1
Q
What is the morphology of Vibrio cholerae?
A
Comma-shaped; gram (-) bacteria
2
Q
What is the reservoir and mode of transmission for Vibrio cholerae?
A
Reservoir = shellfish
MOT = fecal-oral; water
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
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
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
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
7
Q
What is the most common bacterial enteric pathogen in developed countries and important cause of traveler’s diarrhea?
A
Campylobacter jejuni
8
Q
What are the 4 major properties contributing to the virulence of Campylobacter jejuni?
A
- Motility - flagella
- Adherence
- Toxin production - cytotoxin + cholera toxin-like enterotoxin
- Invasion
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
10
Q
What is the association of Campylobacter infection and HLA-B27?
A
Can result in reactive arthritis
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
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)
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)
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
15
Q
Shigella is one of the most common causes of?
A
Dysentery (blood diarrhea)
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
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
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
19
Q
All Shigella spp. carry which virulence plasmids allowing for direct injeciton of bacterial proteins into host cytoplasm?
A
Type III secretion system
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
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
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
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
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)
25
Which treatment is indicated and which is contraindicated in patients w/ *Shigella* infection?
- **Antibiotics** may shorten clinical course
- **Antidiarrheals** = **CONTRAINDICATED** --\> prolong sx's and delay clearance
26
Salmonellosis is usually due to which type of *Salmonella**?*
*Salmonella enteritidis*
27
Salmonella infection is most commonly transmitted how?
Which age groups most affected?
Which time of year do infections peak?
- Meat, poultry, and eggs/milk
- Young children **and** Older adults
- Peak incidence in **fall** and **summer**
28
What are predispositions for the development of Salmonella infection?
1. **Atrophic gastritis** or on **acid-suppressive therapy** (**PPIs**)
2. Genetic **defects** in **TH17 --\> Disseminated salmonellosis**
29
Which virulence factor allows for *Salmonella* invade and infect humans?
Explain the pathogenesis of invasion.
- **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**
30
What do the flagellin and LPS of *Salmonella* activate inside humans are what does this result in?
- **Flagellin** --\> **TLR5** --\> Increased inflammtory response
- **LPS** --\> **TLR4**
31
How do *Salmonella* indirectly cause increased neutrophils and potentiate mucosal damage?
Secrete molecule **inducing epithelial cells** to release **eicosanoid hepoxilin A3**
32
Which immune cells limit infection by *Salmonella?*
**TH1 and TH17**
33
What is essential for the diagnosis of *Salmonella* infection?
Stool culture (+)
34
Typhoid fever (enteric fever) is caused by which organism and its 2 subtypes?
Which subtype is associated with endemic countries and which with travelers?
- *Salmonella enterica*
- Subtypes:
* - Typhi* (endemic countries)
* - Paratyphi* (travelers)
35
What is the reservoir for *Salmonella enterica?*
Mode of transmission?
- Humans = reservoir
- MOT = fecal-oral and water
36
Typhoid fever (*Salmonella enterica)* is strongly associated with travel to which countries?
India, Mexico, Philippines, Pakistan, El Salvador, and Haiti
37
Gallbladder colonization by *S. typhi or S. paratyphi* is associated with?
- Gallstones
- Chronic carrier state
38
Explain the pathogeneis of *S. typhi* infection (i.e., how do they invade?)
- **S****urvive in gastric acid**--\> small intestine --\> taken up by**M 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
39
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?
- **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**
40
What are the phases of Typhoid Fever and symptoms involved in each?
- 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**
41
Are antibiotics recommended for Typhoid Fever?
Yes, can prevent further disease progression
42
In patients with Typhoid Fever, not treated w/ antibiotics what additional signs and symptoms may develop?
- Sustained high fevers
- Abdominal tenderness which may **mimic appendicits**
- **Rose spots** = erythematous maculopapular lesions on chest and abd.
43
Systemic dissemination of *S. typhi* may lead to what complications?
