niti
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Topics: 36
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Trichuris Trichiura:
1. Infective Stage: Egg.
2. Route of Infection: Oral.
3. Vector: None.
4. Intermediate Host: None
5. Reservoir Host: None
6. Pathophysiological basis of disease: Direct damage to colonic tissues.
7. Major pathological consequence: Diarrhea, prolapsed rectum.
8. Diagnostic Stage: Egg
9. Method of Diagnosis: Stool examination.
Ascaris Lumbricoides:
1. Infective Stage: Egg
2. Route of Infection: Oral
3. Vector: None
4. Intermdiate Host: None
5. Reservoir Host: None
6. Pathophysiological Basis of Disease:
Transitory pneumonia due to migrating 3rd stage larvae. Trauma due to
migration of adult worms, secondary septicemia.
7. Major Pathological consequence:
Adult worm migrate to aberrant sites in body (eg. Pancreas, liver, peritoneal
cavity). Intestinal blockage by worm bolus in heavy infections.)
8. Diagnostic Stage: Egg
9. Method of Diagnsis: Stool examination
Strongyloides Stercoralis
1. Infective Stage: Third stage (filariform) larva in soil.
2. Route of Infection: Direct penetration of skin by larva; rarely the oral route. Autoinfection in immunosuppressed patients.
3. Vector: None
4. Intermediate Host: None
5. Reservoir Host: Dog, monkey.
6. Pathophysiological Basis of Disease:
The adults and larvae erode the villus tissue; bacteria are introduced into the tissues by the migrating larvae.
7. Major Pathological consequence:
Acute diarrhea in non-immunosuppressed patients; bacteremia often leading to death in immunosuppressed patients.
8. Diagnosis Stage: Second (rhabditiform) or third stage larva.
9. Method of Diagnosis: Stool examination, duodenal aspirate or “string” test.
Schistosoma Mansoni
1. Infective Stage: Cercaria
2. Route of Infection: Direct penetration of unbroken skin.
3. Vector: None
4. Intermediate Host: Aquatic fresh water snails.
5. Reservoir Host: None
6. Pathophysiological Basis of Disease:
Eggs block the pre-sinusoidal capillaries in liver, blockage of lung capillaries.
7. Major Pathological consequence:
Portal Hypertension, cor pulmonale, esophageal varices, hypersplenism.
8. Diagnostic Stage: Egg
9. Method of Diagnosis: Stool examination or “rectal snip”
Schistosoma Haematobium:
1. Infective Stage: Cercaria
2. Route of Infection: Direct penetration of unbroken skin
3. Vector: None
4. Intermediate Host: Aquatic fresh water snails
5. Reservoir Host: Primates
6. Pathophysiological basis of disease:
Eggs block pre-sinusoidal capillaries of liver, block capillaries of lungs. Eggs in bladder may induce squamous cell epithelioma.
7. Major Pathological Consequence:
Portal hypertension, esophageal varices, cor pulmonale, bladder ca, calcification of bladder with attendant damage to kidneys.
8. Diagnositic Stage: Egg
9. Method of Diagnosis: Microscopical examination of urine.
Schistosoma Japonicum:
1. Infective Stage: Cercaria
2. Route of Infection: Direct penetration of unbroken skin
3. Vector: None
4. Intermediate Host: Aquatic fresh water snails
5. Reservoir Host: Dog, monkey, pig, cattle
6. Pathophysiological basis of disease:
Eggs block the pre-sinusoidal capillaries in liver, capillaries in lungs; rarely capillaries of CNS.
7. Major Pathological consequence:
Portal hypertension, esophageal varices, cor pulmonale, hypersplenism.
8. Diagnostic Stage: Egg.
9. Method of Diagnosis: Stool Examination.
Taenia Saginata:
1. Infective Stage: Cysticercus in tissue of intermediate host.
2. Route of Infection: Oral
3. Vector: None.
4. Intermediate Host: Cattle.
5. Reservoir Host: None
6. Pathophysiological Basis of Disease: None
7. Major Pathological consequence: None
8. Diagnostic Stage: Gravid proglottid – 12 or more branches to the central uterus. Egg identifies Taenia spp. only.
9. Method of diagnosis: Inject gravid proglottid with India ink, count branches of uterus. Clear sticky tape test for egg. Eggs rarely found on stool exam.
Taenia Solium:
1. Infective Stage: Cysticerus in tissue of intermediate hosts.
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: Pig
5. Reservoir Host: None
6. Pathophysiological Basis of disease: None
7. Major Pathological consequence: None
8. Diagnostic Stage: Gravid proglottid – 10 or fewer lateral branches to central uterus. Egg identifies
Taenia spp. only
9. Method of diagnosis: Inject gravid proglottid with India ink, count lateral branches to uterus. Clear
sticky tape test for eggs. Eggs rarely found on stool exam.
