Protozoa and Helminths Flashcards
(140 cards)
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
2
Q
What are the parasites that cause malaria?
A
Plasmodium falciparum,
P. vivax,
P. malariae,
P. ovale
3
Q
What is the geographic distribution of malaria?
A
tropical
subtropical
temperate
(no animal reservoirs)
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
5
Q
What is malaria?
A
disease of erythrocytes and the blood vascular system;
6
Q
What is malaria mediatd by?
A
TNF-alpha
7
Q
What are the symptoms of malaria?
A
Classic fever paroxysm (correlates w/ synchronized rupture of erythrocytes)
8
Q
When will you get classic fever paroxysm w/ P. falciparum caused malaria?
A
sporadic, daily (malignant tertian)
9
Q
When will you get classic fever paroxysm w/ P. vivax caused malaria?
A
every other day (benign tertian)
10
Q
When will you get classic fever paroxysm w/ P. ovale caused malaria?
A
every other day (ovale tertian)
11
Q
When will you get classic fever paroxysm w/ P. malariae caused malaria?
A
every third day (quartan)
12
Q
What are the important clinical and laboratory findings of malaria?
A
anemia, hepatosplenomegaly, hyperimmunoglobulinemia
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).
14
Q
What types of malaria relapse?
Why?
A
vivax and ovale
liver hypnozoites can re-establish infections
15
Q
What types of malaria do NOT relapse but can recrudesce (subclinical infection becomes active clinical disease)?
A
Falciparum and Malariae
16
Q
WHat immune response fights against malaria?
A
innate and acquired
17
Q
How do you diagnose malaria?
A
thick and thin blood films; rapid immunoassays
18
Q
How do you treat malaria?
A
Chloroquine-> kills erythrocytic forms
Primaquine-> prevent relapses with vivax and ovale
19
Q
T or F
drug resistance in malaria is widespread?
A
T, particularly chloroquine resistance
20
Q
How do you prevent/control malaria?
A
chemoprophylaxis; mosquito control with long-lasting insecticidal nets and residual indoor insecticide spraying; NO VACCINE)
21
Q
What is a tick-borne infection that resembles malaria?
A
babesiosis
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
23
Q
If you see things that look like beta fishes surrounding RBCs, what is the parasite?
A
African trypanosomiasis
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
25
What is the common name for African Trypanosomiasis?
African sleeping sickness
26
How prevalent is african trypanosomiasis?
450,000 cases, 50,000 deaths, 55 million people at risk
27
What are the parasites involved with african trypanosomiasis?
Trypanosoma brucei gambiense= west african sleeping sickness (Gambian)
Trypanosoma brucei rhodesiense = East african sleeping sickness (Rhodesian)
28
Where will you find African trypanosomiasis?
subsaharan africa (paralleles tsetse fly distrubtion; many animal reservoir hosts)
29
What is the life cycle of the parasites of African trypanosomiasis?
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
30
Which is more virulent, the eastern or western african sleeping disease?
Rhodesion so eastern
31
What is a chancre?
a painless ulcer, particularly one developing on the genitals as a result of venereal disease
32
What is the clinical presentation of African Trypanosomiasis?
trypanosomal chancre at site of tsetse bite; parasites in bite wound
33
What defines the acute stage of African Trypanosomiasis?
trypomastigotes in blood stream/lymphatics; fever, lymphadenopathy (winterbottom's sign); acute death in Rhodesian disease
34
What defines the chronic stage of African Trypanosomiasis?
parasite invasion of CNS (early in Rhodesian, late in Gambian); somnolence, coma, death
35
How does your immune system defend against African Trypanosomiasis?
antibodies to trypomastigotes; antigenic variation
36
How do you diagnose African Trypanosomiasis?
demonstration of parasites in chancre, blood, or lymph nodes; serology less helpful
37
How do you treat African Trypanosomiasis?
