ICL 3.4 & 3.5: Protozoa Flashcards
(110 cards)
1
Q
what are the 3 types of parasites?
A
- protozoa
- helminths
- arthropods
2
Q
how many cells are protozoa?
A
unicellular eukaryotes
3
Q
what are the two stages that protozoa appear in ?
A
- trophozoites
2. cysts
4
Q
what are trophozoites?
A
a form that protozoa may appear in
feeding stage = absorbs nutrients from the plasma membrane
motile stage
5
Q
what are cysts?
A
a form that protozoa may appear in
non-feeding stage; they rely on stored food
also the non-motile stage
6
Q
what are the different types of motility that protozoa can have?
A
- sporozoans
- flagellates
- amoebozoa
- ciliate
7
Q
what are sporozoans?
A
non-motile trophozoites
8
Q
what are amoebozoa?
A
they have pseudopodia
9
Q
which parasites are sporozoans?
A
- plasmodium
- T. gondii
- C. parvuum
10
Q
which parasites are flagellates?
A
- L. donovani
- T. brucei
- T. cruzi
- G. intestinalis
- T. vaginalis
11
Q
which parasites are amoebozoa?
A
E. histolytica
12
Q
which parasites are ciliate?
A
balantidium coli
13
Q
what disease does plasmodium cause?
A
malaria
plasmodium is a sporozoan = non-motile trophozoite stage
14
Q
what disease does L. donovani cause?
A
leishmaniasis
L. donovani is a flagellate trophozoite stage
15
Q
which disease does T. brucei cause?
A
african trypanosomiasis
16
Q
which 4 parasites cause malaria?
A
plasmodium (sporozoa):
1. P. vivax
- P. falciparum
- P. ovale
- P. malariae
each parasite leads to a different clinical presentation
17
Q
what are the two types of trypanosomiasis?
A
- african trypanosomiasis
presents as either west african vs. east african sleeping sickness
- american trypanosomiasis = chagas disease
2 presentations - acute and chronic
18
Q
where is malaria in the world?
A
mostly africa
but a century ago it was endemic in every continment
most US cases are imported and rare
19
Q
how is malaria transmitted?
A
vector = female mosquitoes (Anopheles genus)
can also be transmitted from blood transfusion, congenitally, sharing needles
20
Q
what is the infection process of plasmodium?
A
- mosquito bites you and the sporozoites in the salivary glands of the mosquito are injected into your blood stream
- parasites go directly to the liver and infect it and multiply there
- parasites multiple till the cell explodes
- the parasites multiple in the RBC until they also burst and then they go onto infect other RBCs
- mosquito then sucks parasites back up next time it bites you
21
Q
what are the symptoms of malaria?
A
clinical presentation varies depending on which plasmodium species is infecting the human, level of parasitemia and immune status
symptoms start out flu-like: fever, chills, headache, myalgias, arthralgias, weakness, NVD –> due to massive release of merozoites into circulation when RBCs burst
each cycle of infection, replication and cell lysis induces another round of symtpoms so like with P. vivax you’ll see symptoms every 48 hours
other symptoms: splenomegaly, anemia, thrombocytopenia, hypoglycemia, pulmonary or renal dysfunction, and neurologic damage
22
Q
what kind of infection is caused by plasmodium vivax?
A
malaria – very high morbidity
invades only young, immature RBCs (reticulocytes) containing the Duffy blood group antigen
felatively “benign” form of malaria (benign tertian malaria)
does not cause red cell adherence to capillaries!!
23
Q
what are the main clinical characteristics of plasmodium vivax?
A
can remain dormant in the liver (hypnozoites) and relapse even after the blood has been cleared of merozoites (i.e. up to ~3 years)
this dormant hypnozoite form is why travelers could appear with the disease long after moving here!
incubation period (10-17 days)
influenza-like symptoms, as described in general malaria clinical features.
most untreated patients can survive, although sequelae can result from relapses (i.e. splenomegaly, liver and kidney damage)
24
Q
how do you diagnose plasmodium vivax?
