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Wrap-Up Block > Clinical Parasitology 2 - Protozoa > Flashcards

Clinical Parasitology 2 - Protozoa Flashcards

0
Q

What kind of disease does Entamoeba histolytica cause?

A

Bloody diarrhea

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1
Q

What kind of organisms are protozoa?

A

Single-celled eukaryotic organisms

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2
Q

How does E. histolytica get into the human host?

A

Ingestion of mature cysts in fecally contaminated food, hands, water

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3
Q

What is the transmission route of E. histolytica?

A

fecal-oral

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4
Q

In the small intestine, the cysts mature into what in the E. histolytica life cycle?

A

Cysts release Trophozoites, which migrate to the large intestine

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5
Q

How do trophozoites cause bloody diarrhea in E. histolytica?

A

Invade the intestinal mucosa causing erosions–> results in abdominal pain, loose stools and flecks of blood

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6
Q

What is the characteristic lesion formed in the intestine by E. hustolytica?

A

Flask-shaped ulcers in large intestine

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7
Q

What other two places can E. histolytica travel in the body? How does it get to each?

A
  1. Liver–> penetrates portal circulation and forma abscesses in liver
  2. Lung–>after portal invasion, spreads above diaphragm and forms pulmonary abscesses

*may also disseminate to brain and abscess there

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8
Q

What is the characteristic appearance of the contents of E. histolytica liver abscesses?

A

“Anchovy paste” aspirate

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9
Q

How is Dx of E. histolytica made?

*How can active vs. asymptomatic carriage be determined?

A

ID of cysts or trophozoites in the stool

  • Trophozoites with RBCs in their cytoplasm suggest active dz; those without likely reflect carriage state only
  • PCR test for amoeba antigen exists also
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10
Q

What is DOC for symptomatic E. histolytica infection?

A

Metronidazole

*Paromomycin for eradication of luminal carriage

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11
Q

What form of E. histolytica is excreted in the feces?

A

Cysts–> trophozoites can convert to a precyst form with two nuclei, that matures into a tetranucleated cyst by the time it leaves the colon. Precysts contain chromotid bodies (aggregates of ribosomes), when these disappear, it is a mature cyst

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12
Q

What kind of organism is Naegleria fowleri?

A

Free-living amoeba that lives in fresh water

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13
Q

How are N. fowleri infections obtained?

A

Swimming in fresh water–> penetrates the nasal mucosa, passes through the cribiform plate and into brain and spinal fluid

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14
Q

What symptoms are seen with N. fowleri infection?

A

Fever, headache N/V, stiff neck–> looks just like a bacterial meningitis

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15
Q

What might CSF analysis show in N. fowleri infection?

A

Increased neutrophils, low glucose, and increased protein

  • is exactly like bacterial meningitis, but gram stain will be negative
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16
Q

Treatent for N. fowleri?

A

Kiss your ass goodbye; 95%+ are dead w/in a week

*intrathecal Amphotericin B has saved a select few people

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17
Q

What kind of organism is Trichimonas vaginalis?

A

Flagellated protozoan (like Giardia lamblia)

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18
Q

How is T. vaginalis transmitted?

A

STD–> men are asymptomatic carriers who pass it on to women

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19
Q

What symptoms are seen in T. vaginalis infection?

A
  1. Vaginal itching
  2. Dysuria
  3. Copious, frothy discharge (usually malodorous)
  4. “strawberry” cervix on speculum exam
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20
Q

How is dx of Trichomonas confirmed?

A

PCR detection of trophozoites in discharge

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21
Q

Tx for trichimoniasis?

A

Metronidazole

*need to treat male partner or woman will be continously reinfected from carrier state

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22
Q

Where does T. vaginalis live in the human host?

A

Female–> lower genital tract

Male–> urethra

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23
Q

How does T. vaginalis replicate? Where in host?

A

Replicates via binary fission; usually in female genital tract

*no cyst stage; and cannot survive outside the host. No known other reservoir hosts

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24
Q

What type of organism is Giardia lamblia? What two forms can it take?

