Deja Review - Chapter 48 Gastrointestinal System

Front 1

CHAPTER 48 - Gastrointestinal System

Back 1

CHAPTER 48 - Gastrointestinal System

Front 2

What are the four primary enteric host defenses against pathogens?

Back 2

1. Gastric acid
2. Intestinal motility
3. Normal enteric flora (crowds out pathogenic species)
4. Intestinal immunity (immunoglobulins and Peyer patches)

Front 3

Through what route are almost all gastrointestinal (GI) pathogens taken in?

Back 3

Oral route. However, keep in mind that many diseases that do not have predominant GI symptoms can also be acquired via the fecal-oral route (eg, polio and botulism).

Front 4

BACTERIAL GASTRITIS AND ULCERS

Back 4

BACTERIAL GASTRITIS AND ULCERS

Front 5

What species of bacteria is strongly urease-positive and causes pathology in the stomach?

Back 5

Helicobacter pylori

Front 6

Why is urease important to H. pylori?

Back 6

Urease converts urea to ammonium ion (and CO2) which neutralizes the stomach pH allowing the bacteria to survive.

Front 7

What diseases are associated with H. pylori infection?

Back 7

Gastritis and peptic ulcers

Front 8

Where does H. pylori cause ulcers?

Back 8

In the gastric antrum and the duodenum

Front 9

Pathology Correlate: What are the four histologic zones of a chronic ulcer (superficial to deep)?

Back 9

1. Necrotic tissue
2. Inflammation
3. Granulation tissue
4. Scar tissue at the base

Front 10

Helicobacter pylori infection is a risk factor for what cancers?

Back 10

Gastric carcinoma and mucosal-associated lymphoid tissue (MALT) lymphomas

Front 11

What three methods can be used to diagnose H. pylori infection?

Back 11

1. Serology antibody test
2. Urea breath test in which the radiolabeled CO2 given off by radiolabeled urea is detected
3. Culture of biopsy from endoscopy

Front 12

What is the combination of medications used to treat H. pylori infection?

Back 12

The original treatment regimen includes the triple therapy of bismuth salts, metronidazole, and either ampicillin or tetracycline. The current regimen of choice is a proton pump inhibitor, amoxicillin, and clarithromycin (available as Prevpac).

Front 13

What are the three curved gram-negative rods that cause disease in the GI tract?

Back 13

1. Helicobacter pylori
2. Campylobacter jejuni
3. Vibrio species

Front 14

TOXIGENIC BACTERIAL DIARRHEA

Back 14

TOXIGENIC BACTERIAL DIARRHEA

Front 15

Which two species of bacteria are the main culprits for diarrhea caused by preformed toxins?

Back 15

1. Staphylococcus aureus
2. Bacillus cereus

Front 16

Which five bacteria are the main culprits for bacterial diarrhea caused by toxin production in vivo?

Back 16

1. Clostridium perfringens
2. Clostridium difficile
3. Bacillus cereus (produces toxins both in vivo and preformed)
4. Enterotoxigenic Escherichia coli (ETEC)
5. Vibrio cholerae

Front 17

What are the stool findings for diarrhea caused by toxigenic bacteria?

Back 17

Generally unremarkable, no white blood cells (WBCs) or red blood cells (RBCs) (except C. difficile, stool may contain cytotoxin)

Front 18

What are the signs and symptoms of diarrhea caused by preformed bacterial toxins?

Back 18

Early-onset diarrhea (6 hours), more vomiting than diarrhea, illness of short duration (12 hours), and no fever

Front 19

What are the signs and symptoms of diarrhea caused by bacterial toxin production in vivo?

Back 19

Later-onset (12-24 hours), abdominal cramping, watery diarrhea. With the exception of E. coli, the symptoms typically resolve within 24 hours; E. coli symptoms last up to 5 days.

Front 20

Which gram-positive coccus causes watery diarrhea via a superantigen enterotoxin that is acid-stable?