A
blood smear
you’ll see:
- single ring forms (literally a ring in the RBC)
- enlarged erythrocytes from the merozoites replicating in RBCs
25
how do you treat plasmodium vivax?
chloroquine followed by primaquine
primaquine is to eliminate hypnozoites; if you don't treat dormant stage you'll have relapses
26
what genetic phenotype protect against plasmodium vivax?
red cell membrane Duffy antigen (chemokine receptor) used by the P. vivax merozoites to enter the red cell
so people who lack the Duffy antigen are resistant to P. vivax!!
this is why Duffy null phenotype is most common in people whose ancestors derive from regions in Africa where vivax malaria is endemic.
27
what are the clinical characteristics of plasmodium ovale?
very similar to P. vivax = also forms hypnozoites and infects immature RBCs
does NOT infect via Duffy antigen so people without Duffy antigen can still be infected
28
what are the clinical characteristics of plasmodium malariae?
can infect only mature RBCs with more rigid cell membranes
so this means you won't see any large erythrocytes with this parasite
no hypnozoites in liver = no relapses after treatment
longest incubation period (18-40 days)
untreated infections can last many years
29
what are the characteristics of plasmodium falciparum?
occurs almost exclusively in tropical and sub-tropical regions
the vast majority of malaria deaths are caused by P. falciparum!! (the most severe disease with more than 5% of all erythrocytes infected)
it does NOT form hypnozoites so there should be no recurrence post 6 months
falciparum infects erythrocytes of any age (no preference)
30
what are the main clinical characteristics of plasmodium falciparum?
shortest incubation period (7-10 days)
no hypnozoites so falciparum should not be suspect if symptoms appear after 6 months-years after exposure
P. falciparum malaria is the most likely to result in fulminating deadly disease if left untreated which is why it's called malignant tertian malaria
31
what are the symptoms of plasmodium falciparum infection?
more severe symptoms = daily chills, fever, nausea, vomiting, diarrhea, abdominal pain and dehydration
anemia: increased inflammation and rupture of RBC's --> toxic cellular debris
fenal failure, hepatic and lung pathology
cerebral malaria, placental malaria
some infections are known as “Blackwater fever” due to hemoglobinuria from RBC lysis and kidney damage
32
why is plasmodium falciparum malaria so deadly?
P. falciparum generates and inserts an adhesive protein into the infected red cell membrane (PfEMP1) --> red cell membrane becomes more “sticky”
PfEMP1 can bind to many host receptors through its multiple adhesion domains which leads to
sequestration for evading spleen-dependent killing = sticky RBCs get stuck in capillaries and never make it to the spleen to get removed from circulation
the consequence of this is obstruction of capillaries!! this can lead to:
1. parasite sequestration in brain and placenta capillaries = complications of cerebral malaria and placental malaria
2. renal failure is due to hemolysis and obstruction of renal capillaries
3. pathological consequences for liver and lung
33
what trait protects against P. falciparum malaria?
sickle cell trait
infected RBCs are “sickled” more readily and eliminated more easily by the spleen and the liver
34
how do you diagnose plasmodium falciparum?
blood smear:
1.
multiple parasites can infect a single RBC = multiple rings = diagnostic
there's also the possibility of mixed infection w/ P. vivax
3. “banana-shaped” crescent gametocytes = diagnostic (literally looks like a bananna
35
how do you treat plasmodium falciparum?
1. Chloroquine (but there's increasing resistance)
2. Artesunate
alternative:
3. Quinine sulfate + doxycycline, clindamycin
4. Atovaquone-proguanil (Malarone)
5. Mefloquine (toxic)
36
is there a malaria vaccine?
it's against plasmodium falciparum
low efficacy though
37
what are the two stages of leishmaniasis?
