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2. GI II Flashcards > Chapter 17: Infectious Enterocolitis > Flashcards

Chapter 17: Infectious Enterocolitis Flashcards

1
Q

What is the morphology of Vibrio cholerae?

A

Comma-shaped; gram (-) bacteria

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2
Q

What is the reservoir and mode of transmission for Vibrio cholerae?

A

Reservoir = shellfish

MOT = fecal-oral; water

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3
Q

Is Vibrio cholerae invasive and which components of the organism are related to its virulence?

A
  • Non-invasive
  • Cholera toxin
  • Flagella for motility and attachment
  • Hemagglutinin for detachment and shedding in stool
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4
Q

In severe cases of Cholera what are the signs and symptoms?

What are the characteristics of the diarrhea?

When is the onset?

A
  • Abrupt onset of vomiting and watery diarrhea after 1-5 day period
  • Voluminous stools resembling rice water and said to have fish odor
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5
Q

What is the rate of diarrhea in severe cases of cholera and what problems can this create?

When do most deaths occur?

Treatment?

A
  • Up to 1L/hr
  • Dehydration, hypotension, cramping, anuria, shock, and LOC
  • Death usually within first 24 hours
  • Timely fluid replacement can save more than 99% of pts
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6
Q

What is the morphology and mode of transmission for Campylobacter spp.?

A
  • Comma-shaped; flagellated; gram (-) bacteria
  • Poulty (undercooked), milk (unpasteurized), other foods
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7
Q

What is the most common bacterial enteric pathogen in developed countries and important cause of traveler’s diarrhea?

A

Campylobacter jejuni

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8
Q

What are the 4 major properties contributing to the virulence of Campylobacter jejuni?

A
  1. Motility - flagella
  2. Adherence
  3. Toxin production - cytotoxin + cholera toxin-like enterotoxin
  4. Invasion
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9
Q

What are some of the signs and symptoms of Campylobacter infection?

How can sx’s of a fever be produced?

A
  • Watery diarrhea, either acute or following an influenza-like prodrome
  • Dysentery (blood stool) in minority of patients
  • Enteric fever if bacteria prolif. in lamina propria and mesenteric LNs
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10
Q

What is the association of Campylobacter infection and HLA-B27?

A

Can result in reactive arthritis

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11
Q

What are 2 possible complications of Campylobacter infection that are not HLA linked?

A
  • Erythema nodosum
  • Guillain-Barre syndrome

*NOT HLA linked, like reactive arthritis

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12
Q

How is the diagnosis of Campylobacter infection made?

Which immune cell infiltrates predominate and where are they found?

A
  • Primarily by stool culture
  • Intraepithelial neutrophilinfiltrates withinsuperficial mucosaandcrypts (cryptitis)
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13
Q

What is the affect of Campylobacter infection on crypt architecture?

A
  • May see neutrophil infiltration of crypts (cryptitis) or crypt abscesses
  • Architecture of cyrpts are PRESERVED (important)
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14
Q

What is the morphology of Shigella?

Mode of transmission?

Reservoir?

A
  • Gram (-); Unencapsulated; Non-motile;Facultative anaerobes

- MOT = fecal-oral, food, water

- Reservoir = humans

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15
Q

Shigella is one of the most common causes of?

A

Dysentery (blood diarrhea)

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16
Q

Where are the most common sites for infection by Shigella and who is most at risk?

Most deaths occur in whom?

A
  • In US and Europe, daycares, migrant workers, travelers, and those in nursing homes
  • Most deaths occurs in children <5 yo
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17
Q

Why is such a low infective dose of Shigella required to cause symptoms?

A
  • Acid-STABLE
  • Able to resist the harsh acidic enviornment of the stomach
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18
Q

Once Shigella are in the intestine how are they taken up and what do they do?

