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Block 6 Week 5 > Protozoa and Helminths > Flashcards

Protozoa and Helminths Flashcards

1
Q

How prevalent is malaria?

A

half the worlds pop is ar risk

250 million cases, > 1.5 million deaths, 91% in Africa and most in chidren < 5 years old

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2
Q

What are the parasites that cause malaria?

A

Plasmodium falciparum,
P. vivax,
P. malariae,
P. ovale

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3
Q

What is the geographic distribution of malaria?

A

tropical
subtropical
temperate
(no animal reservoirs)

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4
Q

What is the life cycle of malaria?

A
  • female anophaeles spp mosquitos take blood meals from infected humans
  • after sexual reproduction, sporozites in salivary glands are infective forms for humans
  • sporozites inculated into human migrate to liver
  • asexual reproduction in hepatocytes
  • merozoites enter blood and penetrate erythrocytes
  • merozoites develop in ertyhrocytes to schizonts
  • merozites rupture host cells and release new merozoites that penetrate new erythrocytes (cause of symptoms and pathology).
  • some merozoites give rise to gametocytes that are picked up during mosquito feeding to complete cycle
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5
Q

What is malaria?

A

disease of erythrocytes and the blood vascular system;

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6
Q

What is malaria mediatd by?

A

TNF-alpha

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7
Q

What are the symptoms of malaria?

A

Classic fever paroxysm (correlates w/ synchronized rupture of erythrocytes)

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8
Q

When will you get classic fever paroxysm w/ P. falciparum caused malaria?

A

sporadic, daily (malignant tertian)

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9
Q

When will you get classic fever paroxysm w/ P. vivax caused malaria?

A

every other day (benign tertian)

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10
Q

When will you get classic fever paroxysm w/ P. ovale caused malaria?

A

every other day (ovale tertian)

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11
Q

When will you get classic fever paroxysm w/ P. malariae caused malaria?

A

every third day (quartan)

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12
Q

What are the important clinical and laboratory findings of malaria?

A

anemia, hepatosplenomegaly, hyperimmunoglobulinemia

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13
Q

What are the disease sequellae (a condition this is the consequence of a previous disease or injury) of malaria?

A

glomerulonephritis, nephrosis, cerebral malaria (most organ systems affected).

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14
Q

What types of malaria relapse?

Why?

A

vivax and ovale

liver hypnozoites can re-establish infections

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15
Q

What types of malaria do NOT relapse but can recrudesce (subclinical infection becomes active clinical disease)?

A

Falciparum and Malariae

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16
Q

WHat immune response fights against malaria?

A

innate and acquired

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17
Q

How do you diagnose malaria?

A

thick and thin blood films; rapid immunoassays

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18
Q

How do you treat malaria?

A

Chloroquine-> kills erythrocytic forms

Primaquine-> prevent relapses with vivax and ovale

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19
Q

T or F

drug resistance in malaria is widespread?

A

T, particularly chloroquine resistance

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20
Q

How do you prevent/control malaria?

A

chemoprophylaxis; mosquito control with long-lasting insecticidal nets and residual indoor insecticide spraying; NO VACCINE)

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21
Q

What is a tick-borne infection that resembles malaria?

A

babesiosis

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22
Q

If you see cross linking or things that look almost like chromosomes in a blood cell what is the parasite?

A

babesiosis

maltese cross is the chromosome looking things

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23
Q

If you see things that look like beta fishes surrounding RBCs, what is the parasite?

A

African trypanosomiasis

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24
Q

If you see things that look like rings with a diamond on them or a bunch of dots in a banana, what is the parasite?

A

P. falciparum malaria

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25
Q

What is the common name for African Trypanosomiasis?

A

African sleeping sickness

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26
Q

How prevalent is african trypanosomiasis?

A

450,000 cases, 50,000 deaths, 55 million people at risk

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27
Q

What are the parasites involved with african trypanosomiasis?

A

Trypanosoma brucei gambiense= west african sleeping sickness (Gambian)
Trypanosoma brucei rhodesiense = East african sleeping sickness (Rhodesian)

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28
Q

Where will you find African trypanosomiasis?

A

subsaharan africa (paralleles tsetse fly distrubtion; many animal reservoir hosts)

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29
Q

What is the life cycle of the parasites of African trypanosomiasis?