1. adult = flagellated, infective form
free promastigote in vector (sandfly)
2. obligate intracelular amastigote = non-flagellated, in mammalian definitive hosts, divides within macrophage, is diagnostic form
38
what are the 3 clinical forms of leishmaniasis?
1. visceral leishmaniasis (kala-azar) = multi-organ infection
2. cutaneous leishmaniasis = ulcerative, skin disfiguring infection
3. mucocutaneous leishmaniasis = destruction of mucous membranes and related tissue structures
39
how is leishmaniasis transmitted?
vector = sandfly
can be zoonotic: sandfly get it from another animal
or can be anthroponotic = sandfly gets it from another human
40
what is the life cycle of leishmaniasis?
1. sandfly takes blood meal from human
2. promastigotes are phagocytized by macrophages
3. promastigotes transform into amastigotes inside macrophages
4. amastigotes multiply in cells and macrophages in various tissues
5. sandfly takes blood meal
6. ingestion of parasitized cell
7. amastigotes transform into promastigote stage in midgut
8. divide in midgut and migrate to probescis
amastigote = intracellular, no flagellum
promastigote = extracellular + flagellum
41
which parasites cause visceral leishmaniasis?
L. donovani
L. infantum
it's opportunistic in AIDS
42
what are the main clinical characteristics of visceral eishmaniasis?
most serious= affects all organs (multi-organ infection); grows in macrophages
fulminating, or chronic and debilitating, or asymptomatic and self-limiting
invasion of the reticulo-endothelial system = enlarged lymph nodes, spleen, liver
fatigue and weakness due to anemia caused by persistent inflammation and hypersplenism (RBC destruction increased)
fever, rigor and chills (often intermittent)
super big stomaches
43
which groups are commonly effected by cutaneous leishmaniasis?
U.S. military deployed in afghanistan, iraq, and kuwait
90% of cases are in afghanistan, brazil, iran, peru, saudi arabia and syria
species that cause it differ worldwide
44
what are the main symptoms of cutaneous leishmaniasis?
cutaneous disease = chronic sore
1st sign = red papule at fly's bite site (2 wks. - 2 mo. post exposure)
irritated lesion, intensely pruritic, and begins to enlarge and ulcerate.
2ndary infection are a big problem.
it's a skin disfiguring infection
slow-healing = lesion may heal w/o treatment in months, but usually leaves a disfiguring scar
45
what is mucocutaneous leishmaniasis? which parasite usually causes it?
least prevalent leishmaniasis
90% of all cases of MCL occur in Bolivia, Brazil and Peru; present also in Central America
produced most often by L. braziliensis
46
what are the main clinical characteristics of mucocutaneous leishmaniasis?
progressive infection; initially cutaneous that does not heal = secondary bacterial infections common = severe mutilation
may involve oral and nasal mucosae = destruction of underlying structures like palate, nasal cartilage
untreated primary cutaneous lesions may develop into the MCL form in up to 80% of cases even many years after primary lesion has healed
47
how do you diagnose leishmaniasis in general?
for all 3 forms:
1. most common: detection of amastigotes (non flagellated form) in macrophages (microscopy)
2. molecular detection methods (most accurate, not common).
48
how do you specifically diagnose mucoid or cutaneous leishmania?
1. amastigotes in stained smears from skin/mucous touch preps or ulcer biopsies
2. promastigotes (flagellated) in culture (ulcer tissue)
49
how do you specifically diagnose visceral leishmania?
amastigotes in biopsy samples: splenic puncture, lymph node aspirates, liver biopsy, sternal aspirates, iliac crest bone marrow, and buffy coat preparations of venous blood
50
how do you treat leishmania?
1. antimonial compounds (e.g. sodium stibogluconate)
highly toxic and becoming non effective
also there's drug resistance, India
2. paramomycin (antibiotic)
follow-up with smears, cultures, and/or PCR is necessary to ensure that treatment has been effective
51
how do you prevent leishmaniasis?
no vaccine
52
what are the 2 forms of trypanosomiasis?