A
  • Taken up by Microfold (M cells)
  • Proliferate intracellularly, escape into LP to be phagocytosed by MØ’s in which they induce apoptosis
  • Inflammatory response damages surface epithelia and allows Shigella access to basolateral membrane for invasion
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19
Q

All Shigella spp. carry which virulence plasmids allowing for direct injeciton of bacterial proteins into host cytoplasm?

A

Type III secretion system

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20
Q

Shigella dysenteriae serotype 1 are able to release which special toxin and what does this cause?

A
  • Shiga toxin Stx
  • Inhibits eukaryotic protein synthesis –> host cell damage + death
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21
Q

Shigella most prominently infect which part of the GI, likely due to what?

What is the morphology of the mucosa?

A
  • Left colon and Ileum –> M cells prominent in Peyers patches here
  • Mucosa = ulcerated + hemorrhagic w/ pseudomembranes
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22
Q

What is the most common clinical presentation of a pt w/ Shigella infection?

A
  • 1 week of diarrhea w/ fever and abdominal pain
  • Initially watery diarrhea may progress to dysenteric phase w/ sx’s lasting up to a month
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23
Q

Complications of Shigella infection are related to which immune system component and presents as a triad of sx’s most commonly in which patient population?

A
  • HLA-B27 in men ages 20-40 yo

1) Sterile reactive arthritis

2) Urethritis

3) Conjunctivitis

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24
Q

The Shigella dysenteriae serotype 1 that secretes shiga toxin is somtimes associated w/ what clinical complication?

A

Hemolytic-uremic syndrome (typically assoc. w/ EHEC)

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25
Q

Which treatment is indicated and which is contraindicated in patients w/ Shigella infection?

A
  • Antibiotics may shorten clinical course
  • Antidiarrheals = CONTRAINDICATED –> prolong sx’s and delay clearance
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26
Q

Salmonellosis is usually due to which type of Salmonella**?

A

Salmonella enteritidis

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27
Q

Salmonella infection is most commonly transmitted how?

Which age groups most affected?

Which time of year do infections peak?

A
  • Meat, poultry, and eggs/milk
  • Young children and Older adults
  • Peak incidence in fall and summer
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28
Q

What are predispositions for the development of Salmonella infection?

A
  1. Atrophic gastritis or on acid-suppressive therapy (PPIs)
  2. Genetic defects in TH17 –> Disseminated salmonellosis
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29
Q

Which virulence factor allows for Salmonella invade and infect humans?

Explain the pathogenesis of invasion.

A
  • Type III secretion system transfers bacterial proteins –> M cells and enterocytes
  • Proteins activate host Rho GTPases –> actin rearrangement and bacterial endocytosis for growth in endosomes
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30
Q

What do the flagellin and LPS of Salmonella activate inside humans are what does this result in?

A
  • Flagellin –> TLR5 –> Increased inflammtory response
  • LPS –> TLR4
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31
Q

How do Salmonella indirectly cause increased neutrophils and potentiate mucosal damage?

A

Secrete molecule inducing epithelial cells to release eicosanoid hepoxilin A3

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32
Q

Which immune cells limit infection by Salmonella?

A

TH1 and TH17

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33
Q

What is essential for the diagnosis of Salmonella infection?

A

Stool culture (+)

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34
Q

Typhoid fever (enteric fever) is caused by which organism and its 2 subtypes?

Which subtype is associated with endemic countries and which with travelers?

A
  • Salmonella enterica
  • Subtypes:
    • Typhi* (endemic countries)
    • Paratyphi* (travelers)
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35
Q

What is the reservoir for Salmonella enterica?

Mode of transmission?

A
  • Humans = reservoir
  • MOT = fecal-oral and water
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36
Q

Typhoid fever (Salmonella enterica) is strongly associated with travel to which countries?

A

India, Mexico, Philippines, Pakistan, El Salvador, and Haiti

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37
Q

Gallbladder colonization by S. typhi or S. paratyphi is associated with?

A
  • Gallstones
  • Chronic carrier state
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38
Q

Explain the pathogeneis of S. typhi infection (i.e., how do they invade?)

