Exam 2 Flashcards
(229 cards)
1
Q
What is the only parasitic protozoan of the small intestine?
A
Giardia lamblia
2
Q
steatorrhea-
A
fatty stool
3
Q
does giardia feed on host tissues?
A
no
4
Q
What host immune response is elicited against giardia?
A
IgA
5
Q
What microscopy shows giardia covering GI tract?
A
SEM
6
Q
When will you see giardia trophs in fecal sample?
A
watery diarrhea (not enough time to encyst)
7
Q
Which tests are for giardia in GI tract?
A
ELISA for parasite antigen string test (enterotest)
8
Q
Rx for giardia:
A
Flagyl (metronidazole)
Tindamax (tinidazole) = DOC
Nitazoxanide
Furazolidone-for children
9
Q
Which two giardia drugs cant be taken with alcohol?
A
flagyl and tindamax
10
Q
The commensal oral trichomonad?
A
T. tenax
11
Q
The commensal GI trichomonad?
A
P. hominis
12
Q
Trichomonas vaginalis:
A
vagina and urethra of females
urethra, seminal vesicles and prostate of male
13
Q
vaginalis trichomoniasis
•Transmission:
•Trophs cannot survive outside host
A
sexual contact
14
Q
What is pathology of T. vaginalis?
A
lyses and eats epithelial cells
15
Q
Dx. of T. vaginalis
A
- wet mount of genital secretions
- OSOM Trichomonas Rapid Test (ELISA tests for parasite antigen, doctor can do this test)
- anaerobic in vitro culture
16
Q
transmission can occur congenitally, but…..
A
parasite does not cross placenta or cervix. infant is infected during birth. RARE
17
Q
Rx for Trichomonas vaginalis
A
Flagyl. 7 day bid or tid (2x a day or 3x a day)
no immunity
18
Q
why is a lysosomal response not initiated in a cell invaded by an apicomplexan
A
they force their way in, they are not endocytized
19
Q
Apicoplast is considered to be a relic of a:
A
chloroplast
20
Q
During schizogony, multiple ______ occur, but only one ____ occurs
A
nuclear divisions
cytokinesis (into as many parts as there are nuclei)
21
Q
chickens infected with eimeria contract “bloody cecum” aka:
A
cecal coccidiosis
22
Q
ingestion of what stage of eimeria infects chickens?
A
sporulated oocyst
23
Q
Chicken host defenses against eimeria:
A
shed epithelial cells, pass with feces before invading cell, macrophages kill a few
24
Q
Isospora belli is now called:
A
Cystoisospora belli
25
```
Isospora belli
-Only Isospora species to infect man!
oDistribution:
oNiche:
oDx:
oRx:
```
- Tropical regions (NOT IN USA)
- small intestine
- oocysts in fecal samples (external sporulation)
- TMP-SMX (Trimethoprim-sulfamethoxazole. A.k.a. Bactrim/ Septra/ Cotrim)
26
What kind of people do Isospora belli infect?
young, old, immunocompromised. Uncommon in immunocompetent
27
considered an "emerging" pathogen
cyclospora cayetanensis
28
```
Cyclospora cayetanensis
distribution-
niche-
symptoms-
-it is self limiting
-sources-
```
- worldwide
- small intestine
- explosive diarrhea
- contaminated food and water
29
Cyclospora catayensis
sporgony occurs where-
oocyst contains what composition of sporozoites/sporocysts-
oocysts are very ______- not easily visualized in unstained fecal sample.
- external
- 2 sporocysts with 2 sporozoites each
- refractile
30
cyclospora cayetanensis
Dx.-
Rx.-
- acid fast stain fecal smear
| - TMP-SMX
31
```
Cryptosporidium parvum
host:
at risk:
has no_______. Those genes are still present though
niche:
```
- vertebrae
- immunosupressed and infants
- apicoplast
- entire GI tract
32
Cryptosporidium parvum:
life cycle direct/indirect?
where does sporogony occur?
what is unique about its niche?
- direct
- inside host
- it creates an intracellular, yet extracytoplasmic niche in intestinal epithelial cells
33
________ can occur when the oocyst of C. parvum are thin walled
autoinfection- they rupture in the same host
34
How strong are the thick walled oocysts of C. parvum?
they are extremely resistant to environment. chlorination will not kill, and will survive weeks to months in moist environment
35
does C. parvum have sporocysts?
| Is it host specific?