1. African trypanosomiasis = sleeping sickness
| 2. American trypanosomiasis = Chagas disease
53
which parasite and what is the vector for African trypanosomiasis?
parasite = Trypanosoma brucei gambiense and T. b. rhodesiense
vector = tsetse fly
54
which parasite and what is the vector for american trypanosomiasis?
parasite = Trypanosoma cruzi
vector = Reduviids
55
where in the world do you see sleeping sickness?
1. T.b. gambiense = Tropical West and Central Africa
| 2. T.b. rhodesiense = found primarily in East Africa, especially cattle-raising countries.
56
what is the microbiology of trypanosoma brucei gambiense and T. b. rhodesiense?
flagellated
extracellular protozoa
57
what is the life cycle of trypanosoma brucei?
1. tsetse fly takes a blood meal
2. injected metacyclic trypomastigotes transform into bloodstream trypomastigoes which are carrier to other sites
3. trypomastigoes multiply by binary fission in various body fluids like blood, lymph, CSF
4. trypomastigotes in blood
5. tsetse fly takes a blood meal
6. bloodstream trypomastigotes transform into procyclic trypomastigoetes in tsetse fly's midgut and multiple
7. procyclic trypomastigotes leave the midgut and transform into epimastigotes
8. epimastigotes multiply in salivary fland and then transform into metacyclic trypomastigotes
starts all over
58
what are the main clinical characteristics of Gambian sleeping sickness?
aka West African sleeping caused by T.b. gambiense
starts as inflamed red lesion at the bite site then spreads to lymph nodes = enlargement
when it's swollen lymph nodes in the next area it's called "Winterbottom sign" and it's characteristic of Gambian trypanosomiasis
then you'll see fever, rash, edema and eventually it'll get to the CNS
CNS involvement = lethargy, tremors, meningoencephalitis
final stages of chronic disease= hemiplegia, incontinence, coma, death.
59
what are the clinical characteristics of East African sleeping sickness?
caused by T.b. rhodesiense
more virulent and shorter incubation period than T. b. gambiense
acute disease (fever, rigors, and myalgia) occurs more rapidly and progresses to a fulminating, rapidly fatal illness death within 12 months if untreated
it develops in greater numbers in the blood
*lymphadenopathy is uncommon
CNS invasion occurs early in the infection
60
what are the 3 stages for african trypanosomiasis?
1. chancre (may devlop at inoculation site)
2. hemolyphatic stage = fever, lymphadenopathy, and pruritus
3. meningoencephalitic stage = invasion of the central nervous system causing headaches, somnolence, abnormal behavior, and leading to loss of consciousness and coma.
61
how do you diagnose african trypanosomiasis?
1. Blood films
2. Lymph node aspirates
3. Spinal fluid
4. Serologic tests
5. PCR (not routine) --> to detect infections and to differentiate species (T. b. gambiense versus T. b. rhodesiense)
62
what will you see in the blood films of african trypanosomiasis infection?
dxtracellular flagellated protozoan
much larger than the red cell, unlike the malaria parasite or the American trypanosome
looks like a fat squigly worm
slide 45
63
how do you treat african trypanosomiasis infection?
Don't cross BBB
1. suramin
2. pentamidine
cross BBB
1. eflornithine (Gambian)
2. melarsoprol (rhodesiense)
64
what immune response does african trypanosomiasis elicit?
surface T.b. has antigenic VSG (variable surface glycoprotein)
different VSGs are expressed by organisms within a population
replacement population to be generated after effective antibody response against the dominant VSG = evasion of response
65
is there a vaccine for african trypanosomiasis?
nope
66
where in the world do you see Chagas disease?
North, Central, and South America
aka american trypanosomiasis
67
which parasite causes Chagas disease?
