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Block 6 - week 5 > Protozoa - Hunter > Flashcards

Protozoa - Hunter Flashcards

1
Q

Name the different types of parasites that cause Malaria.

A
  1. plasmodium falciparum
  2. plasmodium vivax
  3. plasmodium malariae
  4. plasmodium ovale
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2
Q

Describe the epidemiology of malaria.

A
  1. 250 million cases
  2. greater than 1.5 million deaths
  3. 91% of deaths in Africa and most in children younger than 5
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3
Q

What is the geographic distribution of malaria?

A

tropical, subtropical and temperate regions

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4
Q

Are there any animal reservoirs for malaria parasites?

A

no

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5
Q

What is the primary site of infection in malaria?

A

Malaria is primarily a disease of erythrocytes and the blood vascular system. Malaria causes TNF-alpha mediated sepsis.

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6
Q

What is a classic symptom of malaria?

A

Intermittent fevers.

  1. they correlate with the synchronized rupture of erythrocytes
  2. P. falciparum - non-synchronized, sporadic, daily, malignant tertian
  3. P. vivax - every other day, benign tertian
  4. P. ovale - every other day, ovale tertian
  5. P. malariae - every third day, quartan
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7
Q

What are some important clinical findings in malaria?

A
  1. anemia
  2. hepatosplenomegaly - splenomegaly caused because malaria is a polyclonal, non-specific B cell activator
  3. hyperimmunoglobulinemia
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8
Q

What are some important disease sequellae for malaria?

A
  1. glomerulonephritis - immune complex mediated
  2. nephrosis
  3. cerebral malaria - immune complex mediated
  4. most organ systems affected
  5. vivax and ovale malarias can present with relapse while falciparum and malariae do not.
  6. falciparum and malariae malarias can recrudesce - describes when subclinical infection becomes an active clinical disease
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9
Q

Why do vivax and ovale malarias recur or relapse?

A

A form of the parasite called a hypnozoite can colonize the liver and re-establish infection at a later date.

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10
Q

What type of immunity is associated with malaria?

A

Acquired and innate. Inadequate immune response in malnourished.

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11
Q

How is malaria diagnosed?

A
  1. thick and thin blood films to visualize the parasite

2. rapid immunoassay

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12
Q

How is malaria treated?

A
  1. drugs such as chloroquine can kill erythrocytic form
  2. drugs such as primaquine can kill hepatic form and prevent relapse
  3. drug resistance is widespread - especially chloroquine resistance
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13
Q

How can malaria be prevented?

A
  1. mosquito control with long-lasting insecticidal nets
  2. residual indoor insecticide spraying
  3. chemoprophylaxis
  4. no vaccine available
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14
Q

What is another disease that resembles malaria?

A

Babesiosis - a tick-borne infection that is found in the midwest and eastern US. Can be fatal in immune compromised pt. Symptoms include fever, malaise, dark urine, low hemoglobin.

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15
Q

Describe the life cycle of the malaria parasite.

A
  1. Female Anopheles mosquito takes blood meal from infected human
  2. after sexual reproduction, sporozoites in her salivary gland are the infective form for humans
  3. sporozoites inoculated into human after a bite from infected mosquito travel to the liver
  4. sporozoites undergo asexual reproduction in hepatocytes and become merozoites, some can become hypnozoites and stay in liver (depends on spp.)
  5. merozoites enter blood and penetrate an RBC
  6. merozoites develop in RBC into schizonts (structures containing thousands of merozoites)
  7. RBC ruptures and releases merozoites and these invade other RBC’s
  8. Some merozoites leave asexual repro. and undergo sexual repro. in order to become gametocytes that a female anopheles mosquito can pick up from an infected human
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16
Q

What is the vector for malaria parasites?

A

The female Anopheles mosquito.

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17
Q

What is the infective form of the malaria parasite?

A

The sporozoite.

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18
Q

What drug can kill a hypnozoite and stop relapse of malaria?

A

Primaquine.

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19
Q

Which of the malaria parasites is the most malignant?