A

Flagellated protozoan–> has both a trophozoite stage and a cyst stage

*compare to T. vaginalis, also a flagellated protozoan, but doesnt have a cyst stage

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25
Q

What kind of dz in general does G. lamblia cause?

A

Intestinal disease–> most common protozoan intestinal disease in the US

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26
Q

What is the classical case scenaria for getting G. lamblia infection?

A

Campers/ other people in the woods who drink water from clear streams

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27
Q

What is the source of water infection of G. lamblia?

A

Rodents and beaver shit all in the water and you drink it

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28
Q

Other than the Great Outdoors, what environment is G. lamblia common in?

A

Day-care centers

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29
Q

What form in the life cycle of G. lamblia is ingested in contaminated water?

A

Cysts–> also the infectious form via the fecal-oral route like in day care centers

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30
Q

After ingestion, what happens to the G. lamblia cysta?

A

Turn into trophozoites, which multiply via binary fission in the small intestines

*Encystation occurs as parasites move towards colon

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31
Q

What do G. lamblia trophozoites do in the small intestines to contribute to Giardiasis symptoms?

A

Attach to the intestinal wall and interfere with absorption

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32
Q

What are some symtoms due to Giardia lamblia infection?

A
  1. Foul-smelling, bulky diarrhea
  2. Flatulence
  3. Abdominal distention
  • due to Giardia coating the intestines and interfering with fat absorption–> NO BLODD IN STOOL
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33
Q

What histopath changes may be seen due to Giardia infection on intestines?

A

Flattened intestinal epithelium

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34
Q

What confirms the Dx of Giardiasis?

A

ID of cysts and trophozoites in stool

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35
Q

Tx for Giardiasis?

A

Metronidazole

36
Q

What are the two blood-borne flagellates?

A
  1. Leishmania

2. Trypanosoma

37
Q

What organism causes African sleeping sickness?

A

Trypsanosoma brucei

rhodesience and gambiense species exist, both are T. brucei though

38
Q

What organism transmits T. brucei to the human host? Which form of T. brucei is the infectious form transmitted by the bite?

A

Tsetse fly–> trypomastigote is the form transmitted

39
Q

Where does the trypomastigote go once in the person’s bloodstream?

A

To the CNS and lymph nodes

40
Q

What is the first manifestation of T. brucei infection?

A

Chancre (hard, red, painful ulcer) on the skin at the site of the Tsetse fly bite

41
Q

What four symptoms are see with systemic spread of T. brucei?

A
  1. Fever
  2. Headache
  3. dizziness
  4. Lymphadenopathy
42
Q

What is unique about the fevers due to T. brucei infection?

A

They are undulating–> fevers will come and go in a pattern for a few months, likely due to antigenic variation (variant surface glycoproteins)

43
Q

What CNS symptoms eventually develop later on in T. brucei infection, after the waxing/waning fevers?

A
  1. Drowsiness in the daytime
  2. Behavioral changes
  3. Difficulty walking
  4. Slurred speech
  5. Eventually, coma and death
44
Q

What is a main difference between t. brucei gambiense and T. brucei rhoesciense?

A

Gambiense–> “West African sleeping sickness”; slowly progressive fevers, wasting and LATE neuro symptoms

Rhodesiense–> “East African sleeping sickness”; rapid progression from fevers to EARLY neuro disease; death usually within weeks to months

45
Q

What two methods are used to confirm T. brucei infection?

A
  1. Microscopic visualization of trypomastigotes in peripheral blood or lymph nodes
  2. Card agglutination test (assay for anti-T. brucei Abs in serum)
46
Q

What is tx for T. brucei infection if CNS is not involved?

A

Suramin or pentamidine

47
Q

What is tx for T. brucei if there are CNS manifestations? (different 1st line drugs depending on if infection is rhodesiense or gambiense)

A
  1. Melarsoprol (rhodesiense, 1st line; 2nd line for gambiense)
  2. Eflornithine + Nifurtimox (1st line for CNS gambiense)
48
Q

What organism is responsible for American tryanosomiasis?

A

T. cruzi

49
Q

Where is T. cruzi endemic (2 places)?

A

Central and South America

*also found in Mexico and SW U.S.