Back 20

Staphylococcus aureus (symptom of vomiting is usually more prominent than diarrhea). Note that since the bacterium is acid-stable, it is not deactivated by gastric acid.

Front 21

Can the S. aureus toxin be deactivated by boiling?

Back 21

Yes, but the toxin is fairly resistant to heat so boiling must take place greater than 10 minutes at 60°C.

Front 22

Which gram-positive rod causes diarrhea via two enterotoxins, one that is heat-stable and one that resembles cholera toxin?

Back 22

Bacillus cereus

Front 23

What is the mechanism of action for the two toxins of B. cereus?

Back 23

The toxin adenosine diphosphate (ADP)-ribosylates a G protein, stimulating adenylate cyclase and resulting in an increased cyclic adenosine monophosphate (cAMP) level in the enterocyte. The other toxin is a superantigen similar to S. aureus in action.

Front 24

Of the two enterotoxins produced by B. cereus, which one is produced in vivo and which one is preformed?

Back 24

The cholera-like toxin is produced in vivo while the superantigen enterotoxin is preformed.

Front 25

Why does B. cereus survive boiling of food while S. aureus does not?

Back 25

Bacillus cereus produces heat-resistant spores; S. aureus does not produce spores.

Front 26

What organism produces a watery diarrhea with classic findings of rice-water stool and a remarkable amount of fluid loss (7-8 L/d)?

Back 26

Vibrio cholerae

Front 27

What two things must occur in order for V. cholerae to cause disease?

Back 27

1. The bacteria must colonize the small intestine.
2. Bacteria must secrete enterotoxin.

Front 28

Does V. cholerae have a high or low ID50?

Back 28

High. Vibrio cholerae is sensitive to gastric acid so approximately 10 organisms are required for the bacteria to colonize the small intestine, unless the patient is on antacids.

Front 29

What is the reservoir for V. cholerae infection?

Back 29

Contaminated water and food from contaminated water (eg, seafood)

Front 30

Is V. cholerae gram-positive or gram-negative? Is it a rod, coccus, or spirochete?

Back 30

Gram-negative rod but it looks comma shaped. So do not be fooled, it is not a spirochete.

Front 31

What do the two subunits, A (active) and B (binding), in the cholera enterotoxin do?

Back 31

The B subunit binds to a ganglioside receptor on the enterocyte. After binding of the B subunit, the A subunit can then be inserted into the cytosol where it irreversibly activates glomerulosclerosis (Gs) protein through ADP-ribosylation.

Front 32

What happens after cholera toxin activates Gs protein?

Back 32

The active Gs protein causes increased stimulation of membrane-bound adenylate cyclase, which in turn results in increased production of cAMP. cAMP then leads to active secretion of chloride and inhibits absorption of sodium. This creates an osmotic force, resulting in a massive loss of water into the intestinal lumen.

Front 33

What does the CTXφ virus have to do with V. cholerae?

Back 33

The CTXφ virus is a bacteriophage that encodes the cholera enterotoxin. Cholera acquires the toxin through lysogenic conversion.

Front 34

What are the signs and symptoms associated with cholera?

Back 34

Because of massive volume loss and electrolyte abnormalities, patients exhibit hypotension, acidosis (from losing HCO-3), hypokalemia, hyponatremia, and possibly a dilutional hypernatremia from fluid loss. Acute tubular necrosis can eventually ensue and lead to death. Mortality is 40% untreated.

Front 35

What is the treatment for cholera?

Back 35

Intravenous (IV) or oral fluid replacement is imperative as rate of fluid loss is almost as dramatic as exsanguination. Antibiotics are not necessary, but tetracycline or quinolones can reduce the duration of diarrhea.

Front 36

What preventive measures exist against cholera?

Back 36

Public health measures are important (eg, sanitation); vaccination is only 50% effective for 3 to 6 months and it does not prevent transmission; antibiotics are not effective in preventing epidemics.

Front 37

Do patients acquire immunity to cholera after infection?

Back 37

Yes. Prior infection induces a secretory immunoglobulin A (IgA) antibody.