A
  • Survive in gastric acid–> small intestine –> taken up byM cells
  • Bacteria engulfed by mononuclear cells in lymph tissue
  • Can disseminate via lymph and blood causing reactive hyperplasia of phagocytes and lymph tissue throughout body
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39
Q

What is seen morphologically in the Peyer patches, Mesenteric LN’s, Spleen, and Liver of a person with S. typhi infection (typhoid fever)?

Where in the GI are the Peyer Patches affected?

A
  • Peyer patches of terminal ileum –> enlarge, sharply delineated, plateau-like elevations
  • Mesenteric LNs –> enlarged
  • Spleen –> enlarged w/ uniform pale red pulp; prom. phagocyte hyperplasia
  • Liver –> small, scattered foci of parenchymal necrosis in which hepatocytes are replaced by MØ aggregates –> typhoid nodules
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40
Q

What are the phases of Typhoid Fever and symptoms involved in each?

A
  • Pts have anorexia, abd. pain, bloating, nausea, vomiting, and blood diarrhea
  • Followed by short asymptomatic phase
  • Gives way to bacteremia and fever w/ flu-like sx’s
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41
Q

Are antibiotics recommended for Typhoid Fever?

A

Yes, can prevent further disease progression

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42
Q

In patients with Typhoid Fever, not treated w/ antibiotics what additional signs and symptoms may develop?

A
  • Sustained high fevers
  • Abdominal tenderness which may mimic appendicits
  • Rose spots = erythematous maculopapular lesions on chest and abd.
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43
Q

Systemic dissemination of S. typhi may lead to what complications?

A
  • Encephalopathy
  • Meningitis
  • Seizures
  • Endocarditis
  • Myocarditis
  • Pneumonia
  • Cholecystitis
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44
Q

Which patient population is particularly susceptible to developing Salmonella osteomyelitis?

A

Sickle cell disease pts

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45
Q

Which 2 types of Yersiniai cause GI disease?

Which is more common?

A

1) Yersinia enterocolitica = more common
2) Yersinia pseudotuberculosis

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46
Q

Where are Yersinia infections most common?

Mode of transmission?

Time of year infections are most common?

A
  • Europe
  • Pork, milk, water
  • More common in winter
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47
Q

Which cells does Yersinia invade and which virulence factors does it contain allowing for its pathogenicity?

Which system allows for enhanced virulence and systemic dissemination?

A
  • Invades M cells and uses adhesins to bind host β1 integrins
  • Iron uptake system to capture and mediate transport of iron; which enhances its virulence and stimulates systemic dissemination
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48
Q

Which predisposition by some patients increases the chance of developing sepsis and death when infected by Yersinia?

A
  • Pts w/ increased non-heme iron
  • Such as certain chronic anemias or hemochromatosis
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49
Q

Yersinia infections preferentially involve which parts of the GI?

A

Ileum, appendix, and right colon

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50
Q

What are some of the characteristic morpho, histo, and gross changes associated with Yersinia infection?

Predominant immune infiltrate?

A
  • Regional LN and Peyer patch hyperplasia
  • Bowel wall thickening
  • Mucosa overlying lymph tissue –> hemorrhagic, apthous-like erosions, and ulcers
  • Neutrophils and granulomas
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51
Q

Peyer patch invasion with subsequent involement of regional lymphatics by Yersinia can cause symptoms which are confused with what other pathology in teens and young adults?

A

Acute appendicits

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52
Q

What are common extraintestinal symptoms of Yersinia infection?

A
  • Pharyngitis
  • Arthralgia
  • Erythema nodosum
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53
Q

What are some of the postinfectious complications associated withYersinia?

A
  • Reactive arthritis, Urethritis, Conjunctivitis (like Shigella)
  • Myocarditis
  • Erythema nodosum (like Campylobacter)
  • Kidney disease
54
Q

Which subgroup of E. coli is the principal cause of traveler’s diarrhea and spreads via contaminated water/food?

