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Microbiology > Unit 1: Bacterial GI Infections > Flashcards

Unit 1: Bacterial GI Infections Flashcards

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1
Q

Acute disease due to Vibrio cholerae infection of the GI tract

A

Cholera

Disease is distributed worldwide, cause of massive human morbidity and mortality

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2
Q

Clinical manifestation of cholera

A

Bacteria colonize the small intestine mucosa with the colonized mucosa showing NO change in physical integrity

ACUTE AND MASSIVE WATERY DIARRHEA (1L/hour) is the main feature.

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3
Q

Rice water stools

A

Cholera

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4
Q

Why do you end up dying with cholera?

A

Rapid depletion of fluids and electrolytes leading to hypovolemic shock, metabolic acidosis, and death.

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5
Q

Incubation period for cholera

A

1-5 days —> abrupt onset of symptoms

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6
Q

SSx of cholera

A

Muscle cramps, poor skin turbot, wrinkled skin over fingers (‘washerwoman hands’), sunken eyes, missing pulse in extremities

Extreme water stools the cause of most of these (b/c dehydration)

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7
Q

So what does Vibrio cholerae look like?

A 
Gram negative
Bent rod shape (vibrio, duh)
Nonspore-former
Facultative anaerobe
Motile, polar flagellum
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8
Q

Diagnosing cholera

A

Culture!

Final ID is with group specific antisera

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9
Q

Treatment of cholera

A

For the majority of patients, successful therapy usually only requires replacement of fluids/electrolytes

Provide by IV route if patient can’t take oral fluids

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10
Q

Epidemic cholera is now recognized to be caused by the _____ and ______ types.

A

O-1 and O-139

Other types cause diarrheal disease

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11
Q

Cholera is spread through _____________________.

A

Contaminated drinking water (and food)

Not easily spread person-to-person

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12
Q

Causative microbes for cholera are found naturally in ____________________

A

Marine coastal areas and estuaries, including the United States Gulf Coast Region.

Asymptomatic human carriers are important as reservoirs

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13
Q

Massive cholera epidemics have emerged recently in …

A

Haiti and Yemen

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14
Q

Is prophylactic treatment necessary for travelers to cholera endemic regions?

A

Prophylactic tetracycline has been used but NOT typically needed in most people practicing normal hygiene since the infectious dose is high

Primary prevention means is proper control of sewage.

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15
Q

Tell me about these awesome new cholera vaccines…

A

Dukoral - oral, O-1 killed whole cells PLUS choleragen toxioid (may also help prevent traveler’s diarrhea due to ETEC)

Shanchol - oral, I valentines O-1 and O-139 killed whole cells

Vaxchora - oral, attenuated (live) O-1 vaccine FOR TRAVELERS

Euvichol - oral, kill whole O-1 and O-139 cells

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16
Q

The three vibrio species we discussed

A

V. cholerae
V. parahaemolyticus
V. vulnificus

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17
Q

Vibrio species causing a gastroenteritis to a mild cholera-like illness

A

V. parahaemolyticus

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18
Q

The most common cause of food-borne illness in Japan

A

V. parahaemolyticus

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19
Q

Vibrio species with seasonal infection pattern, organism receding in winter

A

V. parahaemolyticus

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20
Q

Where can you find V. parahaemolyticus?

A

Normal inhabitants of coastal ocean and estuary waters

Endemic in US Gulf coast waters, most US cases are frequently associated with mishandling infected seafood (improper refrigeration)

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21
Q

Vibrio species associated with oysters

A

V. vulnificus - also a normal inhabitant of coast marine and estuary waters

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22
Q

Seasonality of V. vulnificus

A

More common when warm

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23
Q

How do V.vulnificus infections normally begin?

A

Wound infections through direct contact of open wound with seawater or oysters

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24
Q

How does one get sepsis from V.vulnificus?

A

Consumption of raw oysters —> eruption of bullous skin lesions, shock

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25
Q

What condition is usually associated with V.vulnificus infection?

A

History of oyster consumption with suspicion of liver dysfunction (commonly, alcoholism)

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26
Q

Treatment for V.vulnificus sepsis

A

Tetracycline

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27
Q

Apparent from wound infections and sepsis, how else might V.vulnificus present itself?

