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Term 5: Infectious Disease > 6/9- Cestodes and Intestinal Protozoa > Flashcards

6/9- Cestodes and Intestinal Protozoa Flashcards

1
Q

What organisms are included in cestodes?

A

- Taenia solium

- Echinococcus granulosis/multilocaris

  • Diphylloborthrium latum (not covered)
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2
Q

What organisms are considered intestinal protozoa?

A
  • Cryptosporidium hominis/parvum
  • Entamoeba histolytica
  • Giardia lamblia
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3
Q

What is the major phyla of helminths?

What classes are within it?

A

Phylum Platyheminthes (flatworms)

  • Class Cestoda (tapeworms)
  • Class Trematoda (flukes)
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4
Q

Identify the different types of tapeworms:

  • Beef:
  • Pork:
  • Fish:
  • Dog:
A

Identify the different types of tapeworms:

  • Beef: Taenia saginata
  • Pork: Taenia solium
  • Fish: Diphyllobothrium latum
  • Dog: Echinococcus granulosus
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5
Q

What is this?

A

Adult tapeworm (can be 20 ft long)

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6
Q

Tapeworm anatomy?

Which part is alive?

A

Scolex is alive (binding head bit); the rest is just reproductive segments/egg sacs

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7
Q

What is taeniaisis (broadly)?

A

Infection with a tapeworm

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8
Q

Where is Taenia saginata found?

Symptoms?

A

(Beef tapeworm)

Worldwide

  • Especially East Africa (Ethiopia)

Usually asymptomatic; intermittent diarrhea

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9
Q

Where is Taenia solium found? Symptoms?

A

(Pork tapeworm)

Worldwide

  • Especially Mexico, Central America, South America, China, Indonesia, Tanzania

Usually asymptomatic; intermittent diarrhea

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10
Q

What is this?

A

Taenia saginata (looks a lot like the other tapeworms too)

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11
Q

Life cycle of Taenia saginata?

A
  • Cysticerci are ingested with raw/undercooked beef
  • Released from muscle in stomach
  • Worms mature and live in small intestine (scolex with four suckers)
  • Adults grow up to ~10m in length
  • Proglottids pass in feces (reproductive sacs)
  • Cow ingests embryonated eggs, hatch, oncospheres migrate to tissues and develop into cysticerci
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12
Q

What is the mode of transmission of T. solium?

A

Fecal oral transmission (test)

- Zoonotic

- Human to human

NOT a soil transmitted helminth

  • Does not require life cycle in soil
  • Eggs can survive in environment for months

Often from undercooked or raw pork

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13
Q

Characteristics of T. solium:

  • length:
  • proglottids:
  • life span:
A

Characteristics of T. solium:

  • length: 6-12 ft (up to 30)
  • proglottids: 300-1000/worm (each with 10,000s of eggs)
  • life span: 10-25 years
  • Can’t distinguish from saginatum grossly (different scolex, but don’t need to know how)
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14
Q

Life cycle of T. solium?

A
  • Cystercerci are ingested with raw or undercooked pork
  • Cysticerci are released from muscle in stomach
  • Adults mature and live in small intestine
  • Adults grow up to 10 m in length (scolex with hooklets and 4 suckers)
  • Proglottids pass in feces
  • Pig ingests embryonated eggs, hatch, oncospheres migrate to tissues, develop to cysticerci
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15
Q

Ingesting the T. ____ egg can cause what?

A

The T. solium egg is the infective stage of neurocysticercosis

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16
Q

Pathogenesis/process of Cysticercosis (T. solium)?

A
  • Embryonated EGGS are ingested
  • Onchospheres hatch in small intestine
  • Onchospheres enter bloodstream, penetrate tissue
  • Causes cysticercus in: muscle, eye, brain (neurocysticercosis)
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17
Q

What is causing the problem in neurocysticercosis?

A

Eggs of T. solium causes cysticercus (space-occupying lesions) in the brain (encapsulated)

  • As cysticercus dies, it elicits an inflammatory response, c/o lymphocytes, plasma cells, and eosinophils
  • Inflammation sets off seizure focus
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18
Q

What is this?

A

Neurocysticercosis (T. solium)

  • space occupying lesion
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19
Q

Underlying mechanisms (pathophysiology) of Neurocysticercosis?

A

1. Mass effect- due to space occupying lesion (if removed, brain can typically refill without too many sequelae)

2. Inflammatory response

3. Obstruction of the foramina and ventricular system of the brain (resulting in hydrocephalus)

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20
Q

Clinical presentation of Neurocysticercosis?

(US and endemic regions)

A

(In young adult with no history of childhood seizures, experience of 1st seizure is HIGHLY probably Neurocysticercosis!)

US:

  • Solitary ring-enhancing lesion on CT/MRI cortex or gray-white junction

Endemic areas:

  • Multiple lesions with increased intracranial pressure
  • Encephalitis
  • Arachnoiditis
  • Hydrocephalus
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21
Q

What is this?

A

Severe neurocysticercosis

  • Holes = cysts, with little central dot = scolex
  • Tissue is not destroyed but pressed!

Picture on the right has scolex within the cyst, but surrounding white area is inflammation

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22
Q

What is this?