A

Enterotoxigenic E. Coli (ETEC)

55
Q

Which age group is particularly susceptible to infection by ETEC?

A

Children <2 yo in developing countries

56
Q

What are the 2 main toxins of ETEC and what is the MOA of each?

Net effect of these toxins?

A
  • Heat-labile toxin (LT) –> similar to cholera toxin (activates AC = incrased cAMP) –> Cl- secretion
  • Heat-stabile toxin (ST) –> homology to guanylin = binds to GC = increased cGMP –> similar effects of LT
  • Toxins cause Cl- + H2O secretion and inhibit fluid absorption
57
Q

What is the clinical manifestations (signs/symptoms) of ETEC infection?

A
  • Secretory, noninflammatory diarrhea –> dehydration
  • Severe cases = shock
58
Q

Which subtype of E. coli is an important cause of endemic diarrhea as well as diarrheal outbreaks in children <2 yo?

A

Enteropathogenic E. Coli (EPEC)

59
Q

EPEC are characterized by their ability to produce what type of lesion?

Describe this lesion

A
  • (A/E) lesions = attaching and effacing
  • Attach tightly to enterocyte apical membranes
  • Cause local loss –> effacement of the microvilli
60
Q

The proteins necessary for creating the A/E lesions seen w/ EPEC infections are encoded by which pathogenicity island?

What are the proteins encoded?

A
  • Locus of enterocyte effacement (LEE)
  • Encodes: Tir –> inserted into intestinal epithelial cell PM and acts as receptor for bacterial outer membrane protein, intimin
  • Encodes: type III secretion system (similar to Shigella)
61
Q

Which bacterial protein encoded by the espE gene is used for molecular detection and diagnosis of EPEC infection?

A

Intimin

62
Q

How is Enterohemorrhagic E. Coli (EHEC) categorized?

A
  • O157:H7
  • non-O157:H7
63
Q

What is the reservoir for EHEC and is transmitted how?

A
  • Cows = reservoir
  • Transmitted via consumption of undercooked beef, also milk and vegetables
64
Q

What is produced by O157:H7 and non-O157:H7 serotypes of EHEC that contributes to its pathogenecity?

Symptoms are similar to infection by what organism?

Which serotype is more likely to produce large outbreaks?

A
  • Shiga-like toxin –> Sx’s similar to S. dysenteriae infection
  • O157:H7 more likely to cause large outbreaks
65
Q

What are the symptoms and complications of EHEC infection, especially by the O157:H7 serotype?

A
  • Bloody diarrhea
  • Hemolytic uremic syndrome (HUS)
  • Ischemic colitis
66
Q

Are antibiotics recommended for treatment of EHEC; why or why not?

A
  • No!
  • Cause increased release of Shiga toxin –> enhancing risk for HUS, especially in children
67
Q

Which E. Coli subtype is bacteriologically similar to Shigella and is transmitted via food, water, or by person-to-person contact?

A

Enteroinvasive E. Coli (EIEC)

68
Q

What toxins are produced by EIEC and what is the clinical course of infection?

A
  • Do not produce toxins
  • Invade epithelial cells and cause non-specific features of acute self-limited colitis
69
Q

Enteroaggregative E. Coli (EAEC) were identified on the basis of their unique what?

A

Unique pattern of adherence to epithelial cells

70
Q

How does EAEC uniquely attach to enterocytes, which virulence factors are used?

A
  • Via adherence fimbriae and are aided by dispersin
  • Dispersin is a surface protein which neutralizes the negative surface charge of LPS
71
Q

Which toxins are produced by EAEC organisms?

A
  • Enterotoxin related to Shigella enterotoxin
  • ETEC ST toxin (heat-stable toxin)
72
Q

What are the clinical manifestations of EAEC infection and which popluation most often affected?