- no, just oocysts with sporozoites within
| - no it is not
36
clinical cryptosporidiosis is characterized by:
profuse, watery diarrhea, abdominal pain, nausea and vomiting
37
cryptosporidiosis in
immunocompromised-
immunocompetent-
asymptomatic-
- dehydration, chronic, possible fatality
- lasts 1-3 weeks, self limiting
- carrier. sheds the infective oocysts
38
If your diarrhea lasts longer than two weeks, you probably have what?
C. parvum or G. lamblia
39
C. parvum
| Dx.
- acid fast stain (oocyst are 5 micrometers, twice as big as C. cayetanensis)
- ELISA test for parasite Ag
- Intestinal biopsy if the other two dont work
40
C. parvum Rx.
Nitazoxanide (Alinia)
41
Nitazoxanide
| static or cidal?
static. for this reason it may not work for immunocompromised individuals
42
Does one acquire an immunity to C. parvum
yes, but only partial. next infection will need to be a bigger dose and symptoms will be milder
43
must use filters of _____ micrometers to filter water for C. parvum
1 micrometer
44
heteroxeneous-
undergoes different sexual reproduction in two hosts
45
Toxoplasma gondii undergoes asexual reproduction in ______ host and sexual reproduction in ________ host
- intermediate
| - definitve
46
Intestinal stages of T. gondii
| Extraintestinal stages of T. gondii
- tachyzoites and bradyzoites
| - sporozoites, merozoites, gametocytes
47
```
T. gondii-
the infective stage-
the intestinal stage-
the sexual stage-
the extra intestinal actives stage-
the extra intestinal dormant stage-
```
```
sporozoite
merozoite
gametocyte
tachyzoites
bradyzoites
```
48
Which T. gondii stage is analagous to gut merozoites?
tachyzoites
49
Why are bradyzoites not attacked by immune system but tachyzoites are?
they have antigenic differences
50
a tissue cyst can be called what 3 things?
zoitocyst, bradycyst, pseudocyst
51
Toxoplasma gondii
intermediate host-
definitive host-
sporogony occurs outside of host how long after a good cat scat?
- any warm blooded host, any nucleated cell
- cats only
- 1-3 days
52
How can you become infected with Toxoplasma gondii?
ingesting bradycysts via undercooked meat, transplacental or blood transfusion tachyzoite, organ transplant bradyzoite, or acquiring sporulated oocysts from cat scat.
53
How does toxoplasma evade host defenses?
prevents fusion of lysosome inside macrophage by surrounding it's vacuole with mitochondria
54
Is apical complex required for entry of macrophage?
no, the macrophage ingests it. It uses the apical complex to invade tissue cells
55
What are the 3 toxoplasmosis syndromes?
Acquired, congenital, recrudescent
56
Acquired toxo-
benign with few to no symptoms. maybe some flu like symptoms, swollen cervical nodes, maybe a little tissue damage.
57
Chronic toxoplasma infection-
asymptomatic, complete immunity, bradycysts remain in tissues for life.
58
how many babies are born with toxoplasmosis every year?
400-4000
59
what toxo stage crosses placenta to infect babies?
tachyzoite
60
when is the most dangerous time for a baby to be infected with toxo?
first trimester.
61
1st trimester
o Infection rates _____ but parasite damage is ______
3rd trimester
o Infection rates ______ but parasite damage is the ______
- lowest, greatest
| - highest, least
62
What are some consequences of congenital toxoplasmosis?
retardation, blindness, seizures, hearing loss, death
63
Babies born symptomatic (with toxo) have a classic triad of symptoms-
hydrocephaly, intracranial calcification of cysts, and chorioretinitis
64
Babies born with asymptomatic toxo may have problems later such as
seizures, retardation, visual problems
65
This kind of toxoplasmosis occurs when someone is infected as an immunocompetent indiv., but then became immunocompromised
recrudescent toxoplasmosis
66
chorioretinitis-
ocular toxoplasmosis
67
Dx of toxoplasmos. (4 methods)
serology (Ab detection), PCR, detection of fetal IgM, detection of fetal IgG
68
2 serological tests for toxoplas.