Cyticerosis due to larval infection with Taenia Solium:
1. Infective stage: Egg
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: Pig and human
5. Reservoir Host: None
6. Pathophysiological Basis of disease:
The hexacanth larva migrates to various areas of the body and encysts, forming a small space-occupying lesion.
7. Major Pathological consequence:
Neurological disturbances related to the space-occupying lesions.
8. Diagnostic Stage: Cysticercus in tissue.
9. Method of diagnosis: Direct – Biopsy
Indirect – Serology (Immunoelectrophoresis) look for “arc 5”
Hydatid disease due to larval infection with Echinococcus Granulosus
1. Infective Stage: Egg
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: Herbivores (eg. Sheep, reindeer) and humans
5. Reservoir Host: None
6. Pathophysiological basis of disease:
The hexacanth larvae migrate to various areas of the body and develop into large, space-occupying lesions referred to as hydatid cysts.
7. Major Pathological consequence:
Obstruction or replacement of tissue by the hydatid cyst. Anaphylaxis due to rupturing of cyst.
8. Diagnostic Stage: Protoscolices or hooklets (“hydatid sand”)
9. Method of diagnosis: Direct – biopsy (contra-indicated)
Indirect – Serology (immunoelectrophoresis), look for “arc 5”
Diphyllobothrium Latum
1. Infective Stage: Plerocerus in raw or unercooked muscle of intermediate host.
2. Route of Infection: Oral
3. Vector: None
4. Intermediate host: Copepods (first intermediate host), fresh water fish (2nd intermediate host).
5. Reservoir Host: Bear, dog
6. Pathophysiological Basis of Disease:
Adult worms accumulate vitamin B12.
7. Major Pathological Consequence: Megalobastic anemia
8. Diagnostic Stage: Egg
9. Method of Dx: Stool Exam
Plasmodium Vivax, Ovale, and Malariae
1. Infective Stage: Sporozoite
2. Route of Infection: Skin – via bite of a mosquito, which introduces sporozoites. Blood transfusions and congenital (rare).
3. Vector: Female anopheline mosquito
4. Intermediate Host: Man
5. Reservoir Host: None
6. Patholophysiological basis of disease:
Direct and indirect destruction of RBC’s by parasites.
7. Major Pathological consequence:
Fever and chills, anemia, splenomegaly.
8. Diagnostic Stage: Asexual and sexual stages of parasites in RBC’s.
9. Methods of Dx: Direct – thin and thick blood films stained with Giemsa.
Indirect – serology (IFA test).
Plasmodium Faciparum:
1. Infective Stage: Sporozoite.
2. Route of Infection: Skin – via mosquito bite, which introduces sporozoites – also via blood transfusion and congenital (rare).
3. Vector: Female anopheline mosquito
4. Intermediate Host: Man
5. Reservoir Host: None
6. Pathological basis of disease:
Destruction of RBCs by parasites. Anoxia caused by blocked capillaries in brain.
7. Major Pathological consequence:
Fever and chills, anemia, splenomegaly, coma, and death
8. Diagnostic Stage: Asexual and sexual stages of parasites in RBCs.
9. Method of Dx: Direct – thin and thick blood films stained with Giemsa.
Indirect – serology (IFA)
Toxoplasma Gondii
1. Infective Stage: Pseudocysts in infected meat, oocysts in cat feces.
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: Man, other mammals, avians (felines considered definitive host).
5. Reservoir host: Virtually all warm-blooded animals.
6. Pathophysiological basis of disease:
Invades virtually all cell types in body. Severity of disease depends upon immunological competence of host.
7. Major pathological consequence:
Acquired – (resembles mononucleosis) – lymphatic involvement.
Congenital – chorioretinitis, hydrocephaly.
8. Diagnostic Stage: Demonstration of pseudocysts containing rophozoites in biopsied material.
9. Method of Dx: Direct – biopsy (rarely successful).
Indirect – serology (IFA- IgG, IFA-IgM, CF test)
Giardia Lamblia:
1. Infective Stage: Cyst
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: None
5. Reservoir Host: Beaver, dog
6. Pathophysiological basis of disease:
Trophozoites attach to intestinal mucosa and cause flattening of villi.
7. Major pathological consequence:
Malabsorption syndrome, crramping diarrhea, wt loss.