A
  • Non-bloody diarrhea (traveler’s)
  • Children/adults in both developing + developed countries
  • Diarrhea may be prolonged in immunodeficient pt
73
Q

Which organism is responsible for Pseudomembranous Colitis?

A

C. difficile

74
Q

Which factor most likely contributes to bacterial overgrowth by C. difficile?

Toxins released by this organism cause what?

A
  • Disruption of normal colonic microbiota by antibiotics; immunodeficiency = pre-disposing factor
  • Toxins cause ribosylation of small GTPases (i.e., Rho) –> disruption of the epithelial cytoskeleton, tight junction barrier loss, cytokine release, and apoptosis
75
Q

Crypts w/ mucopurulent exudate of neutrophils that forms eruption reminiscent of a volcano is characteristic of what infection?

A

C. difficile —> pseudomembranous colitis

76
Q

Diagnosis of C. difficile-associated colitis is usually accomplished how?

A

Detection of C. difficile toxin in stool and supported by histopathology

77
Q

What is a major challenge in C. difficile-associated colitis and a complication which may arise?

A
  • Recurrent infection is common
  • Toxic megacolon may occur
78
Q

Which rare disease, was first described as intestinal lipodystrophy?

A

Whipple Disease

79
Q

How does lymphatic obstruction occur in Whipple Disease?

Leads to what?

A
  • Organism-laden MØ’s accumulate within SI lamina propria and Mesenteric LN’s
  • Malabsorptive diarrhea
80
Q

Postmortem examination of someone with Whipple Disease will show what histological characteristics?

Gross characteristics?

A

- Foamy macrophages in lamina propria and large #s of agyrophilic rods in LN’s

  • Villous expansion caused by dense MØ infiltrate imparting shaggy gross appearance to mucosal surface
81
Q

Which stain is used the visualize macrophages in Whipple Disease?

How can it be differentiated from the similar looking intestinal tuberculosis?

A
  • PAS
  • Used acid-fast to differentiate because T. whippelii will not stain, while mycobacteria will stain (+)
82
Q

In Whipple disease, bacteria-laden macrophages can accumulate where?

A
  • Mesenteric LNs (malabsorption)
  • Synovial membranes (arthritis)
  • Cardiac valves
  • Brain (CNS disease)
83
Q

Whipple disease most commonly affects who?

A

Caucasian men, particularly farmers and those w/ occupational exposure to soil or animals

84
Q

What is the clinial triad of sx’s associated w/ Whipple disease?

A

1) Diarrhea
2) Weight loss
3) Arthralgia

85
Q

Which extraintestinal symptoms of Whipple disease may persist for months or years before malabsorption?

A
  • Arthritis
  • Arthralgia
  • Fever
  • LAD
  • Neuro, Cardiac, or Pulmonary disease
86
Q

Which icosahedral virus w/ a SS-RNA genome is a common cause of gastroenteritis worldwide and severe diarrhea in infants?

A

Norovirus (Caliciviridae family)

87
Q

Local norovirus outbreaks are usually related to what?

Which form of transmission underlies most sporadic cases?

A
  • Contaminated food or water
  • Person-to-person transmission underlies most sporadic cases
88
Q

Where is infectious spread of Norovirus commonly seen?

A
  • Schools, hospitals, and nursing homes
  • Common on cruise ships
89
Q

Norovirus infection is a significant problem in which patient population?

Leads to what problems?

A
  • Immunocompromised (i.e., transplants, tx for GVHD, or HSC transplants)
  • Can have 9 months of persistent diarrhea –> malnutrition and dehydr.
  • Increased morbidity of underlying conditions
90
Q

What type of Virus is Rotavirus?

A

Encapsulated w/ segmented DS-RNA gnoma

91
Q

Which patient population is most vulnerable to infection by Rotavirus?

A

Children between ages 6 -24 months

92
Q

What type of vaccine exists for Rotavirus?

Who is it contraindicated in?

Has been associated w/ what adverse effect?