A

P. falciparum.

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20
Q

Name two parasites than can cause African Trypanosomiasis/ African sleeping sickness.

A
  1. Trypanosoma brucei gambiense

2. Trypanosoma brucei rhodesiense

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21
Q

Which parasite that causes African Trypanosomiasis is found in East Africa?

A

Trypanosoma brucei rhodesiense

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22
Q

Which parasite that causes Trypanosomiasis is found in West Africa?

A

Trypanosoma brucei gambiense

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23
Q

Describe the epidemiology of African Trypanosomiasis.

A
  1. 450,000 cases
  2. 50,000 deaths
  3. 55 million people at risk
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24
Q

What is the distribution of of African Trypanosomiasis?

A

Subsaharan Africa, has many animal reservoirs.

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25
Q

What is the vector of the African Trypanosoma parasites?

A

Tse tse fly. Glossina species.

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26
Q

Which of the two forms of African sleeping sickness is more virulent?

A

The Rhodesian form is more virulent than the Gambian.

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27
Q

What is a characteristic sign of AfricanTrypanosoma infection?

A

A chancre at the site of the Tse tse fly bite - parasites will enter the bite wound.

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28
Q

What are the two stages of African Trypanosoma infection?

A
  1. Acute stage - tryptomastigotes in blood/lymphatics. Causes fever and lymphadenopathy which are called Winterbottom’s sign. Death can occur in the acute stage with Rhodesian disease.
  2. Chronic stage - parasite invasion of CNS followed by somnolence, coma and death. Invasion of CNS happens earlier in Rhodesian infection than Gambian.
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29
Q

What type of immunity is associated with African Trypanososmiasis?

A
  1. antibodies to tryptomastigotes.

2. parasites exhibit a lot of antigenic variation to evade immune response.

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30
Q

How is African Trypanosomiasis diagnosed?

A
  1. demonstration of parasite in chancre, blood or lymph node

2. serology less helpful

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31
Q

How is African Trypanosomiasis treated and prevented?

A
  1. Pre-CNS disease - Suramin
  2. Post-CNS disease - melarsoprol - is a very toxic drug
  3. prevention - avoid Tse Tse fly contact
  4. no vaccine
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32
Q

Describe the life cycle of the African Trypanosoma parasites?

A
  1. Tse Tse fly takes blood meal from infected human
  2. Metacyclic trypomastigotes in fly salivary glands are the infective host for human and a chancre containing parasites develops at site of bite
  3. Trypomastigotes in blood and CNS cause pathology and enter a Tse Tse fly if they bite an infected human
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33
Q

Which parasite causes American Trypanosomiasis?

A

Trypanosoma cruzi.

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34
Q

Describe the epidemiology of American Trypanosomiasis.

A
  1. 120 million at risk
  2. greater than 16 million annual cases
  3. 13,000 annual deaths
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35
Q

What is the distribution of American Trypanososmiasis?

A

Central and South America, Southern US. Has many animal reservoirs.

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36
Q

Describe the symptoms of American Trypanosomiasis.

A
  1. earliest symptoms include a chagoma at the site of reduviid bug bite.
  2. also causes unilateral periorbital edema (Romana’s sign), regional lymphadenopathy.
  3. Acute infection - fever, malaise, hepatosplenomegaly, death occurs 10% of cases when progresses to meningiocephalitis and myocarditis.
  4. Chronic infection - presents with cardiac disease (muscle and nerve damage), gastrointestinal disease including megaesophagus and megacolon, and neurological disease.
  5. tropism of parasite is for cardiac muscle and enteric neurons
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37
Q

How else can transmission occur other than a bug bite?

A
  1. blood transfusion
  2. organ transplant
  3. transplacentally
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38
Q

What kind of immunity is associated with American Trypanosomiasis?

A
  1. Antibody to trypomastigote

2. CD8 T cells kill amastigote infected host cells

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39
Q

How is American Trypanosomiasis diagnosed?

A
  1. amastigotes in tissue
  2. serology
  3. xenodiagnosis
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40
Q

What is xenodiagnosis?