8. Dx Stage: Cysts and trophozoites
9. Method of Dx: Stool exam, duodenal aspirate, “string” test
Entamoeda Histolytica:
1. Infective Stage: Cyst
2. Route of Infection: Oral
3. Vector: None
4. Intermediate Host: None
5. Reservoir Host: None
6. Pathophysiological basis of disease:
Lesions and ulcerations of intestinal mucosa; abscesses of liver and brain all due to secretion of cytotoxic and cytolytic enzymes by the trophozoite.
7. Major pathological consequence:
Diarrhea, dysentery, space-occupying lesion, occasionally death.
8. Diagnostic stage: Cyst and trophozoite
9. Method of diagnosis: Direct – stool exam.
Indirect – serology (IHA, CF, etc.)
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| Haisook
Forum Junior
Topics: 12
Posts: 70
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Is this enough as regards to Parasitology?
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| bactitech
Forum Elite
Topics: 25
Posts: 486
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Do you know what these look like? I'm a medical technologist who performs O&P examinations so I have to know what these look like, but I'm not sure that physicians do.
We have to know sizes, as many parasites, especially the Entamoeba, are differentiated by size and number of nuclei. For example, Entamoeba coli is a bit larger than E. histolytica, and can have more than 4 nuclei in the cyst stage. However, if you only see cysts that have four nuclei, you need to know other methods of differentiation. I'm not sure if med students are required to know this sort of stuff.
I DO think you need to know that Giardia lamblia is the most common parasite found in the US. I am located in the north central midwest and we hardly ever find any other parasites unless the patient has travelled out of the country.
If you are a physician, and confront a patient with longstanding diarrhea, you MUST take a travel history. I was told at a workshop long ago that any patient with diarrhea of more than one month's duration needs to be checked for parasites.
That being said, I see patients whose stools show up on our inoculation bench with every stool test known to man ordered on it. It's especially hilarious to the techs when diarrhea is the diagnosis and we receive rock hard pellets, or perfectly formed stools. Who is kidding who here?
Taking a good thorough travel history AND communicating anything unusual to the microbiology laboratory via the test requisition will ALWAYS stand you in good stead with the techs who perform your patients' testing. Certain parasites are geographical and it helps us immensely to know what's up with the patient. If you call us on the phone to tell us that's even better! 
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| Haisook
Forum Junior
Topics: 12
Posts: 70
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Well bactitech.. thanks for your reply but,
I originally meant if the stuff mentioned above is enough for the USMLE step 1 exam,, you've gone a little divergent, at least for me.
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| mjl1717
Forum Hero
Topics: 955
Posts: 5,451
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Greetings Bachtitech, thank you for everything.!
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| bactitech
Forum Elite
Topics: 25
Posts: 486
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Please do realize, Haisook, that if you get parasitology questions on your examination, they won't be straightforward memorization stuff. When I took parasitology in college, I had a four question blue book final examination that took me three hours to write. Not being a physician, I have no clue as to how much you will need to know. I thought I did answer your inquiry when I asked if you knew what they looked like - your examination may require that you need to know the morphology and/or measurements.
Sorry if you misunderstood my motives. I do think it's important that you know where in the world these parasites exist. This will tie in to travel history. Then again, this may not happen in a Level 1 exam. Perhaps that's later on in your training.
I don't think you can ever have TOO much knowledge. I do know that you're inundated with stuff to learn, too. I used to work in a lab affiliated with a med school.
You're welcome mjl1717 
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| mjl1717
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Posts: 5,451
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Bactittech: 1)Your post was good 2)Haisooks post was originally in the wrong forum, the support forum,(that may be part of the problem) 3)As you say good history and especially travel hisory is important. 4)They could easily show a pic of a schistosome egg and have you name it by the angle of the spicule. Or any other parasite especially Plasmodia. 5)I agree you can never have too much knowledge.
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| bactitech
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That's what I was thinking. They could show you a pic of some fairly obscure parasite, and ask you an equally obscure question about it. We do parasitology unknowns twice a year. Our lead tech in this biyearly exercise worked exclusively doing O&P's at Cleveland Clinic for two years, so she's had LOTS of experience. However, she really has to think about some of the stuff that CAP (accrediting agency) sends sometimes.
The Entamoebas are particularly tricky. Make SURE you count nuclei in the cysts. Trophozoites are even harder to identify. Ent. coli gives a fairly benign prognosis; E. histolytica gives a much worse clinical picture. The sizes overlap also.
Good luck to you all.
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| Haisook
Forum Junior
Topics: 12
Posts: 70
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Well, bactitech..
I could conclude that you speak 'pure' parasitology. In the USMLE exam, we need to know the high yield parts, and the most important info. I appreciate the information you've supplied, but not all of it - I think - is needed by a USMLE-exam-taker.
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