A
  • Live-attenuated
  • Containdicated in pts w/ immunodeficiency
  • Vaccine has been associated with intussusception
93
Q

Rotavirus selectively infects and destroys what?

Mediated by which viral factor?

A
  • Mature enterocytes of the small intestine, villus surface is repopulated by immature secretory cells
  • Mediated by NSP4, which can induce epithelial apoptosis
94
Q

The epithelial damage caused by Rotavirus leads to a loss of which function?

Contributes to the symptoms of infection how?

A
  • Loss of absorptive function
  • Net secretion of H2O + electrolytes w/ osmotic diarrhea which is 2’ to malabsorption
95
Q

Adenovirus is a common cause of which GI dysfunction and in which population?

A

Pediatric diarrhea

96
Q

Small intestinal biopsies of Adenovirus infection show which intestinal changes?

A

Non-specific villous atrophy + compensatory crypt hyperplasia

97
Q

What are 2 common nematodes (round worms) which cause parasitic enterocolitis?

A

1) Ascaris lumbricoids
2) Strongyloides

98
Q

Upon Ascaris lumbricoides return to the small intestine to mature into adult worm, what reaction may induced?

May manifest clinically how?

A
  • Eosinophilic reaction
  • Physical obstruction of intestine or biliary tree
  • Larvae can also form hepatic abscesses and causes Ascaris pneumonitis
99
Q

How does Strongyloides cause infection?

A

Penetrates unbroken skin –> migrate thru lungs –> reside in small intestine where they mature

100
Q

What is unique of Strongyloides life-cycle and because of this infection in which population may pose a serious problem?

A
  • Do NOT require ova or larval stage outside human and the eggs can hatch within intestine
  • Release larvae that penetrate mucosa and cause an autoinfection, hence, infection can persist for life
  • Immunosuppressed can develop overwhelming autoinfection
101
Q

Stronglyloides infection incites a strong ________ reaction and induces _________ eosinophilia

A

Stronglyloides infection incites a strong tissue reaction and induces peripheral eosinophilia

102
Q

Necator duodenale and Ancylostoma duodenale are what type of parasite?

A

Hookworms

103
Q

Necator duodenale and Ancylostoma duodenale get into the GI tract how?

Do what in the duodenum?

A
  • Larva penetrate skin –> systemic cir. –> lungs –> coughed –> swallowed
  • In duodenum worms attach to mucosa, suck blood, and reproduce
104
Q

What do Necator duodenale and Ancylostoma duodenale in the duodenum cause?

Chronic infection can lead to what deficiency?

Diagnosed how?

A
  • Multiple superficial erosions + Focal hemorrhage + Inflammatory infiltrates
  • Iron deficiency anemia (chronic infection)
  • Diagnosed via eggs in fecal smears
105
Q

Enterobius vermicularis is what type of parasite?

A

Pinworm

106
Q

How do the symptoms produced by Enterobius vermicularis lead to infection?

A
  • Adult worms in intestine migrate to anus at night, deposit eggs on perirectal mucosa
  • Eggs cause intense irritation/itching –> contamination of fingers –> human-to-human transmission via fecal-oral route
107
Q

Diagnosis of Enterobius Vermicularis?

A

Scotch tape test

108
Q

Schistosomiasis is a disease of the intestines most commonly taking what form?

Symptoms are caused by?

What are 2 possible symptoms?

A
  • Most commonlytakes form ofadult wormsresiding inmesenteric vs.
  • Sx’s: trapping of eggs in mucosa and submucosa –> granulomatous immune rxn –> bleeding and even obstruction
109
Q

What are the 3 primary species of intestinal cestodes that infect humans?

Which tapeworm does each represent?

A

1) Diphyllobothrium latum –> fish tapeworm
2) Taenia solium –> pork tapeworm
3) Hymenolepis nana –> dwarf tapeworm

110
Q

Which intestinal cestode can occasionally cause B12 deficiency and megaloblastic anemia due to it competing for host dietary B12?