A
  1. When a person who is suspected of being infected is intentionally bitten with a non-infected Reduviid bug
  2. the bug is then tested for presence of parasite
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41
Q

How is American Trypanosomiasis treated and prevented?

A
  1. Acute stage - Benznidazole
  2. chronic stage - no cure
  3. prevention - vector control
  4. no vaccine
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42
Q

What is the vector for American Trypanosomiasis?

A

The Reduviid bug - also called the kissing bug.

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43
Q

Describe the lifecycle of Trypanosoma cruzi.

A
  1. Reduviid bug picks up trypomastigotes in human blood meal - parasites develop in bug hind gut
  2. Bug defecates while feeding on uninfected human and metacyclic trypomastigotes are scratched into the bite wound (bit is itchy)
  3. Trypomastigote in blood travel to various tissues
  4. once in tissue Trypomastigotes become intracellular amastigotes that form pseudocysts in the cytoplasm - especially in heart muscle and nerves
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44
Q

What is another name for American Trypanosomiasis?

A

Chagas disease.

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45
Q

What is Winterbottom’s sign?

A

Posterior cervical lymphadenopathy found in associated with African Trypanosomiasis.

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46
Q

What is Romana’s sign?

A

Unilateral periorbital edema found in association with American Trypanosomiasis.

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47
Q

What is the infective form of the parasite in American Trypanosomiasis?

A

Metacyclic Trypomastigote.

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48
Q

What is the infective form of the parasite in African Trypanosomiasis?

A

Metacyclic Trypomastigote.

49
Q

What parasite causes Visceral Leishmaniasis?

A

Leishmania donovani.

50
Q

Describe the epidemiology of Visceral Leishmaniasis.

A
  1. 350 million at risk
  2. greater than 12 million cases worldwide
  3. greater than 90% mortality rate if untreated
51
Q

What is the geographic distribution of Visceral Leishmaniasis?

A
  1. Tropics and subtropics
  2. E. and W. hemisphere
  3. many animal reservoirs
52
Q

What clinical signs are associated with Visceral Leishmaniasis?

A
  1. similar to P. falciparum infection
  2. fever paroxysms and hepatosplenomegaly - lives in cells of the reticuloendothelial system such as liver, spleen and bone marrow
  3. lab findings - hyperimmunoglobulinemia
53
Q

What disease sequellae is associated with Visceral Leishmaniasis?

A

Post Kala Azar Dermal Leishmanoid or PKDL. This is complication of Visceral Leishmaniasis that presents as a nodular or macular type rash that starts around the mouth and then can spread.

54
Q

How is Visceral Leishmaniasis diagnosed?

A
  1. Giemsa stain of buffy coat WBC’s or bone marrow biopsy - look for amastigotes
  2. serology
55
Q

How is Visceral Leishmaniasis treated and prevented?

A
  1. liposomal amphotericin B
  2. sodium stibogluconate
  3. prevention - vector control
  4. no vaccine
56
Q

What is the vector for Leishmania donovani?

A

The sand fly. Phlembotomus species.

57
Q

Describe the life cycle of Leishmania donovani.

A
  1. Sand fly bites human host and flagellated promastigote is inoculated into human
  2. extracellular promastigotes penetrate epithelial cells, macrophages, or dendritic cells and change to intracellular amastigotes
  3. amastigotes survive within a phagolysosome.
  4. infected cells taken in blood meal infect the sand fly when it bites an infected human
58
Q

What is another name for Visceral Leishmaniasis?

A

It is also called Kala Azar which refers to the blackening of the skin that can occur with some infected individuals.

59
Q

What is the infective form of the parasite Leishmania donovani?

A

Flagellated promastigote.

60
Q

What type of immunity is associated with Visceral Leishmaniasis?

A

CD4 T helper cell activation of macrophages that can kill amastigotes.

61
Q

What parasites cause Cutaneous and Mucocutaneous Leishmaniasis?

A
  1. Leishmania tropica
  2. Leishmania braziliensis
  3. Leishmania mexicana
62
Q

Describe the epidemiology of cutaneous and mucocutaneous leishmaniasis.

