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177 Cards in this Set
- Front
- Back
T/F: Most protozoa are benign
|
True. Most protozoa are neither pathogenic nor parasitic
|
|
T/F: Parasitic protozoa are intracellular.
|
False. Some parasitic protozoa are intracellular, and some multiply in extracellular fluids (eg, blood). In some species, certain stages are extracellular while others are intracellular.
|
|
How do protozoa differ from worms, pathogenically?
|
All protozoa that cause disease in humans must be capable of multiplying in humans (not true of worms)
Eosinophilia is not a usual sign of protozoal infection |
|
Metronidazole is useful against these types of parasitic infections
|
Infection by anaerobic protozoa
|
|
These three protozoa are anaerobes
|
Entamoeba histolytica, Giardia lamblia, Trichomonas vaginalis
|
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Cause of amebiasis
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Entamoeba histolytica
|
|
This parasite is an extracellular protozoan that grows anaerobically
|
Entamoeba histolytica
|
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The simple life cylce of this protozoa involves only humans
|
Entamoeba histolytica
|
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Transmission of Entamoeba histolytica
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Oral-fecal. Human ingests CYSTS (human fecal contamination)
|
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Life cycle of Entamoeba histolytica and Giardia
|
Ingestion of cyst --> cyst opens in intestine releasing parasites --> parasites multiply as trophozoite in large intestine and can then either invade colon wall and multiply or … --> trophozoite changes to cyst --> cysts are excreted in stool
|
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Surivival time of Entamoeba histolytica cysts
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Weeks
|
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Trophozoite
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General term for actively multiplying stage of parasitic protozoa
|
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Infective stage of Entamoeba histolytica
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Mature cyst
|
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Pathogenic stage of Entamoeba histolytica
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Trophozoites
|
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Diagnostic stage of Entamoeba histolytica
|
Cyst in stool, trophozoite in diarrhea
|
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Appearance of Entamoeba histolytica cyst
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4 nuclei and chromatoidal bodies which are linear structures
|
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Dystenteric stool vs diarrhea
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Dystenteric stool contains blood and mucus
|
|
This parasite is morphologically identical to E. histolytica but is nonpathogenic
|
Entamoeba dispar
|
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Ingested RBC's can be seen in these protozoa
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Entamoeba histolytica
|
|
Signs and symptoms of Entamoeba histolytica infection
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Dysentery (blood, mucous stools), invasion of colon mucosa, pain
|
|
Flask shaped ulcers are seen on colonoscopy in this infection
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Entamoeba histolytica
|
|
Common cause of death in E. histolytical infection
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Bowel perforation, liver abscess
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T/F: Most patients with amebic dysentery will have cysts or trophozoites in stool
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True.
|
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Amebic abscess
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Feature of E. histolytica infection. Most commonly in liver but can also appear in brain or lung. It is uniformly fatal in the brain
|
|
Hepatosplenomegaly can be impressive and hard to diagnose in the setting of infection by this parasite
|
Entamoeba histolytica
|
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T/F: The liver abscess seen in E. histolytica accompanies dysentery and excretion of cysts and trophozoites.
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False. Only 10% of liver abscess patients continue to excrete cysts or trophozoites, and only 50% have a hx of dysentery
|
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Diagnosis of amebic abscess
|
(1) serology (anti-parasite Ab)
(2) liver scan (3)trophozoites in aspirate |
|
This parasite has a substantial mortality rate associated with colonic perforation that, even following colectomy, can be fatal
|
Entamoeba histolytica
|
|
Cause of Amebic meningoencephalitis
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Naegleria (an emeba)
|
|
This disease is contracted by swimming in warm, shallow, stagnant water
|
Amebic meningoencephalitis (Naegleria)
|
|
These are three amebic presentations
|
Dysentery, abscess, meningoencephalitis
|
|
These ameba reach brain by a neural route via penetration of the cribiform plate
|
Naegleria
|
|
This disease is usually not diagnosed until autopsy because it is misdiagnosed as bacterial or viral disease
|
Amebic meningoencephalitis (Naegleria)
|
|
Two ways to disinfect water
|
Boil (best)
Halogen treatment |
|
T/F: Compared to water, carbonated water is generally safe
|
True.
|
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T/F: Carbonation disinfects water
|
False. It is useful because the companies that bottle carbonated beverages do not use contaminated water.
|
|
T/F: In the 3rd world, canned foods are generally safe
|
True.