IgG and IgM
69
Toxo serological test
IgM (+) and IgG (-)
IgM (+) and IgG (+)
IgM (-) and IgG (+)
- suspect toxo infection, retest in weeks. If IgG (+) then you have acute toxo. Otherwise it is a false positive
- you are infected but the window is 18 months because thats how long it takes IgM titer to diminish
- We have no idea when you got infected, BUT you will be infected for life
70
PCR to detect toxoplasma in ________
body fluids (CSF/ocular/ amniotic)
71
What fetal Ig definitely means toxo infection?
| What fetal Ig could possibly be toxo infection?
- IgM
| - IgG, either the fetus or mother is infected
72
Fetal toxo Rx.
Spiraycin (DOC) given to mom and crosses placenta
73
Immunocompromised toxo Rx.
Pyramethamine-sulfadiazine (Daraprim)
74
Pyramethamine-sulfadiazine facts:
folic acid antagonist. Do not give to give to pregnant mom or youll be getting some spina bifida
75
If infant is infected (post birth) then give them:
pyramethamine-sulfadiazine AND folic acid to prevent folic acid deficiency
76
To prevent congenital toxoplasmosis, it is important to :
cook all meat, wash raw food, wear gloves when gardening, preggos cant clean litter box and should wash hands after petting a cat. Clean the litter box every day and keep cat indoors and wear gloves when gardening
77
Which two plasmodium have Schuffner's dots?
vivax and ovale
78
Which species will cause recrudescing malaria for decades?
P. malariae
79
Recrudescing/Relapsing malaria, which one involves the liver?
relapsing
80
how many deaths per year are attributed to malaria?
2.7 million
81
What rare ways can malaria transmission occur?
blood transfusion (not that rare in regions where blood isnt screened for malaria), dirty syringes, neonate infected during delivery, and transplacentally (super rare)
82
How many sporozoites are produces per oocyst in malaria?
1,000-2,000
83
```
# of plasmod. merozoites per sporozoite:
falciparum
vivax
malariae
ovale
```
40k
10k
2k
15k
84
Malaria of Plasmodium spp.
oP. falciparum—“_______” [the big killer]
oP. vivax—“_______”
oP. malariae—“_______”
oP. ovale—“______” [confined to W. Africa and W. Pacific]
- malignant tertian malaria
- benign tertian malaria
- quartan malaria
- mild tertian malaria
85
Paroxysm-
- A sudden onset of recurrent signs or symptoms of a disease
| - The periodic spasms of fever and chills (rigor = hot phase/cold phase) in malaria
86
Malaria Rigor- hot and cold stage, describe them
cold stage= paroxysm chills with high fever and shivering (RBCs are rupturing)
hot stage= sense of being very hot with severe headache, dizziness, nausea, etc. followed by profuse sweating (fever has subsided!!)
87
Classic Clinical Signs of the Malaria’s: (9)
o Cyclic high fever (104-106 degrees F)
o Chills
o Headache
o Myalgia (ache all over—flu like)
o Malaise and lethargy
o Anemia (low oxygen levels → low ATP/energy)
• Intravascular hemolysis of RBC’s by parasite → increased loss
• Bone marrow suppression → decrease in RBC replacement
o Enlarged liver and enlarged spleen
o Nausea, vomiting, diarrhea (seen in small children)
o Jaundice
88
2 major factors in the Pathogenesis of the disease called malaria
RBC destruction and the resultant non-specific host inflammatory response
89
Pregnant woman is ___x more likely to die than a normal woman
400
90
Why is falciparum so pathogenic?
-40,000 merozoites per sporozoite
•Infects any and all RBC’s (all ages)
•Greatest parasitemia levels
•Greatest destruction of RBC’s of all the malarias
oHemolysis of both infected and uninfected RBC’s**** important to know
oGreatest anemia
91
___% RBC’s infected w/ falciparum → grave and likely fatal
25
92
deep vascular schizogony-
falciparum does this. only young trophs found in peripheral blood. they sequester in capillary beds of major organs
93
How does falciparum stick to deep vascular capillaries?