A
  1. greater than 2 million new cases in old and new world each year
63
Q

What is the distribution of cutaneous and mucocutaneous leishmaniasis?

A
  1. Tropics and subtropics
  2. E. and W. hemisphere
  3. many animal reservoirs
64
Q

Describe the signs and symptoms of cutaneous leishmaniasis.

A
  1. L. mexicana causes papules and crateriform ulcers on exposed parts of body that are vulnerable to secondary bacterial infections.
  2. cutaneous skin lesions eventually heal and pt left with life-long immunity to reinfection with same parasite
  3. mucocutaneous leishmaniasis caused by L. braziliensis parasites that first form a typical cutaneous lesion. The parasite has tropism for nasopharyngeal tissue and palate. Causes tissue erosion and secondary infections are common.
65
Q

What type of immunity is associated with cutaneous and mucocutaneous leishmaniasis?

A

CD4 T helper cell enhanced killing of amastigotes in macrophage phagolysosome.

66
Q

How is cutaneous and mucocutaneous leishmaniasis diagnosed?

A
  1. skin test

2. needle aspiration or biopsy of ulcers for amastigotes

67
Q

How is mucocutaneous and cutaneous leishmaniasis treated and prevented?

A
  1. sodium stibogluconate (very toxic) used to treat
  2. no vaccine
  3. prevention - vector control
68
Q

Describe the lifecycle of the cutaneous and mucocutaneous leishmania parasites.

A
  1. sand fly bites human and inoculates the flagellated promastigote into the bite wound.
  2. extracellular promastigotes change to intracellular amastigotes when they enter epithelial cells, macrophages and dendritic cells.
  3. sand fly then bites infected human and is infected with the parasite.
69
Q

What is the infective form of the cutaneous and mucocutaneous leishmania parasites?

A

Flagellated promastigote.

70
Q

What is the vector of the cutaneous and mucocutaneous leishmania parasite?

A

The sand fly, Phlebotomus spp.

71
Q

What parasite causes Toxoplasmosis?

A

Toxoplasma gondii.

72
Q

Describe the epidemiology of Toxoplasmosis.

A
  1. 23% of US population is serologically positive

2. 40% of AIDS patients have the disease

73
Q

What is the distribution of Toxoplasmosis?

A

Distribution is worldwide, can infect any mammal.

74
Q

What are the modes of transmission for Toxoplasma gondii?

A
  1. igestion of oocysts shed in feline feces
  2. ingestion of pseudocysts in infected raw or undercooked meat
  3. transplacental transmission of tachyzoites from mother to fetus
  4. transfusion or transplantation transmission of tachyzoites
75
Q

Describe the clinical disease and pathology of Toxoplasmosis.

A
  1. Acute infection - subclinical mono-like syndrome and lymphadenopathy in immunocompetent patients
  2. Chronic infection - usually asymptomatic but pseudocyst rupture can lead to systemic infections, particularly in immunosuppressed pt’s
  3. causes nearly 35% of chorioretinitis cases in children and adults in the US
  4. Congenital infection - primary maternal infection during first trimester of pregnancy causes neurological sequellae including hydrocephalus and often causes chorioretinitis later in life of child. Often is fatal to neonate.
76
Q

What type of immunity is associated with toxoplasmosis?

A
  1. IgG and complement kill extracellular tachyzoites

2. CD4 T-helper cell induced macrophage activation

77
Q

How is toxoplasmosis diagnosed?

A
  1. lymph node biopsy or mouse inoculations of blood or tissue fluid
  2. serology
78
Q

How is toxoplasmosis treated and prevented?

A
  1. Primethamine-sulfadiazine with folinic acid (because drug blocks folic acid pathway for both human and pathogen)
  2. prevention - cook meat, avoid cats during pregnancy
  3. no vaccine
79
Q

Describe the life cycle of Toxoplasma gondii.