Front 38

What is the most common cause of diarrhea in hospitalized patients and a commonly pimped pathogen responsible for diarrhea on hospital rounds?

Back 38

Clostridium difficile

Front 39

What is the classic finding on the colonic mucosa associated with diarrhea caused by C. difficile?

Back 39

Pseudomembranes, hence the disease is called pseudomembranous colitis

Front 40

Considering that C. difficile is carried in the GI tract of 3% of normal people, what is the usual underlying cause of diarrhea?

Back 40

Antibiotics kill the natural flora of the gut allowing an overgrowth of C. difficile. However, C. difficile is mainly a nosocomial infection.

Front 41

What antibiotic is classically associated with pseudomembranous colitis?

Back 41

Clindamycin is classically associated with pseudomembranous colitis.

Front 42

What is the most common antibiotic that causes pseudomembranous colitis?

Back 42

Cephalosporins are the most common cause of C. difficile pseudomembranous colitis because they are used much more frequently than clindamycin.

Front 43

What is the treatment for pseudomembranous colitis?

Back 43

Stop the offending antibiotic causing diarrhea and treat the C. difficile infection with oral metronidazole or vancomycin. Metronidazole is preferred due to concern over the emergence of vancomycin-resistant enterococci (VRE).

Front 44

What species of bacteria causes both gas gangrene and food poisoning?

Back 44

Clostridium perfringens

Front 45

What is the mechanism of action of the C. perfringens enterotoxin?

Back 45

It is a superantigen similar to staphylococcal enterotoxin.

Front 46

What protective characteristic of the bacteria makes them heat resistant?

Back 46

Clostridium perfringens produces heat-resistant spores.

Front 47

What is the laboratory diagnosis for diarrhea caused by C. perfringens?

Back 47

There is none. Be careful not to confuse this with gas gangrene which is caused by the same bacteria. In the case of gas gangrene, tissue samples can be cultured on blood agar to yield double zone hemolysis or they can be cultured on egg yolk agar to show clearing. Stool cultures do not show C. perfringens diarrheal infection.

Front 48

Which gram-negative rod is the principal cause of diarrheal illness in travelers and exists in more than 1000 different antigenic strains?

Back 48

Enterotoxigenic E. coli (ETEC)

Front 49

What two virulence factors must be present in order for ETEC to cause disease?

Back 49

1. Pili (allow attachment of bacteria to mucosal surfaces in jejunum and ileum)
2. Enterotoxins

If only one of these virulence factors is present, then the bacteria will not cause disease.

Front 50

What are the two main types of toxins produced by ETEC and what are their mechanisms of action?

Back 50

1. Heat-labile toxin (LT), which acts through a mechanism similar to cholera toxin (activates adenylate cyclase)
2. Heat-stable toxin (ST), which causes diarrhea by activating guanylate cyclase

Front 51

What type of agar is E. coli grown on?

Back 51

MacConkey agar yielding pink colonies (lactose fermenting). Note that not all E. coli are lactose fermenting (eg, genetic recombination often uses E. coli that cannot ferment lactose).

Front 52

What is the treatment for ETEC-associated diarrhea?

Back 52

As with most watery diarrheas, fluid replacement is most important, but antibiotics shorten the duration of illness (typically fluoroquinolones or trimethoprim-sulfamethoxazole [TMP-SMX]).

Front 53

INVASIVE BACTERIAL DIARRHEA

Back 53

INVASIVE BACTERIAL DIARRHEA

Front 54

What is the classic symptom of diarrhea caused by organisms that invade the enteric mucosa?

Back 54

Bloody diarrhea

Front 55

What are the four main bacterial causes of bloody diarrhea?

Back 55

1. Shigella
2. Salmonella
3. Campylobacter
4. Escherichia coli O157:H7

Front 56

Of the four major causes of invasive diarrhea, which two do not ferment lactose?

Back 56

1. Shigella
2. Salmonella

Front 57

What are some other bacteria that can cause a bloody diarrhea?