It induces a protein "knob" on the RBC membrane that helps them attach
94
Why does falciparum sequester in deep vascular?
-Prevents premature destruction of infected RBC’s by the spleen
95
If you find falciparum late trophs and meronts in peripheral blood, what does this mean?
that person is dying
96
what would a falciparum infected persons liver look like?
it would be black from all the hemozoin
97
falciparum gametocytes appear ____DPI and are viable for ____ days
10
| 4
98
Why does falciparum suppress RBC production as well?
it sucks the iron out of you via hemozoin pigment. WBC production decreases as well
99
In falciparum infections, why are non infected cells destroyed as well?
host inflammatory response
100
```
Cerebral malaria:
major cause of death
sudden onset
Rx. ASAP
always fatal if no Rx
Signs of cerebral malaria:
```
```
•Unconscious with no response to pain (unrousable)
•Hyperthermia (up to 108 degrees)
•Hyperparasitemia
oPeripheral parasitemia—very high
•Convulsions (seizures)
```
101
cerebral malaria is fatal in ______ if untreated, and ____ % die if treated
- 24-72 hours
| - 39
102
cerebral malaria coma pathogenesis: two hypotheses
• Mechanical → _________
• Biochemical → _______
- hypoxia develops
- nitric oxide effect (TNF-alpha induces endothelial cells to release Nitric oxide → crosses BBB (NO has anesthetic properties))
103
**Note falciparum does not only display sequestration, but can also cause:
healthy RBCs to stick to them (‘cyto-adherance’)
104
Results of massive hemolysis of RBCs
-Sever anemia and leucocytopenia (Very low RBC and WNC numbers)
• Caused by combo of hemolysis (RBC) and bone marrow suppression (both RBC and WBCC)
105
Hemoglobinurea
Hemoglobin in urine (this Hb didn’t even get a chance to be broken down into bilirubin)
-happens in falciparum
106
Jaundice-
| can happen from severe infection with:
Liver can’t handle overload of Hb breakdown products (bilirubin). Such an excess of bilirubin that liver can’t metabolize all of it and excess (insoluble, unconjugated) bilirubin deposited in tissue. Causes yellowing of tissues (seen in sclera of eyes and skin)
-falciparum
107
Kidney- Filters _____ substances. CANNOT filter______ substances
•Many valuable substances reabsorbed in proximal tubules
- soluble
| - insoluble or particulate
108
Hemoglobinurea aka "_____"
Black-water fever
109
Hematuria-
| can occur in severe ____ infection
Intact RBC’s in urine
o Only from bleeding lesion in urinary tract
-falciparum
110
Is hemozoin found in urine?
no
111
What organs can falciparum fuck up to kill you?
brain, kidneys
112
severe falciparum kidney damage:
glomerular damage or tubular necrosis
113
Falciparum in Pregnant Women (4 special symptoms)
```
o Severe anemia
o Hypoglycemia
o Very high fevers
o Toxemia
-fetus often dies as well
```
114
Why is a pregnant woman so much more susceptible to falciparum death?
her immune system is dampened to prevent rejection of the "foreign" fetus, so falciparum gets a better jump on her
115
Why does the fetus die from mother malaria infection?
o Anoxia- From mom’s sever anemia (Lack of oxygen for fetus)
o Hyperthermia- From mom’s high fever (Makes uterus like oven/Temp of fetus climbs also)
o If fetus survives—often ‘poor doer’- (Low birth weight/Often succumbs to other childhood illnesses)
116
Plasmodium vivax
Distribution:
Niche:
- Temperate and tropical zones (NOT common in S. Africa)
| - All stages in peripheral blood
117
Plasmodium vivax
•Infects only:
Multiple infections of a RBC?
- reticulocytes (<2% of circulating RBC’s)
| - No multiple infections of one RBC
118
Plasmodium vivax
| Relapsing malaria will reappear how long after initial infection?
5-8 years
119
Plasmodium vivax
NOTE vivax and malariae have much ____ breaks in fever than falciparum
Gametocytes seen within ______ PI
- longer
| - 24 hours
120
Plasmodium malariae
Infects only ____ RBC’s
Duration of infection?