A
  1. sexual reproduction in intestinal epithelium of felines
  2. asexual cycle in rodents and humans begins with ingestion of oocysts or pseudocyst
  3. oocysts become fast growing tachyzoites in hepatocytes and are distributed by infected macrophages throughout the body and form pseudocysts in tissue (slow growing form called bradyzoites)
  4. parasite has tropism for brain, heart and skeletal muscle
  5. tachyzoites can prevent phagosome/lysosome fusion in macrophages
  6. T. gondii is an obligate intracellular parasite
80
Q

What is the infective form of Toxoplasma gondii?

A

Oocyst in feline feces or pseudocyst in raw or undercooked meat. Also could get tachyzoite from transfusion or congenitally.

81
Q

What parasite causes Amebiasis?

A

Entamoeba histolytica.

82
Q

Describe the epidemiology of Amebiasis.

A
  1. greater than 500 million cases worldwide

2. US prevalence is 1-2%

83
Q

What is the distribution of Amebiasis?

A

Worldwide.

84
Q

Describe the disease and pathology caused by Entamoeba histolytic.

A
  1. infections may be asymptomatic - especially cyst carriers
  2. host may exhibit limited diarrhea
  3. can cause ulcerative colitis with associated colicky pain, flatulence, diarrhea and dysentery.
  4. can cause flask-shaped ulcers that can lead to perforations, peritonitis and amebomas.
  5. extraintestinal amebiasis of ten occurs without intestinal symptoms but does cause abscess in the liver - amebic liver abscess.
85
Q

What type of immunity is associated with Amebiasis?

A
  1. IgA

2. CD4 T helper activation of macrophages

86
Q

How is Amebiasis diagnosed?

A
  1. intestinal amebiasis must be considered in any patient with protracted diarrhea or dysentery.
  2. infection diagnosed by finding characteristic trophozoites and cysts on stool exam.
  3. serological tests helpful
  4. diagnosis of Amebic liver abscess - radiography, ultrasonography, CT scan
87
Q

How is Amebiasis treated and prevented?

A
  1. intestinal disease - Iodoquinol
  2. extra-intestinal disease - Tinidazole - need aspiration of liver abscess to confirm first
  3. prevention - sanitary disposal of human feces, water purification
  4. no vaccine
88
Q

What are some other pathogenic Amoebas?

A
  1. Naegleria fowleri
  2. Acanthamoeba spp - causes Amebic meningoecephalitis
  3. Balantidium coli - ciliate
89
Q

What is the life cycle of Entamoeba histolytic?

A
  1. humans ingest cuts that excyst to become trophozoites in the small intestines. Can also be transmitted via anal intercourse.
  2. trophozoites migrate to colon and attach to mucosa.
  3. trophozoites revert to cysts and are passed in the feces to infect new host.
90
Q

What is the infective form of Entamoeba histolytica?

A

Cysts.

91
Q

What parasite causes Giardiasis or intestinalis?

A

Giardia lamblia

92
Q

Describe the epidemiology of Giardiasis?

A

Most common intestinal protozoan parasite in the US.

93
Q

What is the distribution of Giardiasis?

A

World wide - many animal reservoirs, especially the Beaver.

94
Q

What is the pathology caused by Giardiasis?

A
  1. some hosts are asymptomatic
  2. most hosts exhibit some diarrhea that may be fulminate and watery
  3. chronic infections cause flatulence, steatorrhea and malabsorption syndrome leading to weight loss, fatigue, general debility and possibly epigastric pain.
95
Q

What type of immunity is associated with Giardiasis?

A
  1. IgA

2. some evidence for T cells and macrophage involvement

96
Q

How is Giardiasis diagnosed?

A
  1. identification of characteristic trophozoite or cyst in fecal sample or duodenal aspirate
  2. string test
  3. fecal ELISA for antigen
97
Q

How is Giardiasis treated and prevented?

A
  1. Tinidazole or metronidazole
  2. prevention - sanitary disposal of feces, water purification
  3. no vaccine
98
Q

Describe the life cycle of Giardia lamblia.