Back 57

Yersinia enterocolitica, Vibrio parahaemolyticus, enteroinvasive E. coli (EIEC), C. difficile, Bacillus anthmcis (rare)

Front 58

What does methylene blue staining indicate?

Back 58

Leukocytes are present in the stool. This indicates an invasive organism (Shigella, Salmonella, Campylobacter, E. coli O157:H7) and not one of the toxin-producing organisms (except C. difficile).

Front 59

Which curved gram-negative rod causes a bloody diarrhea and is associated with Guillain-Barre syndrome?

Back 59

Campylobacter jejuni

Front 60

Which is the most common cause of diarrhea worldwide: Shigella, Salmonella, or Campylobacter?

Back 60

Campylobacter

Front 61

What is the reservoir for C. jejuni?

Back 61

Domestic animals such as dogs, cattle, and chickens

Front 62

What is the clinical course of the disease?

Back 62

Usually causes enterocolitis with initial watery stools, then lower abdominal pain, bloody mucopurulent diarrhea, and fever. Symptoms usually resolve in 7 days.

Front 63

What autoimmune diseases can develop subsequent to GI infection with Campylobacter?

Back 63

Guillain-Barre syndrome, Reiter syndrome, reactive arthritis

Front 64

How is a laboratory diagnosis made?

Back 64

Campylobacter jejuni must be grown under special conditions to select it. Namely, a blood agar and antibiotic coupled with a temperature of 42°C and an atmosphere of 10% CO2 and 5% O2

Front 65

What is the treatment for C. jejuni diarrhea?

Back 65

Ciprofloxacin or erythromycin can both be given to shorten the duration of symptoms and to prevent the spread of disease to others.

Front 66

Does Shigella have a high or low ID50?

Back 66

Very low. Just hundred organisms can cause disease.

Front 67

What is the animal reservoir for Shigella?

Back 67

None, it only infects humans.

Front 68

Does Shigella cause disease through toxin production or enteroinvasion of the mucosa?

Back 68

Through invasion of the mucosa. Mutated strains without the Shiga toxin still cause disease, but mutated strains that cannot invade do not cause disease.

Front 69

What is the clinical course of the disease?

Back 69

Incubation period of 1 to 3 days, followed by abdominal cramping, fevers, and watery diarrhea for the next 1 to 2 days. Then bloody mucus stools of low volume with rectal urgency and tenesmus with symptoms resolving after a week

Front 70

Does everyone with shigellosis get grossly bloody diarrhea?

Back 70

No, only 40% get gross blood; patients with Shigella dysenteriae are more likely to have severe disease than patient with Shigella sonnei or other Shigella species.

Front 71

What is the treatment for shigellosis?

Back 71

For mild disease, antibiotics are given more to prevent the spread of the bug than to treat the disease. For severe cases, fluoroquinolones or TMP-SMX is given. As always with diarrhea, fluid replacement is essential.

Front 72

Which species of bacteria that produces a bloody diarrhea can be distinguished from Shigella by their ability to produce H2S?

Back 72

Salmonella

Front 73

Is the ID50 for Salmonella higher or lower than Shigella?

Back 73

Much higher. Approximately 100,000 organisms are required. The organism is susceptible to gastric acid, so patients on antacid and/or with a gastrectomy are more susceptible to infection.

Front 74

What are the three clinical syndromes that Salmonella can cause?

Back 74

1. Salmonella enterocolitis
2. Salmonella bacteremia
3. Typhoid fever (do not confuse typhoid fever with typhus)

Note that while Salmonella enterocolitis is the only syndrome that affects the GI system primarily, the intestine is the portal of entry in all three cases.

Front 75

What is the mode of transmission for Salmonella?

Back 75

Domestic pets, poultry, and human being S. Salmonella typhi is only transmitted by human beings.

Front 76

What is the clinical course of Salmonella enterocolitis?

Back 76

Fever, abdominal cramps, bloody or watery diarrhea. Eighty percent of patients will have fecal leukocytes. Symptoms usually resolve within 7 days, though stool cultures can be positive for more than 2 months in 5% to 10% of patients.

