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Flashcards in Anaerobes and H. pylori Deck (41):
1

Describe the normal gut microbiome

Each person has at least 160 different gut microbes

–57 shared by 90% of Europeans

–75 shared by 50%

–Two phyla account for 90% of the species

•Evidence that our core gut microbiome influences our body weight, CV health and tendency to develop of type II diabetes

2

What are the main anaerobic contributors to the gut microbiome?

Bacteriodes and Clostridia (note that anaerobes are the major players in the GI)

•Anaerobes are also prevalent in oral cavity, skin, colon, female genital tract

•Some (Clostridia) found in soil and air as spores

3

Why does oxygen kill anaerobes?

•Anaerobes lack SOD (superoxide dismutase) and catalase

–One of main reasons why the growth of anaerobes is inhibited by oxygen

–These enzymes eliminate the toxic compounds hydrogen peroxide and superoxide which are formed during production of energy by the organism

4

T or F. Anaerobic infections tend to stink

T. The odor is caused by metabolic end-products of the organisms which are mostly organic acids, but note that the lack of putrid smell does not rule out anaerobic infection

Also note that Special transport and culture are required fro anaerobes

5

When do anaerobes typically cause disease (abscesses)?

when they are introduced into normally sterile sites or when the balance of organisms is upset and pathogenic organisms overgrow

–Species found in abscesses often reflect the normal flora in that site.

 

6

T or F. Anaerobic infections are often polymicrobial (mixed anaerobic and facultative aerobic bacteria)

T.

7

Describe Bcteroides fragilis

This is a gram negative bacillus that is one of the most predominant organisms in the human colon and found in the vagina of 60% of women and represents the most common cause of serious anaerobic infections

8

Describe the pathogenesis of Bacteroides fragilis

–Infections usually arise from a break in a mucosal surface (Predisposing factors:  surgery, trauma, chronic disease) and a Polysaccharide antiphagocytic capsule is the important virulence factor

–Host response to the capsule actually plays important role in abscess formation

9

How does Bacteroids fragilis infection present?

BF most commonly causes intra-abdominal infections marked by abscesses or peritonitis. Pelvic or peri-rectal abscesses, bacteremia, and infected decubitus ulcers can occur

In general, B. fragilis causes disease below the diaphragm, but are found in 25% of lung abscesses

–Enterotoxin producing strain can cause diarrhea 

10

How is Bacteroides fragilis diagnosed?

anaerobic cultures 

11

How is BF tx?

resistant to penicillin so tx with metronidazole, carbapenems, and combo beta/lactams with lactamase inhibitors

12

Describe Prevotella melaninogenica (formerly Bacteroides melaninogenicus)

This is a gram negative coccobacillus commonly found in the oral cavity, nasopharynx, GI tract,  and vagina in compromised pts. (it is opportunistic! not commensal)

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13

How does Prevotella melaninogenica present?

–Oral/periodontal abscesses

–Pulmonary abscesses/empyemas

–Chronic otitis

–Sinusitis

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14

Describe Clostridium

Gram +, spore-forming rods (the ONLY anaerobic endospore-forming bacteria).

Note that Clostridium is resistant to both high heat and harsh environments (found in the colon and soil (as spores))

15

What is responsible for the pathogenesis of clostridium?

exotoxins and secreted hydrolytic enzymes

16

Describe Clostridium perfringens

this is a large, 'boxcar' gram+ bacilli found in soil and the colon

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17

How does C. perfringens present?

–Gas gangrene (discussed previously in septic arthritis/myositis lecture)

--Food poisoning

18

Describe C. perfringens induced food poisoning

In this case, heat-resistant spores survive cooking, then spores can germinate in foods such as meats, poultry or gravy at lower temperatures. Following ingestion of large quantity of organisms, C. perfringens enterotoxin is produced in the GI tract induced watery diarrhea with cramps, and minimal vomiting. Resolves in 24 hrs (Outbreaks in psych inpatient facilities have been described)

 

C. perfrigens is an important cause of watery diarrhea in the United States – 3rd most common foodborne illness in the U.S.

19

Describe Clostridium tetani

gram + rod found in soil with spores that usually enters the body through a wound (e.g. nail penetrates the foot) or via 'skin popping"

NOTE: Neonatal tetanus is common in developing countries can occrus when organisms enter the body through contaminated umbilicus or circumcision wounds

20

Describe the pathogenesis of tetanus

 Tetanus occurs when spores of Clostridium tetani, an obligate anaerobe normally present in the gut of mammals and widely found in soil, gains access to damaged human tissue. After inoculation, C. tetani transforms into a vegetative rod-shaped bacterium and produce the metalloprotease tetanospasmin (also known as tetanus toxin, an AB neurotoxin)

This toxin enters at the neuromuscular junction and is transported by motor neurons to ganglia where it binds tightly and irreversibly to ganglioside receptors and blocks release of inhibitory neurotransmitters (glycine and GABA) by its cleaving action on membrane proteines (SNAREs) involved in neuroexocytosis. The net effect is disinhibiton of neurons that modulate excitatory impulses from the motor cortex resulting in increased muscle tone, painful spasms, and widespread autonomic instability 

21

Tetanus occurs when spores of Clostridium tetani, an obligate anaerobe normally present in the gut of mammals and widely found in soil, gains access to damaged human tissue. After inoculation, C. tetani transforms into a vegetative rod-shaped bacterium and produce the metalloprotease tetanospasmin (also known as tetanus toxin).