A

tsetse fly (glossina spp.) takes blood meal on infected human. Metacyclic trypomastigotes in salivary glands are infective forms for human. Trypomastigotes in blood and CNS

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30
Q

Which is more virulent, the eastern or western african sleeping disease?

A

Rhodesion so eastern

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31
Q

What is a chancre?

A

a painless ulcer, particularly one developing on the genitals as a result of venereal disease

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32
Q

What is the clinical presentation of African Trypanosomiasis?

A

trypanosomal chancre at site of tsetse bite; parasites in bite wound

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33
Q

What defines the acute stage of African Trypanosomiasis?

A

trypomastigotes in blood stream/lymphatics; fever, lymphadenopathy (winterbottom’s sign); acute death in Rhodesian disease

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34
Q

What defines the chronic stage of African Trypanosomiasis?

A

parasite invasion of CNS (early in Rhodesian, late in Gambian); somnolence, coma, death

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35
Q

How does your immune system defend against African Trypanosomiasis?

A

antibodies to trypomastigotes; antigenic variation

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36
Q

How do you diagnose African Trypanosomiasis?

A

demonstration of parasites in chancre, blood, or lymph nodes; serology less helpful

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37
Q

How do you treat African Trypanosomiasis?

A

Pre-CNS disease-Suramin

Post-CNS disease-Melarsoprol

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38
Q

How do you prevent and control African Trypanosomiasis?

A

avoid tsetse fly/human contact; NO VACCINE

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39
Q

What is the common name for American trypanosomiasis?

A

Chagas Disease

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40
Q

What is the prevalence of Chagas disease?

A

120 million at risk> 16 million annual cases, 13,000 annual deaths

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41
Q

What is the parasite that causes American Trypanosomiasis (chagas disease)?

A

trypanosoma cruzi

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42
Q

Where do you find trypanosoma cruzi?

A

Central and South America, Southern U.S. (many aminal reservoir hosts)

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43
Q

What is the life cycle/biology of American trypanosomiasis?

A
  • reduviid bug vector (triatoma spp) picks up trypomastigotes in human blood and parasites develop in hind gut
  • Bug defacates while feeding on another human and infective METACYCLIC trypomastigotes are scratched into the bite wound.
  • Trypomastigotes in blood
  • Intracellular Amastigotes form pseudocysts in the cytoplasm of a variety of cells (especially heart muscle and nerves)
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44
Q

What is the earliest clinical presentation of American Trypanosomiasis (Chagas disease, Kissing bug)?

A

chagoma at site of reduviid bite, unilateral periorbital edema (romana’s sign) and regional lymphadenopathy.

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45
Q

What are the symptoms of acute infection of American trypanosomiasis (chagas disease)? What is the fatality rate of acute stage?

A

fever, malaise, hepatosplenomegaly

10% due to meningoencephalitis and mycoarditis

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46
Q

What are the symptoms of chronic infection of American trypanosomiasis?

A

cardiac disease (both muscle and nerve damage) \; GI disease (megaesophagus or megacolon); neurological disease

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47
Q

How can you get transmission of American trypanosomiasis?

A

via blood transfusion, organ transplants, transplacentally

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48
Q

How does your bodies immune system react to American Trypanosomiasis?

A

antibodies to extracellular trypomastigotes; CD8 T cells kill amastigote-infected host cells

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49
Q

How do you diagnoses Amerian trypanosomiasis?

A

amastigotes in tissue; serology; xenodiagnosis

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50
Q

How do you treat American trypanosomiasis ?

A

benznidazole for acute stage

NO cure for chronic stage

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51
Q

How do you prevent/ control american trypanosomosis?

A

vector control; no vaccine

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52
Q

What is the common name for Visceral Leishmaniasis?

A

Kala Azar

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53
Q

What is the prevalence of Visceral Leishmaniasis?

A

350 million at risk, > 12 milion cases worldwide, >90% mortality rate untreated

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54
Q

What is the parasite that causes Visceral Leishmaniasis (Kala Azar) disease?

A

Leishmania donovani

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55
Q

Where do you find Visceral Leishmaniasis (Kala Azar) disease?

A

Tropic, subtropics, E and E hemisphere (many animal reservoir hosts)

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56
Q

What is the life cycle of visceral Leishmaniasis (Kala Azar) disease?