A

Diphyllobothrium latum = fish tapeworm

111
Q

What is the route of transmission for Entamoba histolytica and is most often seen in what countries?

A
  • Fecal-oral
  • Mexico, India, and Columbia
112
Q

Once the cysts of E. histolytica are ingested what occurs in the body?

A

Chitin wall allows resistance to gastric acid –> colonize epi. surface of the colon and release trophozoites

113
Q

Which parts of colon most often affected by E. histolytica?

A
  • Cecum and ascending colon = most often
  • Sigmoid, rectum, and appendix can also be affected
114
Q

What does E. histolytica do in the colon?

Which characteristic ulcer may be seen?

A

Attach to colonic epithelium, induce apoptosis, invade crypts and burrow laterally into LP –> recruits neutrophils = tissue damage –> flask shaped ulcer

115
Q

Somtimes E. histolytica may penetrate which vessles and embolize to which organ?

Causing what?

A
  • Splanchnic vessels –> liver –> producing an abscess
  • Abscess may exceed 10 cm in diameter w/ shaggy fibrin lining
116
Q

Pts w/ E. histolytica infection present with what symptoms?

What are some complications which may occur in some?

A
  • Abdominal pain, bloody diarrhea, and/or weight loss
  • Acute necrotizing colitis and megacolon may occur
117
Q

Where is Giardia lamblia infection endemic, due to cysts being resistant to what?

A
  • Endemic in unfiltered public water supplies
  • Cysts resistant to chlorine
118
Q

Giardia lamblia cause what type of damage/problems in the GI tract?

A
  • Decreased expression of brush-border enzymes (i.e., lactase)
  • Microvillous damage and apoptosis of SI epithelial cells
  • DO NOT invade
119
Q

Which immune system components are important for the clearance of Giardia infection?

A
  • Secretory IgA
  • IL-6
120
Q

Patients with what underlying disorders are often severely affected by Giardia lamblia?

A
  • Immunosuppressed
  • Agammaglobulinemia
  • Malnourished
121
Q

How is Giardia able to evade immune detection?

A

Continous mods of the major surface Ag -> Variant Surface Protein

122
Q

Which characteristic features allow for identification of Giardia when looking at duodenal biopsies?

A
  • Characteristic pear shape
  • Presence of two equally sized nuclei
123
Q

Infection by Giardia is usually detected with what method and samples from where?

A

Immunofluorescent detection of cysts in stool samples

124
Q

Cryptosporidium are most commonly transmitted how?

Oocysts are resistant to?

A
  • Contaminated drinking water
  • Resistant to chlorine
125
Q

Where in the world is Cryptosporidium found, what is the exception?

A
  • Found worldwide
  • Exception is Antartica, because oocysts are killed by freezing
126
Q

Describe how ingested oocysts of Cryptosporidium are able to get into the small intestine?

A
  • Oocyst releases sporozoites following activation of proteases by H+ (stomach)
  • Sporozoites = motile –> special organelle for attaching to brush border and causes eneterocyte cytoskeleton changes
  • Cause enterocyte to engulf the parasite; takes up residence in endocytic vacuole within microvilli
127
Q

Presence of Cryptosporidium within an endocytic vacuole of microvilli leads to what?

Net effect?

A
  • Sodium malabsorption + Chloride secretion
  • Increased tight junction permeability

Net effect = non-bloody, water diarrhea

128
Q

Although the sporozoite is intracellular, how does it appear using light microscopy?

A

Appears to sit on top of epithelial apical membrane

129
Q

Where are the largest concentration of Cryptosporidium found in the GI?

Diagnosed how?

A
  • Terminal ileum and Prox. Colon
  • Diagnosed based on oocysts in stool!
130
Q

How is the diganosis of the intestinal cestodes (tapeworms) made?

A

Proglottids and eggs in the stool

2. GI II Flashcards (12 decks)

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