After reaching the spinal cord and brainstem via retrograde axonal transport and binding tightly and irreversibly to receptors at these sites, tetanus toxin blocks neurotransmission by its cleaving action on membrane proteins involved in neuroexocytosis. The net effect is disinhibition of neurons that modulate excitatory impulses from the motor cortex. Disinhibition of anterior horn cells and autonomic neurons results in increased muscle tone, painful spasms, and widespread autonomic instability.

22

How does tetanus present?

The clinical presentation is marked by strong muscle spasms/spastic paralysis, first as trismus (lock jaw) resulting in a characteristic expression knwon as risus sardonicus. Reflexes become exaggergated and opisthotonos, pronounced arching of the back due to spasm of the strong extensor musles of the back (right) can occur. Respiratory failure typically follows. 

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23

What is the tx of tetanus?

–Wound debridement to eradicate spores

–Human tetanus immune globulin (HTIG) used to neutralize the toxin

–Antibiotics probably play a minor role but they are universally recommended

•DOC metronidazole.  Penicillin is an acceptable alternative

24

T or F. Tetanus does not confer immunity following recovery from acute illness

T. All patients with tetanus should receive active immunization with a total of 3 doses of tetanus toxoid spaced at least 2 weeks apart with the 1st dose given immediately at diagnosis

25

What causes botulism?

Clostridium botulinum

26

What are the forms of botulism?

–Foodborne (classic) botulism (home canned foods like fruits, vegetables; and fish)

–Infant botulism (inhalation or ingestion of spores in carpet or raw honey)

–Wound botulism (Rise in incidence of wound botulism in California due to black tar heroin users.)

–Inhalational (would be an act of bioterrorism)

–Iatrogenic

27

How common is botulism?

 

•110 cases/year reported in the U.S.

–72% infant, 25% foodborne, 3% wound

28

Describe the pathogenesis of C. botulinum

–AB toxins

•8 (A-H) antigenic types

•Most potent bacterial toxin

•Cleave SNARE proteins and prevent release of acetylcholine

29

How does classic (foodborne) botulism occur?

Spores are resistant to heat and germinate after cooking and releases toxins (note that subsequent heating will inactiate the toxin (heat-labile)

30

How does classic botulism present?

–Acute, symmetric descending flaccid paralysis

–Symptoms begin within 12-36 hours post-ingestion

–Nausea, dry mouth, dysphagia, diarrhea, blurred vision

–Paralysis descends to respiratory muscles, trunk and extremities

–Possible death by respiratory failure

31

T or F. Antibiotics are not recommended for infant botulism or for adults with suspected gastrointestinal botulism

T. because lysis of intraluminal C. botulinum could increase the amount of toxin available for absorption

32

Describe infant botulism (aka floppy baby syndrome)

This affects infants aged 1 week-12 months and is marked by infection first then intoxication (due to inhaled spores or raw honey) 

33

How does infant botulism present?

–Presentation and severity variable

–Constipation followed by weakness, feeding difficulties, descending global hypotonia, drooling, anorexia, irritability, weak cry

34

How is botulism tx?

–Mechanical ventilation

–Horse anti-toxin for those over 1 year of age

–Human-derived botulism immune globulin (BIG-IV) available for infants less than 1 year of age

35

T or F. Antibiotic therapy is unproven but recommended for WOUND botulism only. 

T. 

•Not recommended for infant botulism because lysis of intraluminal C. botulinum could increase the amount of toxin available for absorption

36

What is the DOC for wound botulism?

DOC penicillin, metronidazole possible alternative.

 

37

How is H. pylori spread?

human-to-human by fecal-oral or gastric secretions

38

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39

What are the virulence factors of H. pylori?

•Slender, curved gram negative rods

–Motile with polar flagella

–Microaerophilic

•VacA: vaculolating cytotoxin

•PAI encoding Type III secretion system

•Cag: rearranges cytoskeleton

•Urease

40

How does H. pylori cause ulcers?

•Combination of cell destruction by VacA, Cag and immune response leads to ulcers

41

How is H. pylori infection diagnosed?

–Endoscopy with biopsy and culture

–Stool antigen

–Urea breath test

–Serology