|
|
These extracellular protozoa parasites are flagellated
|
Giardia lamblia, Trichomonas vaginalis
|
|
Diagnostic stage of Giardia
|
Trophozoites and cysts in feces
|
|
Infective stage of Giardia
|
Cyst
|
|
Transmission of Giardia
|
Oral-fecal. Human ingests CYSTS (human fecal contamination)
|
|
The cysts of this protozoa opens in the small intestine, releasing parasites that multiply as trophozoites in the duodenum and jejunum
|
Giardia lamblia
|
|
Trophozoites become encysted and excreted in feces when this happens
|
Dehydration of stool mass
|
|
Incubation period of Giardia
|
1-3 weeks
|
|
This protozoa produces diarrhea, foul smelling greasy stools, abd discomfort and nausea
|
Giardia
|
|
This protozoa can cause wt loss due to malabsorption
|
Giardia
|
|
Higher incidents of chronic infection with this protozoa is seen in patients with congenital defects in IgA
|
Giardia
|
|
This protozoa spreads from the GI tract
|
Entamoeba histolytica
|
|
What is the difference in pathogenesis between E. histolytica and Giardia
|
E. histolytica is invasive; Giardia is not
|
|
This protozoa has caused substantial epidemics from municipal water supplies in cities and towns worldwide
|
Giardia lamblia
|
|
T/F: Chlorination kills cysts of Giardia lamblia
|
False. Chlorination does not kill cysts
|
|
This is the best way to prevent Giardia epidemics
|
Filtration of water supply
|
|
Treatment of Giardia
|
Metronidazole
|
|
Beavers are a common cause of municipal water supply contamination with this parasite
|
Giardia lamblia
|
|
This protozoa has no cyst stage
|
Trichomonas vaginalis
|
|
Transmission of Trichomonas vaginalis
|
STD. Trophozoites in vagina or urethra/prostate transmitted by sexual contact or poor hygiene
|
|
The trophozoites of this species of protozoa are relatively hardy
|
Trichomonas vaginalis
|
|
Diagnostic stage of Trichomonas vaginalis
|
Trophozoites in vaginal and prostatic secretions and urine
|
|
Infective stage of Trichomonas vaginalis
|
Trophozoite
|
|
This protozoa has a posterior flagellum, and four anterior flagella
|
Trichomonas vaginalis
|
|
Most infected males are asymptomatic, whereas 10-20% of infected females will have symptoms
|
Trichomonas vaginalis
|
|
Signs and symptoms of Trichomonas vaginalis infection
|
Inflammation, burning, itching, purulent discharge in 10-20% of women. A few men might have nonspecific urethritis.
|
|
Treatment of Trichomonas vaginalis
|
Metronidazole (must include sexual partner)
|
|
Prevention of Trichomonas vaginalis
|
Mechanical barriers (condoms)
|
|
This protozoa is an obligate intracellular parasite
|
Toxoplasma gondii
|
|
T/F: Humans are the definitive host of Toxoplasma gondii
|
False. Humans are an accidental intermediate host.
|
|
Definitive host of Toxoplasma
|
Cat
|
|
Intermediate host of Toxoplasma
|
Mammals (eg, mice), birds
|
|
Cysts that contain dormant parasites of this protozoa are found in muscle and brain
|
Toxoplasma gondii
|
|
Infective stage of Toxoplasma
|
Fecal cysts from cat feces (and *only* cat feces; non-felines who ingest infectious cysts can develop tissue cysts but these are different than the fecal cysts excreted by infected cats)
|
|
Life cycle of Toxoplasma gondii
|
Cat consumes tissue cysts --> parasite grows intracellularly in intestinal mucosa to produce male and female gametes --> gametes fuse to form ZYGOTE --> zygote is excreted from feces as noninfectious fecal cyst --> fecal cyst becomes infectious at ambient temperature for 2 days
|
|
Transmission of Toxoplasma gondii
|
(1) eating undercooked or raw meat with tissue cysts (pork, beef,)
(2) ingestion of fecal cysts from feline contamination |
|
This protozoa causes an often asymptomatic acute infection, followed by chronic infection with cysts in muscle and brain
|
Toxoplasma gondii
|
|
Diagnostic stage of Toxoplasma gondii
|
No diagnostic stage. Dx is serological--look for rise in antibodies, anti-toxo IgM. In AIDS patients, diagnosis can be confirmed by therapeutic trial (pyrimethamine-sulfadiazine)
|
|
Serological tests of Toxomplasma
|
(1) Sabin-Feldman dye test: complement-mediated lysis of parasites in presence of anti-toxoplasma antibody
(2) ELISE or fluorescent antibody test (3) PCR for toxoplasma DNA |
|
Treatment of Toxoplasmosis
|
Pyrimethamine (blocks dihydrofolate reductase) plus sulfadiazine (blocks dihydrofolate synthesis) which act synergistically
|
|
T/F: Most protozoa are benign
|
True. Most protozoa are neither pathogenic nor parasitic
|
|
T/F: Parasitic protozoa are intracellular.