A
  1. human ingests cysts that become flagellated trophozoites in the small intestine
  2. trophozoite attaches to mucosal epithelium with sucking disks, reproduces via binary fission and forms new cysts that pass in feces.
99
Q

What is the infective form of Giardia lamblia?

A

Cysts.

100
Q

What parasite causes cryptosporidiosis?

A

Cryptosporidium parvum.

101
Q

Describe the epidemiology of cryptosporidiosis.

A
  1. widely disributed in US water supplies

2. 10% of AIDS patients have disease

102
Q

What is the distribution of cryptosporidiosis?

A

Worldwide - zoonotic disease.

103
Q

What are the signs and symptoms of cryptosporidiosis?

A
  1. normal host - profuse watery diarrhea with abdominal cramping. Symptoms rapidly abate.
  2. Immune compromised host - onset more gradual but diarrhea more severe and persistent - can lose up to 17 liters per day. Sporozoites can autoinfect. Case fatality rate in AIDS is 50%.
  3. children present with gastroenteritis.
104
Q

What type of immunity is associated with cryptosporidiosis?

A
  1. CD4 T cells

2. IFN-gamma

105
Q

How is cryptosporidiosis diagnosed?

A

Identify oocysts in stool with an acid fast stain. On histopath of intestinal tissue sample can see mild villous atrophy, crypt enlargement and minimal cell infiltrate of lamina propria.

106
Q

How is cryptosporidiosis treated and prevented?

A
  1. nitrazoxanide - both treatment and prophylaxis
  2. rehydration therapy
  3. prevention - proper hygiene (stools highly infective), repair immunodeficiency
  4. no vaccine
107
Q

Describe the life cycle of Cryptosporidium parvum.

A
  1. sporulated oocyst is ingested and sporozoites are released in small intestines mainly in the jejunum.
  2. asexual reproduction occurs in columnar epithelium cells.
  3. some transform into male and female gametocytes
  4. after fertilization, unsporulated oocysts are formed and pass in the feces.
108
Q

What is the infective form of cryptosporidium parvum?

A

Sporulated oocyst.

109
Q

What is an intestinal parasite that is related to cryptosporidium parvum?

A

Cyclospora cayetanensis.

110
Q

What parasite causes Trichomoniasis?

A

Trichomonas vaginalis.

111
Q

Describe the epidemiology of Trichomoniasis.

A
  1. greater than 180 million annual cases worldwide

2. 7.5 million cases a year in US

112
Q

What is the distribution of Trichomoniasis?

A

Worldwide.

113
Q

What is the disease and pathology caused by Trichomonas vaginalis?

A
  1. T. vaginalis has numerous strains and some are more virulent than others.
  2. pH of the vagina becomes more alkaline, allows proliferation of bacterial flora.
  3. 25% of sexually active women will get this infection.
  4. Trophozoites attach to mucosal lining of UG tract and cause contact dependent cytotoxicity.
  5. some infected women are asymptomatic but most have mild vaginal discomfort.
  6. can present with intense vaginal itching and burning with a thick, yellow, blood-tinged discharge.
  7. may see burning on urination
  8. causes increased risk of pre-term births and HIV infection.
  9. men are usually asymptomatic but if prostate is involved then may be groin pain and burning on urination.
114
Q

What type of immunity is associated with Trichomoniasis?

A

IgA

115
Q

How is Trichomoniasis diagnosed?

A
  1. identification of characteristic flagellated trophozoite in discharge fluid
  2. trichonomads may be cultured and are often seen on Pap smear
116
Q

How is Trichomoniasis treated and prevented?

A
  1. Metronidazole or Tinidazole
  2. prevention - condom use during sex, chemotherapy of all partners
  3. no vaccine
117
Q

What is the infective form of Trichomonas vaginalis?

A

Flagellated trophozoite.

118
Q

Describe the life cycle of Trichomonas vaginalis.

A
  1. flagellated trophozoites live in vagina of humans and prostate and urethra of humans.
  2. the flagellated trophozoite is sexually transmitted - no known cyst stage.

Block 6 - week 5 (8 decks)

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