- older
| - considered infected for life
121
Plasmodium malariae
| Trophozoite Morphology:
“band”-shaped trophozoite across RBC
122
Innate Resistance to Malaria:
1. _________ recessive individuals are immune to vivax because organism needs a dominant receptor in order to be able to attach
2. Heterozygote advantage
3. ______ deficient individuals. This enzyme keeps hemoglobin in reduced state in order for RBC’s to carry more oxygen
4. ?
- Duffy Blood Groups
- Sickle cell trait (heterozygote advantage)
- G6PDH
- Beta thalassemia
123
G6PDH confers some resistance to malaria for who? because?
women, because it is an x-linked trait. So, affected males are screwed either way
124
Why does CMI not fight malaria?
RBC's do not have MHC proteins
125
Premunition-
-Situation where low level of parasitemia blocks new infection
126
-With malaria, it is possible to have premunition for ________
decades
127
If you have premonition and then you become completely cured, what is the result?
-Complete (sterile) cure → susceptible again!
128
Malaria Dx. (4 methods):
Microscopy, ELISA, IFA, PCR
129
What is the Dx of choice for malaria?
microscopy of stained peripheral blood smears
130
ELISA for malaria detects:
-Ag of parasite
131
ELISA has 2 types for malaria:
Optimal and Para Site
132
ELISA optimal
It measures:
It is only useful if:
Will detect which ones?
- parasite isoenzymes
- infection is active
- vivax or falciparum. You can thus differentiate between them
133
ELISA Para Site
| -only detects:
P. falciparum
134
Malaria Dx. IFA works by:
| but she considers it a pain in the ass
Ab detection in patient serum (specific schizonts)
135
Malaria Rx.: name all 7 drugs
Quinine, Chloroquine, Mefloquine, Atovaquone, Proguanil, Primaquine, Artemisinins
136
```
Malaria Rx. Quinine
Reserved for:
Kills:
does not kill:
Side effects include:
```
- severe cases and/ or resistant malarial species
- merozoites, schizonts
- hypnozoites, gametocytes
- tinnitus, hearing loss/increased RBC hemolysis/Increased insulin output by pancreas → hypoglycemic shock/Fetotoxic (causes abortions)/Cardiotoxicity—can cause serious cardiac arrhythmias
137
Quinine is the DOC for:
cerebral malaria, severe P. falciparum infection
| --Rapidly absorbed and distributed in body
138
Malaria Rx. Chloroquine
Static or cidal?
what is it?
What is resistant to it?
- cidal
- Synthetic quinine related drug but without its side effects
- P. falciparum- worldwide
139
Malaria Rx.
| Which two drugs are used in tandem?
Atovaquone + Proguanil. • These two are used for prophylasis and Rx
140
Malaria Rx. Primaquine
Kills:
Does not kill:
- Hypnozoites (so vivax and ovale)
| - RBC stages
141
Malaria Rx.
oAntibiotics in combo with quinine in chloroquine-resistant falciparum cases:
Why does this work?
- Clindamycin, Doxacycline, even tetracycline
| - Small circular DNA of apicoplast is similar to bacterial DNA, so antibiotics will work
142
Malaria Rx. Artemisinins
derived from:
Ex. of investigative new drug:
When is this drug administered?
-plants
-Artesunate
•If cerebral malaria and cannot take (quinine/ quinidine)
143
Until malaria spec. is identified, assume it is:
falciparum
144
If you think it is malaria Rx immediately with one of following:
If severe:
If not falciparum, can use:
•Atovaquone-proguanil or Mefloquine
- Quinine in combo with antibiotic
- chloroquin
145
malaria~____ cases reported each year-USA
o Travel history
o Emigration
-1500
146
```
CDC travel recommendations (malaria):
1.
2.
3.
4.
```
1. Prophylaxis (Don’t skip doses!)- Before, during and after trip
2. Sleep under netting
3. Wear Clothing that covers
4. Repellant: DEET
147
Malaria Prevention in Endemic regions
1.
2.
3.
- _________ is one of the most malaria-infested cities in the world
1. Vector Reduction
2. Minimize contact with mosquitos
3. Chemotherapy- Easier said than done
- Apac, Uganda
148
```
Vaccine Research
Clinical trials on:
Vaccine:
Reports indicate about __% effective
Effects last about _____
Helps decrease________
```
- young children in 7 countries in Africa
- subunit of circumsporozoite protein
- 66
- 18 mo.