|
False. Some parasitic protozoa are intracellular, and some multiply in extracellular fluids (eg, blood). In some species, certain stages are extracellular while others are intracellular.
|
|
How do protozoa differ from worms, pathogenically?
|
All protozoa that cause disease in humans must be capable of multiplying in humans (not true of worms)
Eosinophilia is not a usual sign of protozoal infection |
|
Metronidazole is useful against these types of parasitic infections
|
Infection by anaerobic protozoa
|
|
These three protozoa are anaerobes
|
Entamoeba histolytica, Giardia lamblia, Trichomonas vaginalis
|
|
Cause of amebiasis
|
Entamoeba histolytica
|
|
This parasite is an extracellular protozoan that grows anaerobically
|
Entamoeba histolytica
|
|
The simple life cylce of this protozoa involves only humans
|
Entamoeba histolytica
|
|
Transmission of Entamoeba histolytica
|
Oral-fecal. Human ingests CYSTS (human fecal contamination)
|
|
Life cycle of Entamoeba histolytica and Giardia
|
Ingestion of cyst --> cyst opens in intestine releasing parasites --> parasites multiply as trophozoite in large intestine and can then either invade colon wall and multiply or … --> trophozoite changes to cyst --> cysts are excreted in stool
|
|
Surivival time of Entamoeba histolytica cysts
|
Weeks
|
|
Trophozoite
|
General term for actively multiplying stage of parasitic protozoa
|
|
Infective stage of Entamoeba histolytica
|
Mature cyst
|
|
Pathogenic stage of Entamoeba histolytica
|
Trophozoites
|
|
Diagnostic stage of Entamoeba histolytica
|
Cyst in stool, trophozoite in diarrhea
|
|
Appearance of Entamoeba histolytica cyst
|
4 nuclei and chromatoidal bodies which are linear structures
|
|
Dystenteric stool vs diarrhea
|
Dystenteric stool contains blood and mucus
|
|
This parasite is morphologically identical to E. histolytica but is nonpathogenic
|
Entamoeba dispar
|
|
Ingested RBC's can be seen in these protozoa
|
Entamoeba histolytica
|
|
Signs and symptoms of Entamoeba histolytica infection
|
Dysentery (blood, mucous stools), invasion of colon mucosa, pain
|
|
Flask shaped ulcers are seen on colonoscopy in this infection
|
Entamoeba histolytica
|
|
Common cause of death in E. histolytical infection
|
Bowel perforation, liver abscess
|
|
T/F: Most patients with amebic dysentery will have cysts or trophozoites in stool
|
True.
|
|
Amebic abscess
|
Feature of E. histolytica infection. Most commonly in liver but can also appear in brain or lung. It is uniformly fatal in the brain
|
|
Hepatosplenomegaly can be impressive and hard to diagnose in the setting of infection by this parasite
|
Entamoeba histolytica
|
|
T/F: The liver abscess seen in E. histolytica accompanies dysentery and excretion of cysts and trophozoites.
|
False. Only 10% of liver abscess patients continue to excrete cysts or trophozoites, and only 50% have a hx of dysentery
|
|
Diagnosis of amebic abscess
|
(1) serology (anti-parasite Ab)
(2) liver scan (3)trophozoites in aspirate |
|
This parasite has a substantial mortality rate associated with colonic perforation that, even following colectomy, can be fatal
|
Entamoeba histolytica
|
|
Cause of Amebic meningoencephalitis
|
Naegleria (an emeba)
|
|
This disease is contracted by swimming in warm, shallow, stagnant water
|
Amebic meningoencephalitis (Naegleria)
|
|
These are three amebic presentations
|
Dysentery, abscess, meningoencephalitis
|
|
These ameba reach brain by a neural route via penetration of the cribiform plate
|
Naegleria
|
|
This disease is usually not diagnosed until autopsy because it is misdiagnosed as bacterial or viral disease
|
Amebic meningoencephalitis (Naegleria)
|
|
Two ways to disinfect water
|
Boil (best)
Halogen treatment |
|
T/F: Compared to water, carbonated water is generally safe
|
True.