- Encephalopathy
- Meningitis
- Seizures
- Endocarditis
- Myocarditis
- Pneumonia
- **Cholecystitis**
44
Which patient population is particularly susceptible to developing *Salmonella* osteomyelitis?
Sickle cell disease pts
45
Which 2 types of *Yersiniai* cause GI disease?
Which is more common?
1) *Yersinia enterocolitica* = **more common**
2) *Yersinia pseudotuberculosis*
46
Where are *Yersinia* infections most common?
Mode of transmission?
Time of year infections are most common?
- Europe
- Pork, milk, water
- More common in **winter**
47
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?
- 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
48
Which predisposition by some patients increases the chance of developing sepsis and death when infected by *Yersinia?*
- Pts w/ **increased non-heme iron**
- Such as certain **chronic anemias** or **hemochromatosis**
49
*Yersinia* infections preferentially involve which parts of the GI?
Ileum, appendix, and right colon
50
What are some of the characteristic morpho, histo, and gross changes associated with *Yersinia* infection?
Predominant immune infiltrate?
- Regional LN and Peyer patch **hyperplasia**
- Bowel wall thickening
- Mucosa overlying lymph tissue --\> **hemorrhagic**, apthous-like erosions, and ulcers
- **Neutrophils** and **granulomas**
51
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?
Acute appendicits
52
What are common extraintestinal symptoms of *Yersinia* infection?
- Pharyngitis
- Arthralgia
- Erythema nodosum
53
What are some of the postinfectious complications associated with*Yersinia?*
- Reactive arthritis, Urethritis, Conjunctivitis (like *Shigella)*
- Myocarditis
- Erythema nodosum (like *Campylobacter)*
- Kidney disease
54
Which subgroup of *E. coli* is the principal cause of traveler's diarrhea and spreads via contaminated water/food?
**Enterotoxigenic E. Coli (ETEC)**
55
Which age group is particularly susceptible to infection by ETEC?
Children \<2 yo in developing countries
56
What are the 2 main toxins of ETEC and what is the MOA of each?
Net effect of these toxins?
- **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
What is the clinical manifestations (signs/symptoms) of ETEC infection?
- Secretory, **non**inflammatory diarrhea --\> dehydration
- Severe cases = shock
58
Which subtype of E. coli is an important cause of **endemic diarrhea** as well as diarrheal outbreaks in children \<2 yo?
**Enteropathogenic E. Coli (EPEC)**
59
EPEC are characterized by their ability to produce what type of lesion?
Describe this lesion
- (**A/E**) lesions = attaching and effacing
- Attach tightly to **enterocyte apical membranes**
- Cause local loss --\> **effacement** of the **microvilli**
60
The proteins necessary for creating the A/E lesions seen w/ EPEC infections are encoded by which pathogenicity island?
What are the proteins encoded?
- 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
Which bacterial protein encoded by the *espE gene* is used for molecular detection and diagnosis of EPEC infection?
Intimin
62
How is Enterohemorrhagic E. Coli (EHEC) categorized?
- **O157:H7**
- **non-O157:H7**
63
What is the reservoir for EHEC and is transmitted how?
- **Cows** = reservoir
- Transmitted via consumption of **undercooked beef**, also **milk** and **vegetables**
64
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?
- Shiga-like toxin --\> Sx's similar to *S. dysenteriae* infection
- O157:H7 more likely to cause **large outbreaks**
65
What are the symptoms and complications of EHEC infection, especially by the O157:H7 serotype?
- Bloody diarrhea
- Hemolytic uremic syndrome (**HUS**)
- Ischemic colitis
66
Are antibiotics recommended for treatment of EHEC; why or why not?
- No!
- Cause **increased release of Shiga toxin** --\> enhancing risk for **HUS**, especially in **children**
67
Which E. Coli subtype is bacteriologically similar to Shigella and is transmitted via food, water, or by person-to-person contact?