Front 77

What is the treatment for Salmonella enterocolitis?

Back 77

Primarily fluid and electrolyte replacement. Antibiotics should generally be avoided as they do not reduce symptoms or duration of disease and may even prolong excretion of organisms and encourage carrier state. So ciprofloxacin, chloramphenicol, ampicillin, and TMP-SMX are given only to neonates, patients with chronic disease, atherosclerosis, or immunocompromised.

Front 78

What organism in particular causes typhoid fever?

Back 78

Salmonella typhi

Front 79

At what histologic site does S. typhi replicate during intestinal invasion?

Back 79

Within the macrophages concentrated at Peyer patches. This causes hypertrophy and eventual necrosis leading to severe abdominal pain and subsequent ileal perforation.

Front 80

What is the pathogenesis of typhoid fever during primary bacteremia?

Back 80

After 5 to 7 days of replication in the Peyer patches, the S. typhi seeds into the reticuloendothelial system (liver, bone marrow, spleen) through the lymphatic system and blood stream. They continue to undergo intracellular replication.

Front 81

What happens during secondary bacteremia?

Back 81

Salmonella typhi returns to the bowel through roundabout means. After 3 to 5 days of primary bacteremia, infection is established in the gallbladder where the chronic carrier state can persist. Salmonella typhi can silently shed from the biliary tract into the intestine (eg, Typhoid Mary).

Front 82

What are the symptoms during the stage of intestinal invasion?

Back 82

Few symptoms. Mild abdominal pain and sometimes constipation or diarrhea

Front 83

What are the symptoms during primary bacteremia?

Back 83

Fever and rose spots on skin of abdomen. Once seeding takes hold in the reticuloendothelial system (RES), patients have hepatosplenomegaly.

Front 84

What are rose spots?

Back 84

Erythematous macular skin lesions characteristic of S. typhi infections

Front 85

What are the signs and symptoms during secondary bacteremia?

Back 85

Fever/pulse dissociation (high fever with a slow pulse), leukopenia, thrombocytopenia, slightly elevated liver function tests (LFTs)

Front 86

What are the symptoms in chronic carriers?

Back 86

Usually none, but these patients are a public health concern as they are reservoirs for infection.

Front 87

At what stages is the blood culture positive and at what stages is the stool culture positive?

Back 87

Blood cultures are positive during secondary bacteremia. The stool culture can be transiently positive during intestinal invasion but is always positive in chronic carriers.

Front 88

What is the treatment for acute typhoid fever?

Back 88

Fluoroquinolones or third-generation cephalosporin or azithromycin in patients with acute disease

Front 89

What is the treatment for chronic carriers?

Back 89

Long-term (6 weeks) high-dose ciprofloxacin works 80% of the time in patients without gallstones but only 25% of the time in patients with gallstones. Patients who fail therapy require a cholecystectomy.

Front 90

Which gram-negative rod has strains of bacteria that can produce both a watery diarrhea and a bloody diarrhea? The bloody diarrhea variant is the bane of fast food beef.

Back 90

Escherichia coli

Front 91

What specific E. coli strain produces enterohemorrhagic diarrhea?

Back 91

Escherichia coli O157:H7 (EHEC)

Front 92

Why does E. coli O157:H7 produce bloody diarrhea while other strains of E. coli do not?

Back 92

Probably because the O157:H7 strain has a verotoxin that kills cells of the gut mucosa

Front 93

How does E. coli O157:H7 acquire the verotoxin?

Back 93

Through lysogenic conversion

Front 94

In laboratory diagnosis, how is E. coli O157:H7 distinguished from other E. coli strains?

Back 94

It does not ferment sorbitol.

Front 95

Should antibiotics be used in the treatment of diarrhea caused by E. coli O157:H7?

Back 95

No. Treating with antibiotics predisposes to hemolytic-uremic syndrome (HUS) which is potentially life threatening.

Front 96

What is HUS?