|
|
T/F: Carbonation disinfects water
|
False. It is useful because the companies that bottle carbonated beverages do not use contaminated water.
|
|
T/F: In the 3rd world, canned foods are generally safe
|
True.
|
|
These extracellular protozoa parasites are flagellated
|
Giardia lamblia, Trichomonas vaginalis
|
|
Diagnostic stage of Giardia
|
Trophozoites and cysts in feces
|
|
Infective stage of Giardia
|
Cyst
|
|
Transmission of Giardia
|
Oral-fecal. Human ingests CYSTS (human fecal contamination)
|
|
The cysts of this protozoa opens in the small intestine, releasing parasites that multiply as trophozoites in the duodenum and jejunum
|
Giardia lamblia
|
|
Trophozoites become encysted and excreted in feces when this happens
|
Dehydration of stool mass
|
|
Incubation period of Giardia
|
1-3 weeks
|
|
This protozoa produces diarrhea, foul smelling greasy stools, abd discomfort and nausea
|
Giardia
|
|
This protozoa can cause wt loss due to malabsorption
|
Giardia
|
|
Higher incidents of chronic infection with this protozoa is seen in patients with congenital defects in IgA
|
Giardia
|
|
This protozoa spreads from the GI tract
|
Entamoeba histolytica
|
|
What is the difference in pathogenesis between E. histolytica and Giardia
|
E. histolytica is invasive; Giardia is not
|
|
This protozoa has caused substantial epidemics from municipal water supplies in cities and towns worldwide
|
Giardia lamblia
|
|
T/F: Chlorination kills cysts of Giardia lamblia
|
False. Chlorination does not kill cysts
|
|
This is the best way to prevent Giardia epidemics
|
Filtration of water supply
|
|
Treatment of Giardia
|
Metronidazole
|
|
Beavers are a common cause of municipal water supply contamination with this parasite
|
Giardia lamblia
|
|
This protozoa has no cyst stage
|
Trichomonas vaginalis
|
|
Transmission of Trichomonas vaginalis
|
STD. Trophozoites in vagina or urethra/prostate transmitted by sexual contact or poor hygiene
|
|
The trophozoites of this species of protozoa are relatively hardy
|
Trichomonas vaginalis
|
|
Diagnostic stage of Trichomonas vaginalis
|
Trophozoites in vaginal and prostatic secretions and urine
|
|
Infective stage of Trichomonas vaginalis
|
Trophozoite
|
|
This protozoa has a posterior flagellum, and four anterior flagella
|
Trichomonas vaginalis
|
|
Most infected males are asymptomatic, whereas 10-20% of infected females will have symptoms
|
Trichomonas vaginalis
|
|
Signs and symptoms of Trichomonas vaginalis infection
|
Inflammation, burning, itching, purulent discharge in 10-20% of women. A few men might have nonspecific urethritis.
|
|
Treatment of Trichomonas vaginalis
|
Metronidazole (must include sexual partner)
|
|
Prevention of Trichomonas vaginalis
|
Mechanical barriers (condoms)
|
|
This protozoa is an obligate intracellular parasite
|
Toxoplasma gondii, "Spor" protozoa
|
|
T/F: Humans are the definitive host of Toxoplasma gondii
|
False. Humans are an accidental intermediate host.
|
|
Definitive host of Toxoplasma
|
Cat
|
|
Intermediate host of Toxoplasma
|
Mammals (eg, mice), birds
|
|
Cysts that contain dormant parasites of this protozoa are found in muscle and brain
|
Toxoplasma gondii
|
|
Infective stage of Toxoplasma
|
Fecal cysts from cat feces (and *only* cat feces; non-felines who ingest infectious cysts can develop tissue cysts but these are different than the fecal cysts excreted by infected cats)
|
|
Life cycle of Toxoplasma gondii
|
Cat consumes tissue cysts --> parasite grows intracellularly in intestinal mucosa to produce male and female gametes --> gametes fuse to form ZYGOTE --> zygote is excreted from feces as noninfectious fecal cyst --> fecal cyst becomes infectious at ambient temperature for 2 days
|
|
Transmission of Toxoplasma gondii
|
(1) eating undercooked or raw meat with tissue cysts (pork, beef,)
(2) ingestion of fecal cysts from feline contamination |
|
This protozoa causes an often asymptomatic acute infection, followed by chronic infection with cysts in muscle and brain
|
Toxoplasma gondii
|
|
Diagnostic stage of Toxoplasma gondii
|
No diagnostic stage. Dx is serological--look for rise in antibodies, anti-toxo IgM. In AIDS patients, diagnosis can be confirmed by therapeutic trial (pyrimethamine-sulfadiazine)
|
|
Serological tests of Toxomplasma
|
(1) Sabin-Feldman dye test: complement-mediated lysis of parasites in presence of anti-toxoplasma antibody
(2) ELISE or fluorescent antibody test (3) PCR for toxoplasma DNA |
|
Treatment of Toxoplasmosis
|
Pyrimethamine (blocks dihydrofolate reductase) plus sulfadiazine (blocks dihydrofolate synthesis) which act synergistically
|
|
One-eight of the US population is infected sometime in life with this protozoa
|
Toxoplasma gondii
|
|
Infections by this protozoa in immunocompetent people are asymptomatic, but result in encysted parasites.