A

Acute self-limiting diarrhea associated with raw oyster consumption

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28
Q

Antigenic classification scheme used to identify pathogenic forms of Escherichia coli

A 
O antigen (LPS) = serogroup
At least 160 serogroups exist

H antigen (flagella) = serotype

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29
Q

_________ resembles V.cholerae in disease process but usually milder.

A

ETEC (Enterotoxigenic E.coli)

Adheres to mucosa of small intestine and produces symptoms by elaboration of toxins that induce watery diarrhea

Usually only fatal in infants

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30
Q

The most typical disease caused by ETEC in the US

A

Traveler’s diarrhea - partial immunity in adults in endemic/epidemic areas

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31
Q

_________ vaccine MAY offer some protection against traveler’s diarrhea because ETEC toxin is almost identical to __________.

A

Dukoral (cholera) vaccine - choleragen toxin

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32
Q

Diarrhea that becomes bloody after 1-3 days with cramps, vomiting; fever not always present

A

Enterohemorrhagic E.coli (EHEC)

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33
Q

Emerging pathogen, only recently recognized as a cause of disease

A

Enterohemorrhagic E.coli (EHEC)

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34
Q

Eschericia species which releases Shiga-like toxin (SLT)

A

Enterohemorrhagic E.coli (EHEC)

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35
Q

EHEC can be fatal due to …

A

hemolytic uremic syndrom (HUS) development

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36
Q

Predominate form of EHEC

A

O157:H7

But other strains are now designated as STEC (Shiga toxin producing E.coli) that may also induce HUS

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37
Q

Complications of O157:H7 EHEC infection

A

Hemolytic Uremic Syndrom (HUS) - acute renal failure with poor prognosis a few days after bloody diarrhea

HUS only occurs with bacteria that express Shiga toxin (8-10% of O157:H7 infections, higher for O104:H4

More common to see this in elderly and very young patients

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38
Q

Why are O157:H7 infections not typically treated with antibiotics?

A

Risk of HUS induction

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39
Q

What media is used to differentiate O157:H7 for EHEC diagnosis?

A

MacConkey’s sorbitol agar can differentiate it from normal flora E.coli because the pathogenic strain cannot ferment sorbitol and appears white on the plate while other E.coli strains appear bright red/pink

Use of this agar is NOT necessarily automatic - inform the lab that you suspect a case of O157:H7

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40
Q

Treatment for O157:H7

A

Oral rehydration, vigilance for renal function decline

Extreme caution with antibiotics to avoid inducing HUS

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41
Q

Reservoir for O157:H7

A

Cattle

Infections are typically associated with beef and raw milk

Undercooked hamburger is classic infection source

Also being discovered in other food (Veggies) - may reflect low level contamination of food processing plants with cow manure

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42
Q

Person to person transmission of O157”H7 is possible because…

A

It is an extreme low-dose pathogen

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43
Q

E.coli O104:H4

A

New form of Enterogaggregative E.coli that has emerged in Europe, traced to alfalfa sprouts.

HUS production, high case fatality rate

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44
Q

Campylobacter jejuni microbe description

A 
Gram negative
Curved rod (sea gull shaped)
Motile
Microaerophilic
Grows well at 42˚C
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45
Q

Clinical manifestations of campylobacter jejuni infection

A

Incubation period is 1-7 days

Very commonly patient has prodrome with fever, headache, malaise, myalgia 12-24 hours before diarrhea onset

Enteritis with diarrhea - loose stools to frank dysentery, fever, abdominal pain (cramping)

Self-limiting (improvement after several days)

Convalescent carriage and excretion for 2-3 weeks after disease.

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46
Q

Microbe associated with prodrom 12-24 hours before the diarrhea

A

Campylobacter

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47
Q

Severe acute abdominal pain in lower right quadrant that mimics appendicitis

A

Campylobacter

48
Q

Primarily reservoir for campylobacter

A

Intestinal tract of animals, BIRDS especially and transmission by food source primarily

Poultry products are frequently contaminated

49
Q

Eating undercooked chicken is the classic way to get this disease

A

Campylobacter

50
Q

This GI pathogen is unusual in that the highest infection rate is in young adults

A

Campylobacter

51
Q

Campylobacter infections peak when?