Enteroinvasive E. Coli (EIEC)
68
What toxins are produced by EIEC and what is the clinical course of infection?
- Do **not** produce toxins
- Invade epithelial cells and cause non-specific features of **acute self-limited colitis**
69
Enteroaggregative E. Coli (EAEC) were identified on the basis of their unique what?
Unique pattern of **adherence** to **epithelial cells**
70
How does EAEC uniquely attach to enterocytes, which virulence factors are used?
- Via adherence **fimbriae** and are aided by **dispersin**
- **Dispersin** is a surface protein which **neutralizes the negative surface charge of LPS**
71
Which toxins are produced by EAEC organisms?
- Enterotoxin **related to *Shigella* enterotoxin**
- ETEC ST toxin (**heat-stable toxin**)
72
What are the clinical manifestations of EAEC infection and which popluation most often affected?
- Non-bloody diarrhea (traveler's)
- Children/adults in both developing + developed countries
- Diarrhea may be prolonged in immunodeficient pt
73
Which organism is responsible for Pseudomembranous Colitis?
*C. difficile*
74
Which factor most likely contributes to bacterial overgrowth by *C. difficile?*
Toxins released by this organism cause what?
- 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
Crypts w/ **mucopurulent exudate of neutrophils** that forms **eruption reminiscent of a volcano** is characteristic of what infection?
*C. difficile ---\>* pseudomembranous colitis
76
Diagnosis of *C. difficile-*associated colitis is usually accomplished how?
Detection of ***C. difficile* toxin** in stool and supported by histopathology
77
What is a major challenge in *C. difficile-associated* colitis and a complication which may arise?
- **Recurrent infection** is common
- **Toxic megacolon** may occur
78
Which rare disease, was first described as **intestinal lipodystrophy**?
Whipple Disease
79
How does lymphatic obstruction occur in Whipple Disease?
Leads to what?
- Organism-laden MØ's **accumulate** within **SI lamina propria** and **Mesenteric LN's**
- Malabsorptive diarrhea
80
Postmortem examination of someone with Whipple Disease will show what histological characteristics?
Gross characteristics?
**- 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
Which stain is used the visualize macrophages in Whipple Disease?
How can it be differentiated from the similar looking intestinal tuberculosis?
- PAS
- Used **acid-fast** to differentiate because *T. whippelii* will not stain, while mycobacteria will stain (+)
82
In Whipple disease, bacteria-laden macrophages can accumulate where?
- Mesenteric LNs (malabsorption)
- Synovial membranes (arthritis)
- Cardiac valves
- Brain (CNS disease)
83
Whipple disease most commonly affects who?
**Caucasian** men, particularly **farmers** and those w/ occupational exposure to soil or animals
84
What is the clinial triad of sx's associated w/ Whipple disease?
1) Diarrhea
2) Weight loss
3) Arthralgia
85
Which extraintestinal symptoms of Whipple disease may persist for months or years before malabsorption?
- Arthritis
- Arthralgia
- Fever
- LAD
- Neuro, Cardiac, or Pulmonary disease
86
Which icosahedral virus w/ a SS-RNA genome is a common cause of gastroenteritis worldwide and severe diarrhea in infants?
Norovirus (Caliciviridae family)
87
Local norovirus outbreaks are usually related to what?
Which form of transmission underlies most sporadic cases?
- Contaminated food or water
- Person-to-person transmission underlies most sporadic cases
88
Where is infectious spread of Norovirus commonly seen?
- Schools, hospitals, and nursing homes
- Common on **cruise ships**
89
Norovirus infection is a significant problem in which patient population?
Leads to what problems?
- **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
What type of Virus is Rotavirus?
**Encapsulated** w/ segmented **DS-RNA gnoma**
91
Which patient population is most vulnerable to infection by Rotavirus?
Children between ages **6 -24 months**
92
What type of vaccine exists for Rotavirus?