Back 96

Acute kidney failure, hemolytic anemia, microvascular coagulation, and thrombocytopenia

Front 97

What other organism is known to cause hemorrhagic diarrhea and HUS?

Back 97

Shigella, although 70% of hemorrhagic diarrhea-associated HUS in the United States is caused by EHEC.

Front 98

Other than C. jejuni, what curved gram-negative rod causes a bloody diarrhea?

Back 98

Vibrio parahaemolyticus

Front 99

What is the source for V. parahaemolyticus?

Back 99

Contaminated seafood

Front 100

What species of bacteria causes fever, diarrhea, and abdominal pain and is commonly confused with appendicitis?

Back 100

Yersinia enterocolitica

Front 101

VIRAL DIARRHEA

Back 101

VIRAL DIARRHEA

Front 102

What are the typical histologic findings in a patient with viral gastroenteritis?

Back 102

Mild mononuclear infiltration with blunting of intestinal villi

Front 103

What is the pathogenesis of viral diarrhea?

Back 103

A clear pathogenic mechanism is unknown although viruses directly damage the small intestinal villi and may interfere with absorption and enzymatic activity. Rotavirus produces an enterotoxin that may contribute to diarrhea.

Front 104

What is the route of transmission for viral gastroenteritis?

Back 104

Fecal-oral transmission

Front 105

What are the typical signs and symptoms?

Back 105

Low- to moderate-grade fevers, nausea, vomiting, abdominal cramps, and diarrhea. No WBCs or blood in stool

Front 106

What is the course of this disease in healthy adults?

Back 106

Mild and self-limited

Front 107

Is diarrhea a serious medical condition for children?

Back 107

In the United States, approximately 400 children die from complications of diarrhea each year. However, it is estimated that 2 million children worldwide die from complications of diarrhea each year. Children are more susceptible to secondary dehydration and secondary nutrient malabsorption.

Front 108

What two virus families are responsible for the majority of viral gastroenteritis?

Back 108

1. Norwalk virus (also known as norovirus)
2. Rotavirus

Front 109

Which of the above virus families targets adults and which targets infants/young children?

Back 109

Rotavirus targets infants and young children while Norwalk virus targets adults.

Front 110

Which virus is associated with outbreaks in group settings, such as cruise ships, camps, and dorms?

Back 110

Norwalk virus

Front 111

What makes Norwalk virus in particular infectious?

Back 111

Low infectious dose, virus excreted in stool for several weeks after recovery, and resistance to inactivation by chlorination and desiccation (so be more wary about where you swim)

Front 112

What is the treatment for diarrhea caused by Norwalk and/or rotavirus?

Back 112

No antiviral treatments exist. Treatment is supportive and aims at maintaining hydration.

Front 113

What preventive measures can be taken to avoid viral diarrhea outbreaks?

Back 113

Public health measures, such as sewage disposal, and personal hygiene are likely to prevent infection.

Front 114

Which virus causes a nonbloody diarrhea primarily in children younger than the age of 2 years?

Back 114

Adenovirus

Front 115

PROTOZOAL DIARRHEA

Back 115

PROTOZOAL DIARRHEA

Front 116

Which two protozoa produce nonbloody diarrhea?

Back 116

1. Giardia lamblia
2. Cryptosporidium parvum

Front 117

Which bug causes amebic dysentery (bloody diarrhea)?

Back 117

Entamoeba histolytica

Front 118

What is more effective in killing E. histolytica, boiling or chlorination?

Back 118

Boiling. They are heat susceptible but chlorination does not kill them, so beware of the public pool.

Front 119

How is amebic dysentery spread?

Back 119

Fecal-oral route. Ingestion of cysts in contaminated food or water

Front 120

What group in America has a higher incidence of amebic dysentery?

Back 120

Homosexual males

Front 121

Pathology Correlate: What finding on histology is associated with amebic dysentery?

Back 121

Flask-shaped ulcers form once the ameba invades colonic glands and reaches the submucosa.