50
Q

What organism transmits T. cruzi?

A

Reduviid bug (aka “kissing bug”<— WTF?)

*populations of rodents, opossums, and armadillos serve as the reservoir for T. cruzi; is where the reduviid bug gets infected

51
Q

How do reduviid bugs infect humans?

A

Feed on us while we sleep and shits while eating; T. cruzi trypomastigotes are excreted in reduviid feces and they burrow into our skin

52
Q

Once inside human cells, what happens in the life cycle of T. cruzi?

A
  1. Inside cells, trypomastigotes transform into amastigotes

2. Amastigotes replicate via binary fusion inside infected tissue

53
Q

How do amastigotes, once replicated, spread inside the host?

A

Spread via the blood and lymph nodes to distant organs

*are also able to infect macrophages

54
Q

What is the 1st sign of T. cruzi infection?

A

Chagoma–> hardened red area

*is often on the face; called Romaña’s sign

55
Q

What are three symptoms of systemic disease from T. cruzi?

A

Fever, myalgia, lymphadenopathy (also rash)

56
Q

What 2 blood findings are seen in Acute Chagas’ (ameriacn typanisomiasis) disease?

A
  1. parasitemia

2. lymphocytosis

57
Q

What two organs may be involved in acute Chagas’?

A
  1. heart–> tachycardia, EKG changes

2. CNS–> severe meningoencephalitis (usually in young pts)

58
Q

What is the intermediate phase of Chagas’?

A

Acute symptoms (fever, malaise, heart and CNS abnormalities) usually resolve in about a month, although there are usually persistently low levels of parasite in the blood

*most people remain in this Intermediate phase for life and have no further issues

59
Q

What are the three main organs affected by chronic Chagas’ disease, which develops for unknown reasons in people years to decades after intitial, acute disease?

A
  1. Heart
  2. Colon
  3. Esophagus

(heart and some hollow organs)

60
Q

What heart complications may develop in chronic Chagas’ disease? (2 main ones)

A
  1. Arrhythmias (heart block and ventricular tachycardia)
  2. Dilated cardiomyopathy (increased heart size + heart failure)

*#2 is prob the one they’d ax on STEP

61
Q

What complication may occur due to chronic Chagas’ disease in the esophagus and/or colon?

A
  1. Dilated esophagus (lead to dysphagia and odynophagia)
  2. Megacolon(constipation and abdominal pain)
  • destruction of autonomic ganglia
62
Q

How can T. cruzi dx be confirmed?

A
  1. On clinical grounds in endemic regions
  2. Examination of blood smear for motile trypomastigotes
  • also via tissue histological examination
  • in chronic Chagas’ dz, there should be serologic evidence of past T. cruzi infection, either parasitemia or anti-T. cruzi Abs
63
Q

What is treatment for acute Chagas’ disease? (2 drugs)

A

Nifurtimox + benznidazole

  • treating chronic Chagas’ is harder, doesnt respond as well to meds; so best plan is dont get disease (insect repellent and bednets when in endemic areas)
64
Q

What places in the world is Leishmania sp. endemic?

A

Asia, India, Mediterranean, North and Central Africa, Central and South America–> basically everywhere but the U.S.

*8 different species in notes, dont know if they want us to know all that. If you have free time look over it Wally

65
Q

What organism transmits Leishmania spp. to humans?

A

Sandfly

*rodents, dogs, and foxes are the natural reservoirs

66
Q

What form of Leishmania is transmitted by a bite?

A

Promastigote

67
Q

What happens to promastigote of Leishmania once in the body?

A

Taken up by macrophages and differentiates into a nonmotile amastigote
amastigote replicates within phagocytic cells in lymph nodes, spleen, liver and bone marrow (the reticuloendothelial system; makes sense since they replicate in macrophages)

68
Q

What three varieties of Leishmaniasis exist?

A
  1. Cutaneous
  2. Mucocutaneous
  3. Visceral

*depends on the invasiveness of the actual contracted species of Leishmania and the host immune response

69
Q

What are symptoms of cutaneous leishmaniasis?