A

flagellated promastigotes in sand fly vector ( e.g. phlebotomus spp) inoculated into human skin
-extracellular promastigotes penetrate epithelial cells, macrophages, or dendritic cells and change to intracellular amastigotes that survive within phagolysosomes. Infected cells taken in blood meal complete cycle

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57
Q

What is the clinical presentation of Visceral Leishmaniasis?

A

fever paroxysms and hepatosplenomegaly resemble falciparum malaria

58
Q

What are the lab findings in Viseral Leishmaniasis?

A

hyperimmunoglobulinemia

59
Q

What are the disease sequellae of Visceral Leishmaniasis?

A

Post Kala Azar Dermal Leishmanoid (PKDL)

60
Q

How does the immune system react to Viscerl Leishmaniasis?

A

CD4 Th1 T cell activation of macrophages can kill amastigotes

61
Q

How do you diagnose Visceral Leishmaniasis (Kala Azar)?

A

giemsa-stain of buffy coat WBCs or bone marrow biopsy; Look for amastigotes; serology

62
Q

How do you treat Visceral Leishmaniasis (Kala Azar)?

A

liposomal amphotericin B or sodium stibogluconate; drug toxicity)

63
Q

How do you prevent/control Visceral Leishmaniasis?

A

vector control, no vaccine

64
Q

What are the parasites that cause cutaneous and mucocutaneous Leishmaniasis?

A

Leishmania mexicana (chile ulcer)
L. tropica (Dehli boil)
L. braziliensis (espundia)

65
Q

What is the prevalence of Cutenaous and mucocutaneous Leishmaniasis?

A

greater than 2 million new cases in old and new world each year

66
Q

Where will you find cutaeous and mucocutaneous leishmaniasis?

A

Tropic and subtropics, E. and W. hemisphere (many animal reservoir hosts)

67
Q

Tell me about the life cycle of Cuteneous and mucocutaneous Leishmaniasis.

A

flagellated promastigotes in sand fly vector (e.g phlebotomus spp.) inoculated into host skin; extracellular promastigotes change to intracellular amastigotes in epithelial cells, macrophages, dendritic cells.

68
Q

Tell me about the clinical presentation of cutaneous leishmaniasis

A

L. mexicana in cutaneous lesions; papules, ulcers (crateriform) on exposed parts of body (secondary bacterial infections); skin lesions eventually heal with life-long immunity to reinfection with same parasite.

69
Q

Tell me about the clinical presentation of Mucocutaneous leishmaniasis.

A

L. braziliensis parasites found initially in a typical cutaneous lesion; tropism to nasopharyngeal tissue and palate; tissue erosion and secondary infection common

70
Q

How does the immune system respond to Cutaneous and mucocutaneous leishmaniasis?

A

CD4 Th1 T cell-enhanced killing of amastigotes in macrophage phagolysosomes

71
Q

How do you diagnose cutaneous and mucocutaneous leishmaniasis?

A

skin test, needle aspiration or biopsies of ulcers for amastigotes

72
Q

How do you treat cutaneous and mucocutaneous leishmaniasis?

A

sodium stibogluconate; drug toxicity; no vaccine

73
Q

How do you prevent/control cutaneous/mucocutaneous leishmaniasis?

A

vector control, no vaccine

74
Q

If you see focal mass lesions in the brain, what parasite should you be thinking?

A

toxoplasmosis

75
Q

What is the parasite that causes toxoplasmosis?

A

toxoplasma gondii

76
Q

What is the prevalence of toxoplasmosis?

A

23% of US pop serologically positive

40% of AIDS pnts have the disease

77
Q

What is the geographic distribution of toxoplasmosis?

A

worldwide (can infect any animal)

78
Q

What is the life cycle of toxoplasmosis?

A
  • sexual cycle in intestinal epithelium of felines
  • asexual cycle in rodents and humans begins with ingestion of oocytes.
  • Fast growing tachyzoites in tissue can beome slow growing bradyzoites in pseudocysts (mainly in heart, brain, skeletal muscle). Human are usually “dead end” hosts.
79
Q

T. gondii is an obligate (extracellular/intracellular) parasite

A

Intracellular

80
Q

Tachyzoites prevent what?

A

phagolysosome/ lysosome fusion in host macrophages

81
Q

How do you transmit toxoplasmosis?