Front 122

How is the aspirated substance from E. histolytica liver abscesses classically described?

Back 122

Brownish-yellow pus that looks like anchovy paste

Front 123

What distinguishes E. histolytica from other amebae?

Back 123

A cyst with four nuclei

Front 124

What is the treatment for E. histolytica infection?

Back 124

Metronidazole

Front 125

How is G. lamblia spread?

Back 125

Fecal-oral or anal-oral route

Front 126

What groups in America have a higher incidence of giardiasis?

Back 126

Homosexual males and hikers who drink from freshwater sources

Front 127

Is Giardia common in the United States?

Back 127

Yes, approximately 5% of stool samples in America contain Giardia cysts.

Front 128

Which site of the GI tract does G. lamblia primarily infect?

Back 128

Duodenum

Front 129

What are the symptoms associated with giardiasis?

Back 129

Nonbloody, foul-smelling diarrhea, flatulence, and weight loss with chronic disease. No fever

Front 130

How is giardiasis diagnosed?

Back 130

Trophozoites in stool have a characteristic appearance, pear-shaped with two nuclei, four pairs of flagella, and a suction disk. Sometimes small intestine aspirate (string test) or biopsy is needed.

Front 131

What is the treatment for giardiasis?

Back 131

Metronidazole

Front 132

For what population of patients in particular is cryptosporidiosis a major concern?

Back 132

Immunocompromised patients, especially AIDS patients

Front 133

OTHER Gl INFECTIONS

Back 133

OTHER Gl INFECTIONS

Front 134

Which virus, and to which family of viruses does it belong to, causes worldwide food-related acute hepatitis?

Back 134

Hepatitis A virus (HAV), picornavirus

Front 135

Which virus, and to which family of viruses does it belong to, causes contaminated water-associated acute hepatitis noted for its high mortality in pregnant women in the developing countries?

Back 135

Hepatitis E virus (HEV). HEV is now classified into its own hepevirus genus with no assigned family.

Front 136

Which virus, and to which family of viruses does it belong to, causes acute hepatitis acquired through contaminated needles that develops into chronic hepatitis 85% to 90% of the time?

Back 136

Hepatitis C virus (HCV), flavivirus

Front 137

Which virus, and to which family of viruses does it belong to, causes acute or chronic hepatitis depending on the method of transmission?

Back 137

Hepatitis B virus (HBV), hepadnavirus; vertical (neonatal) transmission associated with a high risk of chronic hepatitis, horizontal (needle/transfusion) transmission associated with acute hepatitis, and a much lower risk of chronic hepatitis

Front 138

Which virus, and to which family of viruses does it belong to, causes fulminant hepatitis and is a defective virus?

Back 138

Hepatitis D virus (HDV), delta virus; HDV requires HBV coinfection

Front 139

Which hepatitis viruses are enveloped? Which are transmitted through fecal-oral route?

Back 139

HBV, HCV, and HDV are enveloped viruses and cannot survive the GI tract. HAV and HEV are nonenveloped and transmitted via the fecal-oral route.

Front 140

Chronic infection with what parasite can cause portal hypertension (most common cause worldwide), cirrhosis, and even pulmonary hypertension?

Back 140

Schistosoma mansoni

Front 141

What two species of parasites can potentially cause intestinal obstruction causing patients to present with acute abdominal pain?

Back 141

1. Ascaris lumbricoides
2. Diphyllobothrium latum

Front 142

What type of anemia is D. latum infection associated with? Why?

Back 142

Megaloblastic anemia. Diphyllobothrium latum may interfere with vitamin B 12adsorption.

Front 143

What two species of nematodes can cause microcytic anemia?

Back 143

1. Ancylostoma duodenale (hookworm)
2. Necator americanus (hookworm)

Front 144

What nematode is a common cause of perianal pruritus in young children?

Back 144

Enterobius vermicularis

Front 145

What cestodes cause tapeworm infections?

Back 145

Taenia solium (pork),
Taenia saginata (beef),
D. latum (fish),
Echinococcus granulosus (dog)