|
Toxoplasma gondii
|
|
Signs and symptoms of Toxoplasma gondii infection
|
Only a few primary infections are sympomatic. Lymphadenitis, myalgia, headache, fatigue, fever; in more severe cases, encephalitis, myocarditis, hepatitis, pneumonia
|
|
Infection by this is seen in HIV infection with a CD4 count < 100
|
Toxoplasma gondii
|
|
Serologic diagnosis is not possible in this infection in this type of person
|
Toxoplasmosis in AIDS patients--since disease is almost due to reactivation rather than primary infection, so the patient will already be seropositie (unless they are late in their disease and immune system is shot, wherein they will be seronegative)
|
|
This protozoa causes transplacental infection in primary infection of the mother
|
Toxoplasma gondii. Improve outcome by giving chemotherapy during pregnancy.
|
|
Manifestations of congenital disease due to Toxoplasma
|
Microcephaly, hydrocephalus, mental retardation, blindness, recurrent chorioretinitis (visual defects)
|
|
Cats should be avoided in pregnancy for this reason
|
Toxoplasma gondii can infect transplacentally and cause congenital defects
|
|
These are the four "spor" intestinal parasites
|
Cryptosporidium, cyclospora, isospora, microsporidia
|
|
What do the four "spor" intestinal parasites have in common?
|
(1) obligate intracellular
(2) diarrhea (mild-to-moderate, self-limiting) (3) severe, protracted diarrhea in immunosuppressed (eg, AIDS) (4) fecal-oral transmission (5) diagnostic stage is fecal cyst (6) cysts are resistant to chlorination |
|
Food-borne epidemics cause by this parasite from imported produce (eg, raspberries) are regularly seen in the US
|
Cyclospora (Cyclosporidiosis)
|
|
Diagnostic stage of cyclospora and cryptosporidium
|
Acid-fast (red stained) cysts in feces
|
|
This protozoa forms lumps protruding from the plasma membrane of the intestinal epithelium
|
Cryptosporidium
|
|
This "spor" intestinal parasite is zoonotic
|
Cryptosporidium
|
|
T/F: Chronic latent infection can occur in cryptosporidium
|
False. Chronic latent infection does not occur. The implication of this is that AIDS patients acquire it as an exogenous infection (vs. toxoplasma encephalitis, which is a reactivation)
|
|
This extracellular organism was mistaken as a protozoan but now known to be a fungus
|
Pneumocystis jirovecii
|
|
Clinical presentation of PCP
|
Sudden onset, fever, cough, dyspnea
|
|
Nearly all adults are seropositive for this
|
Pneumocystis
|
|
Diagnostic stage of pneumocystis
|
Cyst in stained bronchoscopy specimen, lung bx, transtracheal aspirate, or induced sputum
|
|
This organism grows in the alveolus, and its life cycle is poorly understood
|
Pneumocystis
|
|
Infection by this is seen in HIV infection with a CD4 count < 200
|
Pneumocystis jirovecii
|
|
AIDS, organ transplants, cancer chemotherapy, leukemia, infants with severe malnutrition all predispose to disease caused by this infection
|
Pneumocystis jirovecii
|
|
Untreated cases of this disease are 50-100% fatal
|
Pneumocystis pneumonia (PCP)
|
|
Treatment of PCP
|
Bactrim (Trimethoprim/Sulfadioxide)
|
|
Diseases in AIDS that are primary infections, and reactivation of latent infections.
|
Toxo is reactivation. Cryptosporidum is new infection (no latent stage). PCP is unknown.
|