A

Summer months

52
Q

Complications of Campylobacter infection

A 
Reiters syndrome (urethritis, polyarthritis, conjunctivitis)
In HLA-B27 individuals, mostly males

Guillain-Barré syndrome
Paralytic syndrome due to immune attack on myelinated peripheral nervous system tissues

53
Q

Chief known precipitation of Gillian-Barre paralytic syndrome

A

Campylobacter jejuni

54
Q

Important clues to diagnosing Campylobacter

A

Fever and prodrome

55
Q

Treatment for Campylobacter

A

Erythromycin

56
Q

Overview of H. Pylori

A

Chronic active gastritis and peptic ulceration

Gram negative, curved rods
Highly motile
Copious production of urease

57
Q

Clinical manifestations of H.pylori infections

A

Epithelial cells of pylori are primary targets

Gastritis, cramps, halitosis, nausea, and vomiting

Eradication of bacteria is not necessarily correlated with relief of symptoms

58
Q

H.pylori virulence factors

A

Urease - produces CO2 and NH4+ that raises pH and protects H.pylori - allows infection to be detected

59
Q

Source/reservoir of H.pylori

A

Probably humans

60
Q

Risks/associations for H.pylori

A

Smoking is a risk factor

Association with stomach adenocarcinoma

61
Q

Diagnosis of H.pylori

A

Histology also detection in biopsy samples plus culture

CLO test - detection of urease activity in biopsy tissue by pH change

62
Q

H.pylori treatment

A

Optimal abx therapy not yet evolved

Combo of antibiotics (tetracycline) pluse bismuth-containing drugs

Patient may be re-infected after antibiotic eradication (by family/contacts)

63
Q

Clinical manifestations of shigella infections

A

Facultative intracellular enteric bacilli causing an inflammatory disease of the large bowel

Invades and multiplies in colon epithelial cells

Incubation period is 72 hours

Disease ranges from moderate diarrhea to severe dysentery

Initial symptoms - fever, cramps, vomiting, watery diarrhea which progresses to dysentery in severe forms - blood, mucous and PMN’s in stools, fever, cramps

64
Q

Description of shigella

A 
Gram negative rods
Nonspore-former
Facultative anaerobe
Nonmotile (usually)
Lactose nonfermenting
65
Q

How to diagnose shigellosis

A

Suspect in any patient with fever and diarrheal disease

Blood and mucous in feces plus acute onset suggest invasive disease

PMNs and RBCs on microscopic exam of feces suggest invasive disease but not seen in diarrhea caused by enterotoxins

66
Q

What is special about culturing shigella?

A

Must plate samples QUICKLY

Choice of precise sample influences probability of success

Blood-tinged flecks of mucus are ideal samples for the micro lab

67
Q

Treatment of shigella

A

Usually self-limiting in otherwise healthy patients

Fluid replacement

Effective antibiotic therapy may shorten course and eliminate carrers but is problematic b/c many shigella are multiple antibiotic resistant

68
Q

Complications of shigella

A

Shedding during convalescence is typical and long-term carrier state is possible

Reiter’s syndrome in HLA B27 individuals (nonspecific acute inflammatory arthritis)

Hemolytic uremic syndrome (HUS)
S.dysenteriae (type 1 infection) is a Shiga toxin producer
Acute renal failure with poor prognosis

69
Q

Types of bacteria that have Reiter’s syndrome as complications

A

Shigella (esp S.dysenteriae)

Campylobacter

70
Q

_______ are the soles reservoir for the shigella species

A

Humans

Person-to-person is the primary mode of transmission

71
Q

The four species of Shigella

A

Group A - S.dysenteriae
Group B - S.flexneri
Group C - S.boydii
Group D - S.sonnei

72
Q

In the US, cases are primarily due to which two species of shigella

A

S.flexneri and S.sonnei

73
Q

Age group most susceptible to shigella

A

Children age 1-4

74
Q

Shigella prevention

A

Hand washing in the single most important control measure

Education

Supervised hand washing for kids

75
Q

Salmonella microbes are the normal gut flora of _____

A

Birds and other animals

Human infection is primarily through food contamination

76
Q

Clinical manifestations of salmonella infections

A

Incubation of 12-48 hours

Sudden onset of disease - fever, chills, cramps, diarrhea, vomiting

2-3 days duration in normal host

77
Q

Patients at greater risk for Salmonella infection

A 
Infants
The elderly
Cancer patients
AIDS patients
Diabetics
Persons on abx therapy
78
Q