- morbidity (sickness) and mortality (sickness → death)
149
```
Vector of:
B. bigemina:
B microti:
B. duncani:
B. divergens:
B. canis:
```
- Boophilus annulatis
- Ixodes scapularis (deer tick)
- unknown
- Ixodes ricinus (Europe)
- Rhipicephalus sanguineous and Dermacentor variabilis
150
Babesia sporozoites undergo ______ not _______
binary fission, not multiple fission
151
Babesia gametes are called:
[“ray bodies”]
152
(Babesia) Humans are “dead-end hosts”; only mode of transmission is:
blood transfusions
153
Babesia tick species as vector: will determine_______
mammalian host
154
```
Ticks
-Each egg produced by female will be:
-Fall into three categories according to number of hosts
1 Host ticks-
2 Host ticks-
3 Host ticks (Ixodes scapularis)-
```
- infected with Babesia spp.
- Entire LC on 1 host (transovarial transmission)
- Larva and nymph on 1st host, adult on 2nd host
- Each stage on a different host (larva, nymph, adult)
155
Ticks get on a host by:
climbing on top of vegetation (i.e. blade of grass) and crawling onto a host that walks near them
156
Babesiosis in man (B. microti)
called “______”
Clinical presentation if immunocompetent:
Population at risk:
• Can be life threatening with hemolytic crisis and severe anemia
- Nantucket fever
- headache, fever, malaise (~2 wks and flu-like)- Mild and self-limiting in immunocompetent individuals
- Immunocompromised, Splenectomized
157
why are splenectomized individuals at risk for babesiosis
spleen’s non-immune role in defense is to detect all abnormal RBCs filtering through sinuses in the organ
158
Which tick can give you a double whammy bite and why?
Deer tick (Ixodes scapularis) because can also carry: Lyme disease (Borrelia burgdorferi)
159
__________ is like a slightly more severe form of microti
| In immunocompromised individuals, __% mortality in microti and __% mortality in duncani
Babesia ducani.
5%
11%
160
________ is like microti, but extremely severe
__% fatality
Can even kill ______
- Babesia divergans
- 42
- immunocompetent
161
Babesia bigemina (cattle, possibly humans)
Led to first realization that:
symptoms:
-arthropods, insects, arachnids can transmit diseases!!!
-Anemia, Hemoglobinuria (due to intravascular hemolysis → release of hemoglobin → overwhelming enzymes that metabolize it → hemoglobin in urine), with high mortality rates in adults
-
162
```
Babesia canis
Clinical syndrome: wide range:
Cerebral babesiosis →
There is evidence that it can also spread by:
Rx:
```
- Sub-clinical to hemolytic crisis
- fatal
- bite (infected dog has oral lesions and bites uninfected dog.
- none, dog's fucked
163
Babesia infection
Dx:
Rx:
- organisms in smears
| - Clindamycin + quinine (DOC); also Azithromycin and atovaquone
164
Babesia Rx.
Divergens may require:
Canis:
- complete blood transfusion
| - no Cure! Dog infected for life
165
2 groups of helminthes:
platyhelminthes and nematodes
166
2 groups of platyhelminthes:
trematodes and cestodes
167
Platyhelminthes
Acoelomic-
Ttissue called _______ fills the body spaces
- No body cavity
| - parenchyma
168
Platyhelminthes
Have what body systems:
Dont have what body systems:
Digestive system ends in:
- Nervous, muscular, excretory systems
- circulatory, respiratory, or skeletal system
- blind sac
169
Digenetic Trematodes = “____”
flukes
170
Trematode eggs will be killed by:
freezing and drying
171
Snail is infected by trematode by 2 ways:
* “chemical homing device”—snail mucous trail attracts
| * Alternate mode: un-hatched egg must be eaten by snail
172
Trematode sporocyst is called a "______"
| It can produce ____ or _____
germinal sac
| -more sporocysts or redia
173
Redia
________ digestive system that contains __________
Feed on:
Produce ______ or ______-
- Rudimentary
- Mouth, pharynx, short gut
- host tissues, sporocysts other redia
- more redia or cercaria
174
Does cercaria have digetive system?