Pre-CNS disease-Suramin
| Post-CNS disease-Melarsoprol
38
How do you prevent and control African Trypanosomiasis?
avoid tsetse fly/human contact; NO VACCINE
39
What is the common name for American trypanosomiasis?
Chagas Disease
40
What is the prevalence of Chagas disease?
120 million at risk> 16 million annual cases, 13,000 annual deaths
41
What is the parasite that causes American Trypanosomiasis (chagas disease)?
trypanosoma cruzi
42
Where do you find trypanosoma cruzi?
Central and South America, Southern U.S. (many aminal reservoir hosts)
43
What is the life cycle/biology of American trypanosomiasis?
- 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)
44
What is the earliest clinical presentation of American Trypanosomiasis (Chagas disease, Kissing bug)?
chagoma at site of reduviid bite, unilateral periorbital edema (romana's sign) and regional lymphadenopathy.
45
What are the symptoms of acute infection of American trypanosomiasis (chagas disease)? What is the fatality rate of acute stage?
fever, malaise, hepatosplenomegaly
| 10% due to meningoencephalitis and mycoarditis
46
What are the symptoms of chronic infection of American trypanosomiasis?
cardiac disease (both muscle and nerve damage) \; GI disease (megaesophagus or megacolon); neurological disease
47
How can you get transmission of American trypanosomiasis?
via blood transfusion, organ transplants, transplacentally
48
How does your bodies immune system react to American Trypanosomiasis?
antibodies to extracellular trypomastigotes; CD8 T cells kill amastigote-infected host cells
49
How do you diagnoses Amerian trypanosomiasis?
amastigotes in tissue; serology; xenodiagnosis
50
How do you treat American trypanosomiasis ?
benznidazole for acute stage
| NO cure for chronic stage
51
How do you prevent/ control american trypanosomosis?
vector control; no vaccine
52
What is the common name for Visceral Leishmaniasis?
Kala Azar
53
What is the prevalence of Visceral Leishmaniasis?
350 million at risk, > 12 milion cases worldwide, >90% mortality rate untreated
54
What is the parasite that causes Visceral Leishmaniasis (Kala Azar) disease?
Leishmania donovani
55
Where do you find Visceral Leishmaniasis (Kala Azar) disease?
Tropic, subtropics, E and E hemisphere (many animal reservoir hosts)
56
What is the life cycle of visceral Leishmaniasis (Kala Azar) disease?
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
57
What is the clinical presentation of Visceral Leishmaniasis?
fever paroxysms and hepatosplenomegaly resemble falciparum malaria
58
What are the lab findings in Viseral Leishmaniasis?
hyperimmunoglobulinemia
59
What are the disease sequellae of Visceral Leishmaniasis?
Post Kala Azar Dermal Leishmanoid (PKDL)
60
How does the immune system react to Viscerl Leishmaniasis?
CD4 Th1 T cell activation of macrophages can kill amastigotes
61
How do you diagnose Visceral Leishmaniasis (Kala Azar)?
giemsa-stain of buffy coat WBCs or bone marrow biopsy; Look for amastigotes; serology
62
How do you treat Visceral Leishmaniasis (Kala Azar)?
liposomal amphotericin B or sodium stibogluconate; drug toxicity)
63
How do you prevent/control Visceral Leishmaniasis?
vector control, no vaccine
64
What are the parasites that cause cutaneous and mucocutaneous Leishmaniasis?
Leishmania mexicana (chile ulcer)
L. tropica (Dehli boil)
L. braziliensis (espundia)
65
What is the prevalence of Cutenaous and mucocutaneous Leishmaniasis?
greater than 2 million new cases in old and new world each year
66
Where will you find cutaeous and mucocutaneous leishmaniasis?
Tropic and subtropics, E. and W. hemisphere (many animal reservoir hosts)
67
Tell me about the life cycle of Cuteneous and mucocutaneous Leishmaniasis.