Trypanosoma cruzi
aka American trypanosomiasis
68
what is the microbiology of trypanosoma cruzi?
flagellated
obligate intracellular protozoa
69
what is the vector for Chagas disease?
vector = reduviid bug aka the kissing bug or the assassin bug
direct correlation between infected wild-animal reservoir hosts and the presence of infected bug nests in human’s homes --> zoonosis
70
what is the life cycle of trypanosoma cruzi?
1. T. cruzi is passed in the feces of reduciid bug and get inside the skin
2. the parasite invades and multiplies intracellularly
3. amastigotes encyst in tissue cells
4. trypomastigotes evolve in the cells and rupture out into blood and get into lymphatics too
there's a predilection for striated muscle, including the heart
5. parasite it taken up by the bug during blood feeding
6. epimastigotes multiply in the guy of vector
71
how is Chagas disease transmitted?
1. reduviid bug
2. contaminated blood transfusions or by organ transplants
3. infected women can pass the infection to their babies during pregnancy (congenital), at delivery, or while breastfeeding
4. eating uncooked food contaminated with infected bug feces (mucosal entry)
5. occupational exposure (research)
72
what are the main clinical characteristics of an acute T. cruzi infection?
erythematous, indurated area (chagoma/ bite site) --> rash and edema around the eyes and face = Romaña‘s sign
most common and severe in children <5 years old
usually CNS involvement
fever, chills, malaise, myalgia, and fatigue (flu-like)
positive smear, positive culture, positive PCR result
73
what are the main clinical characteristics of a chronic T. cruzi infection?
~ 30% of infected individuals get “mega-syndrome” even over 10 yrs. post-infection = myocarditis, dilated cardiomyopathy, enlargement of esophagus and colon = mega-colon and mega-cardiopathy
it's a major cause of cardiomyopathy in Central and South America
CNS involvement may produce brain granulomas = cyst formation, meningoencephalitis
negative smear, positive PCR results; diagnosis based on serologic testing
74
how do you diagnose Chagas disease?
1. acute stage = thick and thing blood films; you'll see T. cruzi trypomastigotes in blood
2. chronic stage = organisms leave the bloodstream and become difficult to find
so instead you have to do a biopsy of lymph nodes, liver, spleen, or bone marrow (amastigote)
3. xenodiagnosis in endemic areas
serologic; PCR
75
how do treat Chagas?
1. nifurtimox
2. benznidazol
these two are mainly against the acute phase
we don't actually have anything effect against the chronic disease...
76
is there a vaccine for Chagas disease?
nope
77
what is Chagas disease most notorious for?
can cause heart failure and death, most commonly among latin american immigrants
78
what are the 2 most important among the intestinal protozoa?
1. Entamoeba histolytica
2. Giardia intestinalis
cryptosporidium is another common pathogen found in the intestinal tract
79
how are intestinal protozoa transmitted?
fecal-oral
80
which parasite causes giardiasis?
giardia duodenalis (lamblia or intestinalis)
transmitted fecal-oral (cysts in water)
effects small intestine
81
where in the world do you see giardiasis?
worldwide
more prevalent tropical and developing countries
in USA, most common protozoal pathogen reported causing GI infection
82
what is the morbidity and mortality of giardiasis?
ranges from asymptomatic to acute intestinal symptoms including diarrhea (foul smelling / fatty --> chronic malabsorption), bloating, flatulence
never fatal
asymptomatic carriers (~50%) can shed cysts for yrs. / IgA deficient indivs. are very susceptible
83
how do you diagnose giardiasis?
detection of parasite in feces [trophozoites (flagellated/motile) and cysts]
84
how do you treat giardiasis?
metronidazole
85
how do you prevent giardiasis infections?
avoid fecal contamination of food or water
boil water (kills cysts)- resistant to chlorination
86
which parasite causes cryptosporidiosis?