yes
175
Cercaria
| Have ________ at anterior to escape from snail host AND gain entry to next host
-penetration glands
176
Sexual reproduction for trematodes can come in what forms:
self-fertilization, cross-fertilization, and normal separate sexes
177
Schistosomiasis
No. __ on WHO list of major diseases to be eradicated
Distribution:
- ___ million affected each year; ___ million at risk
Mostly in _____
Estimated ______ deaths per year
- 2
- Africa, Asia, South America, and Caribbean
- 250
- 850
- Africa
- 200,000-400,000
178
```
Schistosoma haematobium
Dist:
Host Niche:
Reservoir:
Niche:
Egg:
IH:
```
- Africa and Middle East
- urinary bladder veins
- No animal reservoirs
- Urinary tract disease
- Ovoid with terminal spine
- Bulinus spp.
179
```
Schistosoma japonicum
Distribution:
Niche:
Reservoir:
Disease in:
Egg:
IH:
```
- Far East except Japan (eradicated in 1977)
- superior mesenteric veins of small intestine
- zoonotic (RH: cattle, water buffalo)
- Intestine and liver disease
- Round and rudimentary spine (may not be visible)
- Oncomelania spp.
180
```
Schistosoma mansoni
Distribution:
Niche:
Reservoir:
Disease in:
Egg:
IH:
```
- Africa, Middle East, and New World (Caribbean and S. America)
- inferior mesenteric veins of large intestine
- No animal RH’s
- Intestine and liver disease
- Ovoid with lateral spine
- Biomphalaria spp.
181
Schistosomes (literally means ‘______’)
split body
182
Schistosomes are _______ (male and female have different body shape)
Female resides in male's ___________
- dimorphic
| - gynecophoral canal
183
Schistosome life cycle excludes what stages?
redia and metacercaria
184
```
Schistosome cercaria
Attracted to:
Release:
Point of entry:
sheds what outside:
sheds what inside host:
```
- skin secretions
- signal to others
- hair follicle
- tail
- outer coat
185
Why does Schisto. cercaria shed coat?
This organism has gone from a hypotonic, freshwater environment to an isotonic environment. It also needs to absorb nutrients through its tegument
186
Schistosomes
| cercaria called a _____ upon host entry
schistosomule "little schistosome"
187
first stop for a schistosome in DH
liver (for a month)
188
Schistosome camouflages itself in two major ways:
1.
2.
1. Coats its outer surface with host plasma proteins
2. Produces a surface molecule on their outer membranes that mimics part of the host MHC I molecule
o Parasite DOES NOT pull the MHC I molecules off a nucleated cell (these proteins are integral proteins that do not shed!)
189
Egg travel plan
S. mansoni and S. japonicum:
S. haematobium:
- Blood vessel (three layers) → intestine wall → feces
| - Blood vessel → bladder wall → urine
190
Egg SEA stimulates:
* Stimulate granuloma formation (macs, eos, lymphocytes) around eggs
* Stimulate production of TNF-alpha by macs
191
Schisto. Eggs that don't make their destination are either _____ or _____
* Trapped in gut or bladder wall
| * OR are swept away in circulation
192
Schistosomiasis—the disease—3 phases:
Migratory, acute, chronic
193
Migratory Schistosomiasis
-Repeated infections →
When in lungs and heavy infection, symptoms could be:
- transient cercarial dermatitis at penetration site
| - Possible cough and low fever
194
Acute schistosomiasis
aka:
only occurs if heavy infection
“______” clinical signs occur with onset of egg production
- katayama fever
| - Flu-like
195
Katayama fever
Eggs in feces?
Results from:
Increase in TNF-alpha by macrophages, causes 2 things:
- may not be there yet
- inflammatory and immune response to SEAs
- Helps increase inflammation AND ‘Vitamin’ for parasite—enhances egg production
196
How many eggs can japonicum make per day?
3,000
197
Why does haematobium not cause katayama fever?
only produces 30 eggs per day
198
Chronic schistosomiasis requires:
-Repeated exposure to heavy infections (takes years)
199
S. mansoni and S. japonicum chronic infection
Intestinal and liver problems
chronic diarrhea, may contain? May result in?