Description of salmonella microbes

A 
Gram negative rods
Nonspore-former
Facultative anaerobe
Motile
Lactose nonfermenting
79
Q

What’s special about salmonella nomenclature

A

Serological variants (“serovars”) are named as if they are true species

Salmonella typhi —> Typhoid fever
Salmonella typhimurium —> food poisoning

80
Q

Diagnosis of salmonella

A

Sample any food remaining to culture
Fecal matter
Blood if fever is evident (but might not be present in blood if in peak of fever)

Fluorescent Antibody (FA) tests allow for rapid and accurate serological confirmation - each isolate is typed by state lab personnel

81
Q

Treatment of salmonellosis

A

Supportive therapy for patients of otherwise normal good health

Maintain fluid and electrolytes

Abx not required if disease is not systemic - AIDS patients require special care

82
Q

Primary reservoirs for salmonella

A 
Animals/foods of animal origins:
• Eggs
• Beef products and cattle
•Pigs and pork products
• Also companion animals and pets
83
Q

Usual route for infection with salmonella

A

Contaminated food or water

84
Q

Peaks of incidence for salmonella

A

Infants more susceptible - highest incidence in infants and children 6 months to 5 years

Infection has a strong seasonal trend - sharp increases are evident in summer and fall

85
Q

Convalescent salmonella patients

A

A convalescent carrier state is recognized, 1-2 months duration, infants may shed for up to a year

86
Q

Reasons why salmonella infections are increasing

A

Food processing changes - shift to large scale facilities increases risk of massive common source outbreaks

“Modified atmosphere packaging” intended to keep produce fresh-looking promotes growth of pathogens

Changing consumer preferences for fresh food items (ie salads) has led to more cases by cross-contamination

Changes in animal husbandry promote pathogen colonization/transfer
• Feeding of slaughterhouse remains and fish meal to chickens
• Chicken infections lead to egg contamination in utero, so even an untracked egg is unsafe

87
Q

Why are most eggs pasteurized in the US now?

A

Chicken infections with salmonella can lead to egg contamination in utero - even an uncracked, clean egg can be unsafe

88
Q

What is pseudomembranous colitis?

A

An antibiotic-induced disease caused by Clostridium difficile

89
Q

Description of C.diff microbe

A

Gram positive bacillus
Anaerobic
Spore former (subterminal)

90
Q

Clinical manifestations of C.difficile

A

Difficult to distinguish from ulcerative colitis, crohn’s disease, chronic IBD on clinical findings alone

Three types of disease resulting from C.difficile are at issue:
A. Diarrhea with lower abdominal cramping - no systemic symptoms
B. Severe colitis w/o pseudomembrane - profuse diarrhea, pain, and systemic symptoms (fever, nausea, malaise, dehydration)
C. CLASSIC PSEUDOMEMBRANOUS COLITIS (PMC) - same suite of symptoms for severe colitis, with elevated yellowish plaques 2-10mm over inflamed regions of mucosa

91
Q

PMC diagnosis

A

Detection of toxin in feces

Gram stain of stool will reveal gram positive rods with subterminal spores

Culture

Many hospitals screen all abx-associated diarrhea patients for toxin

92
Q

PMC treatment

A

Fluid and electrolyte replacement

Discontinue abx therapy

Administer new abx (oral vanco or metro)

Experimental treatment based on reconstitution of bowl flora undergoing trial

93
Q

PMC complications

A

A significant fraction of patients (10-20%) will relapse and some will suffer multiple relapses

94
Q

Main predisposing factor for C.difficile

A

Disruption of normal gut flora (secondary to abx treatment) —> subsequent colonization by C.diff and release of toxins

10% of pop carries C.diff bacteria as normal flora w/o problem

95
Q

Clostridium perfringens type A is a common cause of …

A

Acute food borne diarrheal disease in the US

96
Q

What does C.perfringens typeA look like?