A

Skin ulcer develops at site of sandfly bite (called “oriental sore)

  • heals in ~ 1 year, leaving a depigmented scar
  • this variety sometimes seen in Texas
70
Q

Dx of cutaneous leishmaniasis?

A

Scrapings of ulcer base reveal Leishmania

71
Q

What are symptoms of mucocutaneous leishmaniasis?

A

Initially the same as cutaneous (ulcer); however, months to years later, ulcers arise in the mucous membranes of mouth and nose

*if untreated, may erode nasal septum, soft palate, and lips; death may result due to secondary bacterial infection

72
Q

What are symptoms of visceral leishmaniasis (Kala-azar)?

A

Months after infection–> fever, anorexia, weight loss, abdominal pain and distention (distension due to massive hepatosplenomegaly, remember these organisms multiply in the RES)

*often seen in children; over 90% fatality rate if untreated

73
Q

What two blood abnormalities may occur in visceral leishmanasis?

A
  1. Anemia

2. Low WBC

74
Q

How is dx of visceral leishmaniasis made?

A
  1. Liver and spleen biopsy demonstrating protozoa

2. High titers of anti-leishmanial IgG levels

75
Q

What is tx for all forms of leishmaniasis?

A

Sodium stibogluconate (an antimonial)

76
Q

What two parasites are often found in AIDS patients, other than Cryptosporidium?

A
  1. Toxoplasma gondii

2. Pneumocystis carinii

77
Q

What two ways can humans be infected with Toxoplasma gondii?

A
  1. Ingestion of cysts in raw/undercooked meat

2. Contact with cat feces (up to 80% of cats in U.S. are infected)

78
Q

What is Toxoplasmosis gondii the most common cause of in AIDS patients?

A

CNS infection–> causes an encephalitis

*often due to reactivation of latent organism in immunocompromised people; infection doesnt usually cause any symptoms in those w/ intact immune systems

79
Q

What symptoms can be seen in a person with CNS infection due to T. gondii?

A

Headache and focal neuro signs (seizures, gait instability, weakness, sensory loss)–> acts very similar to a CNS mass

  • outside CNS may cause fever, lymphadenopathy, hepatosplenomagaly, or pneumonia; frequently infects the retina (chorioretinitis) producing white, fluffy cotton like patches surrounding a red retina
80
Q

Other than immunocompromised, what other pt. population is at risk of infection with T. gondii?

A

Newborns–> of mothers with infection, 5-10% have miscarriage, 10% of newborns will have brain damage; 10% will have vision loss. But 70% of births will be normal

*pregnant women SHOULDNT PLAY WITH CAT SHIT

81
Q

How can dx of toxoplasmosis be made?

A
  1. CT scan of brain showing constrast-enhancing mass
  2. Retinal examination revealing retinal inflammation

**in all susceptible pts, Toxoplasma gondii is toxic to BRAIN and EYES

82
Q

Tx for T. gondii? (2 dug regimen)

A

Sulfadiazine + pyrimethamine

83
Q

What kind of issues can Cyrptosporidium infection cause?

A

Usually severe diarrheal disease, esp. in AIDS/immunocompromised and in young children (daycare centers)

*also can be transmitted infected water; not killed by chlorine

84
Q

What form of Cryptosporidium is ingested? Where in body does life cycle occur?

A

Round oocyst–> life cycle occurs within intestinal epithelial cells

85
Q

After oocysts infect intestinal epithelial cells, what do they differentiate into? (specifically what does each of the four sporozoites each oocyte contains differentiate into)

A

Merozoites (these grow via asexual reproduction)–> some differentiate into male gametes, others into females; gametes fuse to form oocyst

86
Q

What are the symptoms of Cryptosporidiosis?

A

Severe diarrhea and abdominal pain

  • severity depends on inoculum; pts can lose b/n 3-17 L of stool/day
  • in I.C. patient, may disseminate to gallbladder, biliary tract, or lung
87
Q

How is Cryptosporidium infection dx’d?

A

Via antigen testing or stool microscopy

88
Q

Tx for Cryptosporidiosis?

A

Nitazoxamide

*also want to tx that fluid loss via the anus. supportive care

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