A

Intraventricular neurocysticercosis in 4th ventricle (left lateral Luschka)

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23
Q

Treatment for Neurocysticercosis (same for intestinal parasites)

A

Anti-parasitics

- Albendazole (highest efficacy)

  • Praziquantel (can be used w/ or w/out albendazole; 2nd line therapy)

Steroid administration to reduce inflammation of dying parasite

Anti-epileptics in patients with documented seizures

  • To prevent further seizures
  • Need to treat for 1-2 years
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24
Q

Forms of hyatid disease?

A

(Dog tapeworm)

  • Echinococcus granulosus- unilocular hydatid
  • E. multilocularis- alveolar or mutlilocular hydatid
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25
Q

What is this?

A

Echinococcus granulosus

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26
Q

What patients have positive serology for T. solium:

taeniaisis (digestive) or Neurocystercercosis?

A

Both!

Must diagnose Neurocystercercosis with CT because positive serology may be a result of GI infection

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27
Q

Where is Echinococcus granulosus found (what organisms and what geography)?

A

Adult parasites of dogs (small tapeworm)

  • Mainly sheep but also cattle, horse, and camel strains (intermediate hosts)

Worldwide distribution

  • China, Africa, Southern hemisphere, E European countries
28
Q

When does E. granulosus cause disease in humans? Symptoms? Diagnosis?

A
  • Liver and lung cysts when human becomes accidental intermediate host
  • Radiographic diagnosis
29
Q

Life cycle of Echinococcus?

A

(Don’t need to know super well)

  • Adult in small intestine
  • Embryonated egg in feces of dog
  • Ingestion of eggs by intermediate host (e.g. sheep, goats, sometimes humans)
  • Oncosphere hatches, penetrates intestinal wall
  • Hydatid cyst in liver, lungs, etc.
  • Protoscolex from cyst
  • Scolex attaches to intestine and grows into adult
30
Q

Pathology of unilocular hyatid infection?

A
  • Space-occupying lesion
  • Cysts can grow to large size (golf ball size common, soccer ball not uncommon)
  • Can prove fatal depending on location

Cysts located in many sites:

  • Liver (60%)
  • Lungs (20%)
  • Kidney, bone, CNS (under 3%)

Leakage of hyatid fluid can occur during biopsy/surgery

31
Q

What is this?

A

Hyatid cyst

32
Q

How are hyatid cysts diagnosed (many different tests/features)?

A
  • Slow-growing cystic tumor
  • Hx of residence in endemic area
  • Imaging with Xray, US (great), CT scans and MRI where there is CNS involvement
  • Serological tests
  • Surgery
  • Protoscolex is diagnostic (special hooks); also wall of cyst
33
Q

What interventions can be used for Echinococcosis?

A

Albendazole (6 mo - 1 yr)

Surgical (PAIR)

  • Puncture of cyst
  • Aspiration
  • Injection of chemicals (ethanol)
  • Reaspiration
34
Q

What are the 3 intesetinal protozoan infections focused on in this lecture?

A
  • Giardiasis
  • Cryptosporidiosis
  • Amebiasis
35
Q

Characteristics of Giardia lamblia?

A
  • Primitive eukaryote
  • Lacking mitochondria
  • Pear-shaped
  • Flagellated
  • Zoonotic host (from mammals- most commonly, beavers)
  • Smiley face/owl-eyes
36
Q

Transmission of Giardia lamblia? Life cycle?

A

(Don’t need to know too much)

Fecal-oral transmission

  • Commonly from infected water Ecystation triggered in GIT and small intestine colonized by trophozoites before encystation in distal small or large intestine. Then giardia cysts are excreted in feces
37
Q

Clinical symptoms of Giardia lamblia infection?

A

Asymptomatic giardiasis (60%; more in kids)

Acute giardiasis

  • 1-4 wks incubation
  • Loose, foul-smelling stools
  • Steatorrhea (fat malabsorption)
  • Cramping, bloating, nausea
  • Anorexia, malaise, weight loss
  • No blood

Chronic giardiasis

  • Steatorrhea
  • Growth delays
  • Often seen in those with IgA deficiency
38
Q

What is seen in chronic giardiasis malabsorption?

A
  • Second to CF as cause of steatorrhea
  • Toddlers
  • Growth delays
  • Increased fat excretion in stool
  • Decreased serum carotene
  • Abnormal xylose absorption
39
Q

Diagnosis for Giardia lamblia?

A
  • Fecal examination (not great; only seen in 30%)
  • Duodenal aspiration biopsy
  • Fecal antigen test
  • Serum antibodyu
  • PCR (what he uses)
40
Q

Treatment of Giardiasis? Rate of relapse?

A
  • Metronidazole
  • Nitazoxanide (suspension for pediatric use)
  • Tinidazole
  • Albendazole (need longer course)

10-20% relapse

41
Q

Characteristics of Cryptosporidium parvum?

Causes what? What main populations?

A
  • Coccidian protozoa
  • Infects gastric and respiratory epithelium of vertebrates
  • Obligate intracellular
  • Small (2-6 um) parasite
  • Important pathogen in children and HIV pts
  • Even asymptomatic infxn may cause failure to thrive in children
42
Q

Life cycle of C. parvum?