Cryptosporidium hominis and parvum
transmitted fecal-oral via consumption of oocysts, waterborne, or by contact with cattle
87
where in the world do you see cryptosporidiosis?
worldwide
88
what is the morbidity/mortality of cryptosporidiosis?
generally self-limiting diarrhea (watery), but much more severe in AIDS patients and can be fatal
more common in summer months
89
how do you diagnose cryptosporidiosis?
detection of oocysts in feces by acid-fast staining or fluorescent staining (specific antibodies)
90
how do you treat cryptosporidiosis?
supportive care mainly
paramomycin and nitazoxanide have some clinical effect, and anti-diarrheal agents
91
how do you prevent cryptosporidiosis?
avoid fecal contamination of food or water from both human and cattle (resistant to chlorination; boil to kill)
prevent by filtering city water supplies
92
which parasite causes amebiases/amebic dysentery?
entamoeba histolitica
transmitted fecal-oral
effects the colon
93
where in the world do you see amebiases/amebic dysentery?
worldwide
more prevalent tropical and developing countries
NOT a zoonosis
94
what is the morbidity and mortality of amebiases/amebic dysentery?
general asymptomatic or mild symptoms severe symptoms include dysentery (bloody) and spread to other organs that can be fatal (liver abscess, less freq. in lung and brain) --> trophozoites adhere to human cells and secrete toxins and enzymes (tissue destruction).
95
how do you diagnose amebiases/amebic dysentery?
detection of multinucleated cyst or trophozoite (+/-red blood cells) (intraintestinal)
CT scan, serology (extra-intestinal)
96
how do you treat amebiases/amebic dysentery?
metronidazole
97
how do you prevent amebiases/amebic dysentery?
avoid fecal contamination of food or water
98
which parasite causes trichomoniasis?
Trichomona vaginalis
transmitted during sexual intercourse
affects = urogenital tract, vagina, urethra, prostate and epididymis
99
what is the morbidty and mortality of trichomoniasis?
general asymptomatic or mild vaginitis or urethritis
foul smelling greenish discharge; itching and burning
never fatal
100
how do you diagnose trichomoniasis?
detection of parasite in from vagina urethral, prostatic secretion [trophozoites (flagellated), no Cyst (and troph doesn’t survive in environment)
ONLY motile flagellated organism found in vaginal or urethral discharge (wet mounts)
101
how do you treat trichomoniasis?
metronidazole
102
how do you prevent trichomoniasis?
safe sex practices
103
what is the fun fact about trichomoniasis?
major cause of infertility and preterm labor in women and low birthweight in babies
every year 8 million people are newly infected with trichonmoniasis
104
which parasite causes toxoplasmosis?
toxoplasma gondii
infects brain and eyes
105
how is toxoplasmosis transmitted?
Ingestion of food or water contaminated with mature oocysts (maturation 24hrs) from cat feces (i.e. kitty litter), ingestion of raw or undercooked meat containing tissue cysts, congenitally (chorioretinitis, heydrocephalus, intracranial calcifications)
106
what is the morbidity/mortality of toxoplasmosis?
Ingested parasites penetrate intestinal wall --> spread through body via blood --> damages distant tissues (mononucleosis type symptoms) --> dormant cyst
Benign disease in immunocompetent persons and only results in serious disease if obtained congenitally (if mother infected during pregnancy) or if immunocompromised (most common cause of encephalitis in AIDs patients (cysts rupture --> encephalitis, necrotic brain lesions --> CT/MRI shows ring enhancing lesions)
107
how do you diagnose toxoplasmosis?
serology
108
how do you treat toxoplasmosis?
pirimethamine
sulfadiazine
109
how do you prevent toxoplasmosis?
avoid ingestion of contaminated food or water or raw meat (cooking @160ºF kills tissue cysts)
110
what's the fun fact about toxoplasmosis?
leading cause of foodborne illness and death
more than 60 million people in the US are chronically infected
infections in pregnany woman can lead to birth defects in their babies and infections in immunocompromised individuals can be deadly