A
  • ingestion of oocytes she in feline feces
  • ingestion of pseudocysts in infected raw or undercooked meat
  • transplacental transmission (tachyzoits) from mother to fetus
  • transmission via transfusion or transplantation (tachyzoites)
82
Q

What are the clinical manifestations of acute toxoplasmosis?

A

subclinical “infectious mononucleoisis-like” syndrome in immunocompetent individuals (lymphadenopathy); severe systemic manifestation and HIGH mortality in immunosuppressed individual (e.g encephalitis in AIDS patients)

83
Q

What are the clinical manifestations of chronic toxoplasmosis?

A

usually asymptomatic, but pseudocyst rupture can lead to systemic infections, particularly in immunosuppressed individuas
and HIGH mortality in immunosuppressed individuals

84
Q

What are the clinical manifestations of congenital infection of toxoplasmosis?

A

Most infants develop chorioretinitis later in life; neurological sequellae include hydrocephalus; often FATAL

85
Q

When do you get congenital infection of toxoplasmosis?

A

primary maternal infection during first trimester of pregnancy 1/1000 live births in the US.

86
Q

How does your immune system respond to toxoplasmosis?

A

IgG and complement kill extracellular tachyzoites; CD4 Th1 cell-induced macrophage activation

87
Q

How do you diagnose toxoplasmosis?

A

lymph node biopsy or mouse inovulations of blood or tissue fluid; serology

88
Q

How do you treat toxoplasmosis?

A

pyrimethamine-sulfadiazine with folinic acid

89
Q

How do you prevent/control toxoplasmosis?

A

cook meat; avoid cats during pregnancy NO VACCINE

90
Q

What is the prevalence of amebiasis?

A

greater than 500 million human cases worldwide. U.S prevalence 1-2%

91
Q

What is the parasite that causes amebiasis?

A

Entamoeba histolytica

92
Q

What is the geographic distribution of amebiasis?

A

worldwide (evolving problem in male homosexuals)

93
Q

What is the life cycle of amebiasis?

A

humans ingest cysts

  • become trophozoites in s. intestine
  • migrate to colon and attach to mucosa
  • revert to cysts and passed in feces
94
Q

What is the clinical manifestation of amebiasis?

A

Asymptomatic or limite diarrhea. May result in ulcerative colitis.
Flask shaped ulcers may lead to perforations, peritonitis, and amebomas

95
Q

Extraintestinal amebiasis often occurs (blank) intestinal symptoms.

A

without

96
Q

What is the most common abscess caused by amebiasis?

A

amebic liver abscess

97
Q

How does your immune system respond to amebiasis?

A

IgA; CD4 Th1 activation of macrophages

98
Q

How do you diagnose amebiasis?

A

look for protracted diarrhea or dysentary; infections are diagnosed by finding characteristic trophozites and cysts on stool exam
serological tests
look for amebic liver abscess

99
Q

How can you find an amebic liver abscess?

A

radiography, ultrasonography, CT scans

100
Q

How do you treat amebiasis?

A

Iodoquinol-for intestinal disease
Tinidazole plus iodoquinol-for extraintestinal disease
Aspiration of liver abscesses may be indicated

101
Q

How can you prevent/control amebiasis?

A

sanitary disposal of human feces; water purification; no vaccine

102
Q

What are some other pathogen amoebas?

A

-Naegleria fowleri; Acanthamoeba spp. (amebic eningoencephalitis); -Balantidium coli (ciliate)

103
Q

What is the most common intestinal protozoan parasite in the US?

A

giardiasis

104
Q

What is the parasite that causes giardiasis?

A

giardia lamblia

105
Q

If you see blue floaty things that look like an alien head on histopath what are they?

A

giardia

106
Q

What is the geographic distrubition of giardia?

A

worldwide (many animal reservoir hosts)

107
Q

What is the life cycle of giardia?

A

human ingests cysts that become flagellated trophozoites in S. intestin.
trophozite attaches to mucosal epithlium w/ sucking disks, reproduces by binary fission, forms new cysts that pass in feces

108
Q

What are the clinical manifestations of giardiasis?

A

some hosts asymptomatic

most exhibit diarrhea (fulminate and watery)

109
Q

What will chronic infections of giardiasis look like?

A

flatulence, steatorrhea and malabsorption, weight loss, fatigue, general debility, patient may experience epigastric pain.