A

(Don’t need to know too much)

  • Oocyst is ingested along with fecally contaminated water or food (into reservoir host)
  • Sporozoites released from oocyst in small intestine
  • Sporozoites attach to surface of columnar epithelial cells
  • Local weird stuff~ macrogamont is fertilized
  • Unsporulated oocyst passes in feces
  • Oocyst is ingested along with fecally contaminated water or food
43
Q

Differenc ein transmission of C. parvum vs. C. hominim?

A

C. parvum is zoonotic while

hominim is person-to-person

44
Q

What is this?

A

Transmission EM of Crytosporidium

45
Q

Epidemiology of Cryptosporidium parvum:

  • Prevalence of active infxn:
  • Seroprevalence:
  • Seasonal peaks:
A

Epidemiology of Cryptosporidium parvum:

  • Prevalence of active infxn in N. America: 1-3%
  • Seroprevalence: 25-35%
  • Seasonal peaks: late summer and early fall
46
Q

Transmission of C. parvum?

A

Person-to-person

  • Outbreak in day care centers
  • 2ndary spread from day care centers

Zoonotic transmission

  • Farmers and animal handlers

Waterborne infection

- Swimming pool/water parks- normal chlorination is not effective; need hyperchlorination (and then draining)

  • (also public drinking water)
47
Q

What can be used to stain/identify C. parvum in feces?

A
  • Acid fast staining
  • Immunofluorescence staining
48
Q

Treatment for Cryptosporidium?

A

Nitazoxanide

  • Oral suspension
  • Interferes with pyruvate ferredoxin reductase (PFOR) enzyme-dependent electron transport
  • Effective in pediatric pts for Giardia and Cryptosporidium
  • Safety and efficacy in HIV pts not yet established
  • Good choice in kids (increased compliance because of good taste and low side effects)
49
Q

What organisms cause amebiasis?

A
  • Entamoeba histolytica
  • Entamoeba dispar
50
Q

What is the frequency/regionality of amebiasis?

A
  • Important pathogen in India, Africa, Latin America, Central and S AMerica
  • In US- overall prevalence is 4%
  • 33% in Hispanic immigrants and

17% in immigrants from Asia or other Pacific islands

51
Q

What causes human amebiasis?

A

Entamoeba histolytica

52
Q

T/F: Entamoeba dispar is capable of causing disease

A

False; E. dispar is non-pathogenic

53
Q

Peak seropositivity for human amebiasis in what age group?

A

5-9 year olds

54
Q

Amebiasis most commonly affects what SE groups?

A

All SE groups

55
Q

What is the most commonly affected population in the US for amebiasis?

A

Hispanic males 20-40 yo

56
Q

What is this?

A

Entamoeba histolytica (although can’t really differentiate form dispar?)

57
Q

Life cycle of Entamoeba histolytica?

A
  • Cysts ingested along with fecally contaminated food or water
  • Trophozoites invade tissues of colon
  • Cause abscess (brain, liver) or flask-shaped ulcer
  • Trophozoites encyst in colon
  • Cysts pass with fezes (quadranucleate cysts)
58
Q

Clinical symptoms of amebiasis?

A
  • Asymptomatic colonization
  • Amebic dysentery
  • Amebic colitis
  • Liver abscess
59
Q

Signs and symptoms of amebic colitis?

A
  • Gradual onset
  • H/O symptoms > 1 wk
  • Dysentery (diarrhea, abdominal pain, fever, blood and stools)
  • Weight loss
  • Immigrant/traveler from endemic area
60
Q

What is this?

A

Amebic colitis

61
Q

Signs and symptoms of amebic liver abscess?

A
  • History of symptoms > 4 wks
  • Fever
  • Abdominal tenderness in RUQ
  • Hepatomegaly
  • Jaundice
  • Diarrhea
  • Weight loss
  • Immigrant/traveler from endemic area
62
Q

What is this?

A

CT of Amebic Liver Abscess

63
Q

Characteristics of amebic liver abscess?

A

Aspiration of anchovy paste

64
Q

Amebic colitis and liver abscess is estimated at ____ cases annually worldwide, resulting in ___ deaths

A

Amebic colitis and liver abscess is estimated at 40-50 million cases annually worldwide, resulting in 110,000 deaths

65
Q

Diagnosis of amebiasis?

A

Microscopy

  • Single stool exam (30-50% sensitivity)
  • Erythrophagocytic amebae
  • Liver aspirate (20% sensitive) Stool antigen detection Stool PCR Serology
  • IHA
  • 99% sensitive for liver abscess
  • 88% sensitive for amebic colitis
  • Remains positive for years

Colonoscopy + wet prep

Radiographic imaging

66
Q

Treatment of amebiasis?

A

Asymptomatic colonization treatement with luminal agent alone:

  • Paromomycin
  • Iodoquinol

Invasive amebiasis (colitis, dysentery, liver abscess)

  • Metronidazole + luminal agent
  • Percutaneous drainage not usually required

Term 5: Infectious Disease (18 decks)

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