.

A

S. haematobium

68
Q

This parisite, when an adult, stays in the venous plexis of intestine. Eggs migrate through the intestine and liver and are then released in stool.

A

S. mansoin & S. japonicum

69
Q

Patient comes in with allergic dermatitis associated wtih cercarial penetration of skin. She has no acute symptoms, but has a fever, cough, and abdominal pain. Further testing revealed pyelonephritis.

A

Schistosomiasis

70
Q

Acute schistosomiasis, arising 4-6 weeks afte infection, causes what condition?

A

Katayama Fever

71
Q

Granulomatous lesions that interfere with organ function, causing problems such as liver damage, urinary obstruction, pyelonephritis, and bladder cancer are caused by what?

A

Chronic illness as a result of Schistosomiasis

72
Q
A

S. mansoni egg in liver, surrounded by granuloma

73
Q
A

S. haematobium eggs in bladder wall, surrounded by granuloma

74
Q
A

S. heamatobium & S. mansoni eggs

75
Q

What is the treatment for Schistosomiasis?

A

Praziquantel

76
Q

How would you control Schistosomiasis?

A

Education

Bio-control agents - against snails

use of molluscicides

Drainage of marsh areas

77
Q

What are the 4 fliarial parasites?

A

Wuchereria bancrifti

Brugia malayi

Onchocerca volvulus

Loa loa

78
Q

Which filarial parasites cause lymphatic filiarasis in the form of elephantiasis?

A

Wuchereria bancrifti

Brugia malayi

79
Q

Describe the life cycle of W. bancrofti and B. malayi.

A
80
Q

In what parts of the world are you likely to encounter lymphatic filariasis?

A

Tropics & subtropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America

81
Q

What causes River blindness?

What is the vector?

A

Onchocerca volvulus

Black flies

82
Q

Describe the life cycle of Onchocerca volvulus

A
83
Q

Inflammatory response to microfilariae of this parasite has lead to nodules, depigmentation, skin thickening, and intense itching. After migration to the eye, the microfiliariae cause blindness - River blindness.

A

Onchocercosis

84
Q

How do you diagnose River blindness?

A

Demonstration of microfilariae in skin snip preparation

85
Q

How is River blindness treated?

A

Surgical removal of nodules containing adult worms

Ivermectin

86
Q

How do you control River blindness?

A

Avoid insect bites

Mass prophylaxis with ivermectin and diethylcarbanizine

87
Q

Transmitted by the deer fly, Chrysops, infects the host with his filarial disease

A

Loiasis

88
Q

Adult worms live in CT under skin and between fascial layers overyling somatic muscles. Produce thousands of microfilariae daily. Adults migrate frequently. Usually no permanent damage.

A

Filarial Deases - Loiss

89
Q

Describe the life cycle of Loa loa.

A