-blood from ulcerating granulomas. anemia and iron deficiency
200
S. mansoni and japonicum chronic infection can cause gut wall fibrosis, leading to:
erosions--> ulcers, fibrosis around tissue masses aka pseudotubercules
201
Schistosome eggs within granulomas are still viable, meaning they still:
produce SEA
202
Schistosome J and M Chronic infections: may have few to no eggs in feces because:
(difficult for eggs to pass through now!)
203
gut wall fibrosis can lead to ______ extending into gut lumen and obstructing it
polyps
204
fibrosis of liver veins is called:
periportal or pipestem fibrosis
205
S. japonic. and mansoni chronic liver problems
______ of small veins causes blood flow resistance
Portal hypertension- slowed blood flow to liver, shunts it to _______ where the same situation will occur
-occlusion
-spleen
-
206
Enlarged ________ will occur from chronic J and M schisto.
liver and spleen
207
Children with chronic schist are stunted ______ and ______
physically and mentally
208
in very severe chronic schistosomiasis, liver and spleen enlargement are progressed to:
end result is chronic passive congestion of liver
hepatosplenomegaly
209
(fluid accumulation in abdominal cavity)-
Ascites
210
DO NOT SAY THAT THE EGGS BLOCK THE _____________; IT’S THE SMALL VEINS IN THE LIVER
HEPATIC PORTAL VEIN
211
do you remove ascitic fluid from a patient? why or why not?
no, the body will try to compensate for the treatment by bringing fluid from other parts of the body to the infected site
212
Severe liver congestion will allow schistosome eggs to bypass it and get to:
this leads to:
- lungs
| - Loss of functioning lung tissue, Pulmonary hypertension, Heart failure can result!
213
will haematobium cause granulomas in the bladder?
no, just fibrosis and calcification
214
S. haematobium can lead to _________ OF THE BLADDER. derived from ______ formation
squamous cell carcinoma
| polyp
215
Hematuria-
blood in urine
216
S. haematobium
| It is very rare, but possible for eggs to show up in:
fecal smear (migrate from bladder wall through rectal wall
217
If S. haema. damages bladder enough, urine flow will be obstructed, causing:
obstructive nephropathy (damages ureters then kidney
218
Obstructive nephropathy will cause _______ in kidneys
pressure necrosis (urine cysts)
219
_______ deaths per year from renal failure due to S. haema.
150,000
220
3 diagnostic methods for schistosomes
finding eggs, observe buildup of chronic fibrous tissue, ELISA
221
If there is a buildup of chronic fibrous tissue in gut and bladder, doctor may perform:
* Rectal biopsy to find trapped eggs
| * Bladder biopsy to find trapped eggs
222
ELISA for schistosomes detects:
Host Ab
223
Requirements for schistosomiasis:
Fecal/urine contamination, snail vector present
224
Schistosome risk factors:
* Traditions and customs
* Human wastes for fertilizer
* Streams as human waste disposal sites
* Wading, bathing, playing in contaminated water
225
Schistosome Rx:
Praziquantel (DOC)
226
```
Praziquantel
Efficacious:
Ease of Rx (oral)
No significant side effects
Low cost! (30 cents per person)
MOA (mechanism of action):
```
- (1 does kills all adults)
| - dual effect= Disrupts parasites tegument—“unmasks worm” and Disrupts flow of Ca++ in nervous system of worm killing it
227
Immunity to schistosomes
“_______”- A type of protective immunity but takes years to develop
Immunity has no effect on _____, it is directed at:
Removal of adults (Sterile cure) BUT:
- Concomitant
- No effect on adults (immune response not directed against adults). Stops cercaria → prevents new infections and buildup of worm burden
- susceptible to re-infection
228
Prevention/ Control
Vector control—
Biological control =
Re-engineering of water resource development projects
- difficult and not eco-friendly-Molluscicides are nasty
| - add predator snails that will eat snail vectors
229
Cercarial Dermatitis aka
| leads to a _______ rash, which is very itchy and lasts a few months
- “Swimmers itch” “Swamp itch” “Nutria itch”
| - maculopapular