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
Tell me about the clinical presentation of cutaneous leishmaniasis
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
Tell me about the clinical presentation of Mucocutaneous leishmaniasis.
L. braziliensis parasites found initially in a typical cutaneous lesion; tropism to nasopharyngeal tissue and palate; tissue erosion and secondary infection common
70
How does the immune system respond to Cutaneous and mucocutaneous leishmaniasis?
CD4 Th1 T cell-enhanced killing of amastigotes in macrophage phagolysosomes
71
How do you diagnose cutaneous and mucocutaneous leishmaniasis?
skin test, needle aspiration or biopsies of ulcers for amastigotes
72
How do you treat cutaneous and mucocutaneous leishmaniasis?
sodium stibogluconate; drug toxicity; no vaccine
73
How do you prevent/control cutaneous/mucocutaneous leishmaniasis?
vector control, no vaccine
74
If you see focal mass lesions in the brain, what parasite should you be thinking?
toxoplasmosis
75
What is the parasite that causes toxoplasmosis?
toxoplasma gondii
76
What is the prevalence of toxoplasmosis?
23% of US pop serologically positive
| 40% of AIDS pnts have the disease
77
What is the geographic distribution of toxoplasmosis?
worldwide (can infect any animal)
78
What is the life cycle of toxoplasmosis?
- 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
T. gondii is an obligate (extracellular/intracellular) parasite
Intracellular
80
Tachyzoites prevent what?
phagolysosome/ lysosome fusion in host macrophages
81
How do you transmit toxoplasmosis?
- 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
What are the clinical manifestations of acute toxoplasmosis?
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
What are the clinical manifestations of chronic toxoplasmosis?
usually asymptomatic, but pseudocyst rupture can lead to systemic infections, particularly in immunosuppressed individuas
and HIGH mortality in immunosuppressed individuals
84
What are the clinical manifestations of congenital infection of toxoplasmosis?
Most infants develop chorioretinitis later in life; neurological sequellae include hydrocephalus; often FATAL
85
When do you get congenital infection of toxoplasmosis?
primary maternal infection during first trimester of pregnancy 1/1000 live births in the US.
86
How does your immune system respond to toxoplasmosis?
IgG and complement kill extracellular tachyzoites; CD4 Th1 cell-induced macrophage activation
87
How do you diagnose toxoplasmosis?
lymph node biopsy or mouse inovulations of blood or tissue fluid; serology
88
How do you treat toxoplasmosis?
pyrimethamine-sulfadiazine with folinic acid
89
How do you prevent/control toxoplasmosis?
cook meat; avoid cats during pregnancy NO VACCINE
90
What is the prevalence of amebiasis?
greater than 500 million human cases worldwide. U.S prevalence 1-2%
91
What is the parasite that causes amebiasis?
Entamoeba histolytica
92
What is the geographic distribution of amebiasis?
worldwide (evolving problem in male homosexuals)
93
What is the life cycle of amebiasis?
humans ingest cysts
- become trophozoites in s. intestine
- migrate to colon and attach to mucosa
- revert to cysts and passed in feces
94
What is the clinical manifestation of amebiasis?
Asymptomatic or limite diarrhea. May result in ulcerative colitis.
Flask shaped ulcers may lead to perforations, peritonitis, and amebomas
95
Extraintestinal amebiasis often occurs (blank) intestinal symptoms.
without
96
What is the most common abscess caused by amebiasis?
amebic liver abscess
97
How does your immune system respond to amebiasis?
IgA; CD4 Th1 activation of macrophages
98
How do you diagnose amebiasis?
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
How can you find an amebic liver abscess?
radiography, ultrasonography, CT scans
100
How do you treat amebiasis?
Iodoquinol-for intestinal disease
Tinidazole plus iodoquinol-for extraintestinal disease
Aspiration of liver abscesses may be indicated
101
How can you prevent/control amebiasis?
sanitary disposal of human feces; water purification; no vaccine
102
What are some other pathogen amoebas?
