Infectious Enterocolitis, Anaerobic Infections, and H. pylori

Question 1

What anaerobes do we need to know for this block?

Answer 1

Anaerobes​

Bacteroides fragilis, Prevotella
Clostridium perfringens, tetani, botulinum, difficile​

Question 2

Where are anaerobes most commonly found?
• which genus may also be found in the soil and air?

Answer 2

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

​

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

Question 3

Why is the growth of anaerobes inhibited by oxygen?

Answer 3

Anaerobes lack SOD (superoxide dismutase) and catalase​

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

Question 4

Why are anaerobic infections, often, but not always associated with a foul smell?

Answer 4

Metabolic end products of Anaerobic Infections Stink

Question 5

What are two features to remember about the composition of absesses that are caused by anaerobic organisms?

Answer 5

• Species found in abscesses often reflect the normal flora in that site.​
• Anaerobic infections are often polymicrobial (mixed anaerobic and facultative aerobic bacteria)​

Question 6

Bacteroides fragilis
• Gram Stain and Structure
• Where is it found?

Answer 6

Gram negative bacillus​

Predominant organisms in the human colon (1011/g of feces) and found in vagina of 60% of women​

Question 7

T or F: Bacteroides fragilis is the the 2nd most common cause of serious anaerobic infections.

Answer 7

FALSE, it is the #1 cause of serious anaerobic infections in humans

Question 8

Bacteriodes fragilis
• Major Virulence factor
• What role does this play in the formation of abscesses?

Answer 8

Polysaccharide capsule antiphagocytic important virulence factor​

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

Question 9

What are the common predisposing factors to infection by bacteriodes fragilis?

Answer 9

Pathogenesis​

Infections usually arise from a break in a mucosal surface​
• Predisposing factors: surgery, trauma, chronic disease​

Question 10

What clinical finding are typical in a B. fragilis infection?

Answer 10

Clinical findings​

• In general, B. fragilis causes disease below the diaphragm (lung abscess being the exception)​​*
  1. Most frequently cause intra-abdominal infections – ​abscesses or peritonitis​
  2. Pelvic or peri-rectal abscesses, bacteremia, infected decubitus ulcers can occur
  3. Found in about 25% of lung abscesses​

Question 11

T or F: B. fragilis can have an enterotoxin that causes diarrhea.

Answer 11

True, some strains are associated with enterotoxin

Question 12

Bacteroides fragilis
• Diagnosis
• Treatment

Answer 12

Diagnosis​
Anaerobic cultures​

Treatment​
Resistant to Penicillin. ​

Universally susceptible to metronidazole, carbapenems, combination beta-lactam and beta-lactamase inhibitors (PIP/TAZO, AMOXI/CLAV)

Question 13

Prevotella melaninogenica
• Gram Stain and Structure
• Typical Location
• Type of Pathogen

Answer 13

Gram negative coccobacillus​

Commonly found in the oral cavity, also GI tract, vagina, nasopharynx​

Opportunistic pathogen​

Question 14

Prevotella melaninogenica
• Types of opportunistic infections it can cause?

Answer 14

Clinical findings​
• Oral/periodontal abscesses​
• Pulmonary abscesses/empyemas​
• Chronic otitis​
• Sinusitis​

Question 15

Clostridium spp.
• what staining and structural features are common to all types?

Answer 15

Gram positive, spore-forming rods​
The only anaerobic endospore-forming bacteria​
• Resistant to high heat​
• Resistant to harsh environment​

Question 16

Clostrium spp.
• what is key to the pathogenesis of this species?
• where are they found?

Answer 16

Exotoxins and secreted hydrolytic enzymes responsible for pathogenesis​

Found in the colon and soil (spores)​

​

Question 17

Clostridium perfringins
• Describe the pathogenesis of food poisoning caused by this bug.
• how long before disease onset?
• how long before resolution?

Answer 17

1. Heat-resistant spores survive cooking, then spores can germinate in foods such as meats, poultry or gravy at lower temperatures.​
2. Following ingestion of large quantity of organisms, C. perfringens enterotoxin is produced IN the GI tract​ (not preformed)
3. 8-16 hour incubation period characterized by watery diarrhea with cramps; minimal vomiting. Resolves in 24 hours.​

Question 18

How clostridium tetani typically introduced into a wound?