A 
Gram positive
Rod shaped
Nonmotile
Anaerobe (aerotolerant)
Spore-former
97
Q

Clinical manifestations of C.perfringens type A infections

A

Short incubation period

Moderate severe diarrhea, abdominal cramping (no vomiting)

Complete recovery in a day

98
Q

Epidemiology of clostridium perfringens

A

Common member of gut flora of humans and animals

Consumption of grossly contained meat/poultry. Contaminated meat with cooking that is inadequate to destroy spores; food is allowed to stand w/o refrigeration, enabling spores to germinate; When vegetative cells are eaten, stomach acid induces sporulation and producation of enterotoxin

99
Q

Diagnosing clostridium perfringens

A

Onset and course of disease is FAST

HIGH dose organism

Detection of large numbers of this microbe in food and feces

100
Q

Treatment for Clostridium perfringens

A

Fluid replacement if necessary

101
Q

Description of Bacillus cereus

A

Gram positive
Rod shaped
Aerobic
Spore former

102
Q

Two disease forms observed involving B.cereus…

A

1) Emetic form - preformed toxin is ingested, causing GI symptoms 1-5 hours after ingestion of contaminated food (vomiting, cramps, diarrhea)
2) Diarrheal form - Ingestion of large numbers of vegetative cells that produce enterotoxin after exposure to stomach acid; Abdominal pain, profuse watery diarrhea 1-17 hours after ingestion of contaminated food.

103
Q

Treatment of B.cereus infection

A

Relief of symptoms

104
Q

Diagnosis of B.cereus

A

Afebrile disease with a fast onset and course

High index of suspicion if upper GI illness is evident 1-5 hours after eating or lower illness 5-17 hours after eating

B.cereus disease is often confused with clostridial or staph food poisoning

To Dx, isolate more than 10^5 B.cereus per gram of food or feces

105
Q

Spores of Bacillus cereus are commonly found on …

A

grains and vegetables, esp rice

106
Q

Prevention of B.cereus infection

A

Prevent poisoning sequence by proper food handling. Prompt refrigeration of all grain foods after cooking.

107
Q

__________ is second only to Salmonella as a cause of food borne disease

A

Staphylococcal food borne diseases

108
Q

Staphylococcal GI disease is caused by…

A

Consumption of heat stable preformed toxin in foods

Under the proper set of conditions, it is possible to have disease without colonization or infection of the host with this agent

109
Q

Clinical manifestations of staphylococcal infections

A

Acute emetic and diarrheal disease caused by the ingestion of preformed heat stable toxin

Short incubation period of 1-6 hours after food consumption

Nausea, vomiting, diarrhea, cramps, acute salivation

Self-limiting - complete recovery in 1-4 days

110
Q

Primary virulence factor for staphylococcal infections

A

Enterotoxin A - water soluble, heat stable (tolerates boiling for 30 min)

Emetic response is elicited by this toxin - absorbed in gut, stimulus reaches CNS and sends impulse to the vomiting center

Diarrheal effects - enhanced fluid transmucosal movement into lumen coupled with decreased water absorption

111
Q

The source of staphylococcal GI infections

A

Humans are the source of the organisms and accidentally inoculate food during preparation.

Toxin is undetectable in food, the food quality appears fine, there is no smell or bad taste.

Toxin produced quickly in warm conditions in a few hours

112
Q

Diagnosis of staphylococcal intoxication

A

Afebrile disease, not directly communicable

High index of suspicion with short time between eating and symptoms eruption

Custard filled baked goods, canned foods, processed meats, potato salad

Enterotoxin tests are available and reliable

113
Q

Treatment of staphylococcal intoxication

A

Symptomatic relief

Abx are of no benefit b/c it’s an intoxication, not infection

Toxemia like this are short duration since no additional growth of organism/production of toxin will occur after food ingestion

114
Q

Prevention of staphylococcal intoxication

A

Examination of food handlers

Proper refrigeration

115
Q

Common characteristics of food borne diseases

A

Staphylococcus, B.cereus, C.perfringens

Abx not useful, because they’re all intoxications
Not directly transmissible between patients
Afebrile
Toxemia - fast onset and course
Common factors - inadequate cooking, re-heating, or refridgeration of foods

Microbiology (6 decks)

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