Who is it contraindicated in?
Has been associated w/ what adverse effect?
- Live-attenuated
- Containdicated in pts w/ **immunodeficiency**
- Vaccine has been associated with **intussusception**
93
Rotavirus selectively infects and destroys what?
Mediated by which viral factor?
- **Mature enterocytes** of the **small intestine**, **villus surface** is repopulated by **immature secretory cells**
- Mediated by **NSP4**, which can induce **epithelial apoptosis**
94
The epithelial damage caused by Rotavirus leads to a loss of which function?
Contributes to the symptoms of infection how?
- Loss of absorptive function
- Net secretion of **H2O + electrolytes** w/ **osmotic diarrhea** which is **2' to malabsorption**
95
Adenovirus is a common cause of which GI dysfunction and in which population?
Pediatric diarrhea
96
Small intestinal biopsies of Adenovirus infection show which intestinal changes?
Non-specific **villous atrophy** + **compensatory crypt hyperplasia**
97
What are 2 common nematodes (round worms) which cause parasitic enterocolitis?
1) Ascaris lumbricoids
2) Strongyloides
98
Upon *Ascaris lumbricoides* return to the small intestine to mature into adult worm, what reaction may induced?
May manifest clinically how?
- Eosinophilic reaction
- Physical obstruction of **intestine** or **biliary tree**
- Larvae can also form **hepatic abscesses** and causes ***Ascaris*** pneumonitis
99
How does *Strongyloides* cause infection?
Penetrates unbroken skin --\> migrate thru lungs --\> reside in small intestine where they mature
100
What is unique of *Strongyloides* life-cycle and because of this infection in which population may pose a serious problem?
- 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
*Stronglyloides* infection incites a strong ________ reaction and induces _________ eosinophilia
*Stronglyloides* infection incites a strong **tissue** reaction and induces **peripheral** eosinophilia
102
Necator duodenale and Ancylostoma duodenale are what type of parasite?
Hookworms
103
Necator duodenale and Ancylostoma duodenale get into the GI tract how?
Do what in the duodenum?
- Larva penetrate skin --\> systemic cir. --\> lungs --\> coughed --\> swallowed
- In duodenum worms attach to mucosa, suck blood, and reproduce
104
What do Necator duodenale and Ancylostoma duodenale in the duodenum cause?
Chronic infection can lead to what deficiency?
Diagnosed how?
- Multiple superficial **erosions** + Focal **hemorrhage** + Inflammatory **infiltrates**
- **Iron deficiency anemia** (chronic infection)
- Diagnosed via **eggs in fecal smears**
105
Enterobius vermicularis is what type of parasite?
Pinworm
106
How do the symptoms produced by Enterobius vermicularis lead to infection?
- 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
Diagnosis of Enterobius Vermicularis?
Scotch tape test
108
Schistosomiasis is a disease of the intestines most commonly taking what form?
Symptoms are caused by?
What are 2 possible symptoms?
- **M****ost commonly**takes form of**adult worms**residing in**mesenteric vs.**
- **Sx's:** trapping of eggs in mucosa and submucosa --\> **granulomatous** immune rxn --\> **bleeding** and even **obstruction**
109
What are the 3 primary species of intestinal cestodes that infect humans?
Which tapeworm does each represent?
1) Diphyllobothrium latum --\> **fish tapeworm**
2) Taenia solium --\> **pork tapeworm**
3) Hymenolepis nana --\> **dwarf tapeworm**
110
Which intestinal cestode can occasionally cause **B12 deficiency** and **megaloblastic anemia** due to it competing for host dietary B12?
***Diphyllobothrium latum =*** **fish tapeworm**
111
What is the route of transmission for *Entamoba histolytica* and is most often seen in what countries?
- Fecal-oral
- Mexico, India, and Columbia
112
Once the cysts of *E. histolytica* are ingested what occurs in the body?