Answer 18

Spores found in soil. Portal of entry usually a wound site (eg. nail penetrates the foot)​

Also can be introduced during “skin-popping”​

**Contrast this to botulism that is ingested

Question 19

How does the Tetanus (metalloprotease) toxin work?

Answer 19

Tetanus toxin (tetanospasmin): AB neurotoxin ​

Enters at the neuromuscular junction and is transported by motor neurons to ganglia​

Toxin binds tightly and irreversibly to ganglioside receptors and blocks release of inhibitory neurotransmitters (glycine and GABA) by its cleaving action on membrane proteines (SNARE) involved in neuroexocytosis. 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 ​

Question 20

How do patients infected by Tetanus often present clinically?
• what is often the first presenting symptom?

Answer 20

Clinical presentation​
• Characterized by strong muscle spasms/spastic paralysis​
• Trismus (lock jaw) first​****
• Characteristic grimace known as risus sardonicus​
• Exaggerated reflexes​
• Opisthotonos: pronounced arching of the back due to spasm of the strong extensor muscles of the back​
• Respiratory failure can occur​

High mortality rate​

Question 21

Clostridium Tetanae
• how would you treat this infection?

Answer 21

1. Wound debridement to eradicate spores​
2. Human tetanus immune globulin (HTIG) used to neutralize the toxin​
3. Antibiotics probably play a minor role but they are universally recommended​
   • DOC metronidazole. Penicillin is an acceptable alternative​
4. Tetanus Vaccine at the time of diagnosis and 2 more doses after

Question 22

T or F: Tetanus vaccine is not necessary in people who have been infected with the actual bug.

Answer 22

False, Tetanus does not confer immunity following recovery from acute illness​

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​

Question 23

How is botulism typically acquired?

Answer 23

Ways to get 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​
• Inhalational (would be an act of ​bioterrorism)​
• Iatrogenic​

Question 24

What is the most common type of botulism?

Answer 24

Infant > Food > Wound

Question 25

What should you NOT give in the treatment of botulism?

Answer 25

Antibiotics are not recommended for infant botulism or for adults with suspected gastrointestinal botulism because lysis of intraluminal C. botulinum could increase the amount of toxin available for absorption

Question 26

How does botulism toxin work?

Answer 26

Pathogenesis​

AB toxins​

8 (A-H) antigenic types​

Most potent bacterial toxin​

Cleave SNARE proteins and ​prevent release of acetylcholine​

​

Question 27

What is the clinical presentation of botulism acquired by eating contaminated food?

Answer 27

Clinical presentation​
•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​

Question 28

What causes floppy baby syndrome?
• who do we see this in?

Answer 28

C. botulinum causes botulism - we see this in children 1 wk to 12 mo old.

Question 29

How do kids most often get infected with C. botulinum?
• how does it present?

Answer 29

Infection first then intoxication​ (because the spores can grow in young GI tract)
• Inhale or ingest spores (environmental dust) or honey​

Clinical presentation​
• Presentation and severity variable​
• Constipation followed by weakness, feeding difficulties, descending global hypotonia, drooling, anorexia, irritability, weak cry​

Question 30

What is the treatment for botulism infections?
• how does this differ on the basis of age?

Answer 30

Treatment​
• 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​
• Antibiotic therapy unproven but recommended for WOUND botulism only. DOC penicillin, metronidazole possible alternative.​

Question 31

Why are antibiotic contraindicated in infantile botulism?

Answer 31

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

Question 32

How can botulism be prevented?

Answer 32

Prevention​

Proper cooking/canning

Question 33

H. pylori
• Structure, Staining, Metabolism, Motility

Answer 33

Slender, curved gram negative rods​

Motile with polar flagella​

Microaerophilic​

Question 34

H. pylori
• what factors allow it to cause ulcers?

Answer 34

VacA: vaculolating cytotoxin​

Cag: rearranges cytoskeleton​ (Cag = cytoskeleton associated gene)

Question 35

H. pylori
• is Urease positive
• Has a PAI encoding a type III secretion system

Answer 35

H. pylori
• is Urease positive
• Has a PAI encoding a type III secretion system