110
Q

How does the immune system respond to Giardiasis?

A

IgA, T lymph and macrophages

111
Q

How do you diagnose Giardiasis?

A

identify trophozite or cyst in fecal sample or duodenal aspirate (string test) fecal ELISA for antigen

112
Q

How do you treat Giardiasis?

A

tinidazole or metronidazole

113
Q

How do prevent or control Giardiasis?

A

sanitary disposal of feces; water purfication, especially stream water, NO VACCINE

114
Q

What is an acid fast microorganism that appears like red circles on a histop slide?

A

Cryptosporidium parvum

115
Q

What is the prevalences of cryptosporidosis?

A

10% of AIDS patients, organism widely distributed in US water supply

116
Q

What is the parasite that causes Cryptosporidiosis?

A

cryptosporidium parvum

117
Q

What is the geographic distribution of Cryptosporidosis?

A

worldwide (zoonotic disease)

118
Q

What is the life cycle of cryptosporidosis?

A
  • sporulated oocyst ingested
  • sporozoites released into s. intestine (mainly jejunum)
  • asexual reproduction in columnar cells
  • some become male and some female gametes
  • fertilization creates unsporulated oocysts and then these are passed in feces
119
Q

What is the clinical manifestations of cryptosporidiosis?

A

Children present with gastroenteritis
normal host: diarrhea, abdominal cramping,
immunocompromised host: severe diarrhea (17 liters daily) case fatality in AIDS is 50%

120
Q

What does the lab show in cryptosporiodosis?

A

mild villous atrophy
crypt enlargement
minimal mononuclear cell infiltrate of lamina propria

121
Q

How does your immune system react to cryptosporidiosis?

A

CD4 T lymph and IFN gamma

122
Q

How do you diagnose cryptosporidosis?

A

oocysts in stool

123
Q

How do you treat/prophylaxis of cryptosporidosis?

A

nitrazoxanide; rehydration therapy

124
Q

How do you prevent/control cryptosporidiosis?

A

stools highly infectious; proper hygiene; repair immunodeficiency; NO VACCINE

125
Q

What is a related intestinal parasite to cryptosporidiosis?

A

cyclospora cayetanensis

126
Q

What am i referring to?
In the present outbreak, 636 cases have been reported in 23 states. CDC says that evidence points to contaminated salad greens from Mexico.

A

Cyclospora cayetanensis oocysts

127
Q

If you see a histo slide of a ying yang sign what is it?

A

Trichomoniasis

trichomonas vaginalis

128
Q

What is the prevalence of trichomoniasis?

A

greater than 180 milion a year. 7.5 million cases/yr US

129
Q

What is the parasite that causes trichomoniasis?

A

trichomonas vaginalis

130
Q

What is the geographic distribution of trichomoniasis?

A

worldwide

131
Q

What is the life cycle of trichomoniasis?

A

flagellated trophozoites live in vagina, prostate and urethra

132
Q

(blank) is a venereal disease

A

trichomoniasis

133
Q

T.vaginalis has numerous strains, some more virulent than others; pH of vagina becomes more (blank), allows proliferation of bacterial flora; (blank) sexually active women will get this infection.

A

alkaline

25%

134
Q

In trichomoniasis, Trophozoites attach to mucosal lining of (blank) ; contact-dependent cytotoxicity caused by parasitic enzymes.

A

urogenital tract

135
Q

How will trichomoniasis present in women?

A

Some infected women are asymptomatic, but most have mild vaginal discomfort. Can present with intense vaginal itching or burning with a thick, yellow, blood-tinged discharge; burning on urination also occurs. Increased risk of pre-term births and HIV

136
Q

How will trichomoniasis present in men?

A

Men are usually asymptomatic; if prostate involved, there may be groin pain and burning on urination

137
Q

How does our immune system respond to trichomoniasis?

A

IgA

138
Q

How do you diagnose trichomoniasis?

A

identify flagellated trophozoite in discharge fluid

Trichomonads can be cultured (seen on pap smear)

139
Q

How do you treat trichomoniasis?

A

metronidazole or tinidazole (some drug resistant strains)

140
Q

How do you prevent and control trichomoniasis?

A

condom, chemotherapy of ALL partners NO VACCINE

Block 6 Week 5 (10 decks)

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