**Chitin** wall allows resistance to **gastric acid** --\> colonize **epi.** surface of the **colon** and release **trophozoites**
113
Which parts of colon most often affected by *E. histolytica?*
- Cecum and ascending colon = **most often**
- Sigmoid, rectum, and appendix can also be affected
114
What does *E. histolytica* do in the colon?
Which characteristic ulcer may be seen?
Attach to colonic epithelium, induce apoptosis, invade crypts and burrow laterally into LP --\> recruits neutrophils = tissue damage --\> **flask shaped ulcer**
115
Somtimes *E. histolytica* may penetrate which vessles and embolize to which organ?
Causing what?
- **Splanchnic vessels** --\> **liver** --\> producing an **abscess**
- Abscess may **exceed 10 cm** in diameter w/ **shaggy fibrin lining**
116
Pts w/ *E. histolytica* infection present with what symptoms?
What are some complications which may occur in some?
- Abdominal pain, **bloody diarrhea**, and/or weight loss
- **Acute necrotizing colitis** and **megacolon** may occur
117
Where is *Giardia lamblia* infection endemic, due to cysts being resistant to what?
- **Endemic** in **unfiltered public water supplies**
- Cysts resistant to **chlorine**
118
*Giardia lamblia* cause what type of damage/problems in the GI tract?
- **Decreased** expression of **brush-border enzymes** (i.e., **lactase**)
- **Microvillous damage** and **apoptosis** of **SI epithelial cells**
- DO NOT invade
119
Which immune system components are important for the clearance of *Giardia* infection?
- **Secretory IgA**
- **IL-6**
120
Patients with what underlying disorders are often severely affected by *Giardia lamblia?*
- Immunosuppressed
- Agammaglobulinemia
- Malnourished
121
How is *Giardia* able to evade immune detection?
Continous **mods** of the **major surface Ag -\> Variant Surface Protein**
122
Which characteristic features allow for identification of *Giardia* when looking at duodenal biopsies?
- Characteristic **pear shape**
- Presence of **two equally sized nuclei**
123
Infection by *Giardia* is usually detected with what method and samples from where?
**Immunofluorescent** detection of **cysts** in **stool samples**
124
Cryptosporidium are most commonly transmitted how?
Oocysts are resistant to?
- Contaminated drinking water
- Resistant to **chlorine**
125
Where in the world is Cryptosporidium found, what is the exception?
- Found **worldwide**
- Exception is **Antartica**, because **oocysts** are **killed by freezing**
126
Describe how ingested oocysts of Cryptosporidium are able to get into the small intestine?
- 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
Presence of Cryptosporidium within an endocytic vacuole of microvilli leads to what?
Net effect?
- **Sodium malabsorption** + **Chloride secretion**
- Increased tight junction permeability
Net effect = **non-bloody, water diarrhea**
128
Although the sporozoite is intracellular, how does it appear using light microscopy?
Appears to sit on top of epithelial apical membrane
129
Where are the largest concentration of *Cryptosporidium* found in the GI?
Diagnosed how?
- **Terminal ileum** and **Prox. Colon**
- Diagnosed based on **oocysts in stool!**
130
How is the diganosis of the intestinal cestodes (tapeworms) made?
**Proglottids** and **eggs** in the **stool**
2. GI II Flashcards
flashcards
Decks in class (12)
# Cards
-
Chapter 16: Head and Neck89
-
Chapter 17: Infectious Enterocolitis130
-
Chapter 17: Stomach153
-
Chapter 17: Small Intestine and Colon180
-
Chapter 17: The GI Tract - Congenital Abnormalities and Esophagus86
-
Chapter 19: The Pancreas65
-
Chapter 18: Liver Diseases174
-
Chapter 18: Cholestatic Disease99
-
Chapter 18: Malignant Tumors39
-
Chapter 18: Gall Bladder53
-
Arnce DSA25
-
Immuno of IBD58