-Naegleria fowleri; Acanthamoeba spp. (amebic eningoencephalitis); -Balantidium coli (ciliate)
103
What is the most common intestinal protozoan parasite in the US?
giardiasis
104
What is the parasite that causes giardiasis?
giardia lamblia
105
If you see blue floaty things that look like an alien head on histopath what are they?
giardia
106
What is the geographic distrubition of giardia?
worldwide (many animal reservoir hosts)
107
What is the life cycle of giardia?
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
What are the clinical manifestations of giardiasis?
some hosts asymptomatic
| most exhibit diarrhea (fulminate and watery)
109
What will chronic infections of giardiasis look like?
flatulence, steatorrhea and malabsorption, weight loss, fatigue, general debility, patient may experience epigastric pain.
110
How does the immune system respond to Giardiasis?
IgA, T lymph and macrophages
111
How do you diagnose Giardiasis?
identify trophozite or cyst in fecal sample or duodenal aspirate (string test) fecal ELISA for antigen
112
How do you treat Giardiasis?
tinidazole or metronidazole
113
How do prevent or control Giardiasis?
sanitary disposal of feces; water purfication, especially stream water, NO VACCINE
114
What is an acid fast microorganism that appears like red circles on a histop slide?
Cryptosporidium parvum
115
What is the prevalences of cryptosporidosis?
10% of AIDS patients, organism widely distributed in US water supply
116
What is the parasite that causes Cryptosporidiosis?
cryptosporidium parvum
117
What is the geographic distribution of Cryptosporidosis?
worldwide (zoonotic disease)
118
What is the life cycle of cryptosporidosis?
- 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
What is the clinical manifestations of cryptosporidiosis?
Children present with gastroenteritis
normal host: diarrhea, abdominal cramping,
immunocompromised host: severe diarrhea (17 liters daily) case fatality in AIDS is 50%
120
What does the lab show in cryptosporiodosis?
mild villous atrophy
crypt enlargement
minimal mononuclear cell infiltrate of lamina propria
121
How does your immune system react to cryptosporidiosis?
CD4 T lymph and IFN gamma
122
How do you diagnose cryptosporidosis?
oocysts in stool
123
How do you treat/prophylaxis of cryptosporidosis?
nitrazoxanide; rehydration therapy
124
How do you prevent/control cryptosporidiosis?
stools highly infectious; proper hygiene; repair immunodeficiency; NO VACCINE
125
What is a related intestinal parasite to cryptosporidiosis?
cyclospora cayetanensis
126
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.
Cyclospora cayetanensis oocysts
127
If you see a histo slide of a ying yang sign what is it?
Trichomoniasis
| trichomonas vaginalis
128
What is the prevalence of trichomoniasis?
greater than 180 milion a year. 7.5 million cases/yr US
129
What is the parasite that causes trichomoniasis?
trichomonas vaginalis
130
What is the geographic distribution of trichomoniasis?
worldwide
131
What is the life cycle of trichomoniasis?
flagellated trophozoites live in vagina, prostate and urethra
132
(blank) is a venereal disease
trichomoniasis
133
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.
alkaline
| 25%
134
In trichomoniasis, Trophozoites attach to mucosal lining of (blank) ; contact-dependent cytotoxicity caused by parasitic enzymes.
urogenital tract
135
How will trichomoniasis present in women?
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
How will trichomoniasis present in men?
Men are usually asymptomatic; if prostate involved, there may be groin pain and burning on urination
137
How does our immune system respond to trichomoniasis?
IgA
138
How do you diagnose trichomoniasis?
identify flagellated trophozoite in discharge fluid
| Trichomonads can be cultured (seen on pap smear)
139
How do you treat trichomoniasis?
metronidazole or tinidazole (some drug resistant strains)
140
How do you prevent and control trichomoniasis?
condom, chemotherapy of ALL partners NO VACCINE
