Infectious Enterocolitis, Anaerobic Infections, and H. pylori Flashcards
What anaerobes do we need to know for this block?
Anaerobes
Bacteroides fragilis, Prevotella
Clostridium perfringens, tetani, botulinum, difficile
Where are anaerobes most commonly found?
• which genus may also be found in the soil and air?
Anaerobes are also prevalent in oral cavity, skin, colon, female genital tract
Some (Clostridia) found in soil and air as spores
Why is the growth of anaerobes inhibited by oxygen?
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
Why are anaerobic infections, often, but not always associated with a foul smell?
Metabolic end products of Anaerobic Infections Stink
What are two features to remember about the composition of absesses that are caused by anaerobic organisms?
- Species found in abscesses often reflect the normal flora in that site.
- Anaerobic infections are often polymicrobial (mixed anaerobic and facultative aerobic bacteria)
Bacteroides fragilis
• Gram Stain and Structure
• Where is it found?
Gram negative bacillus
Predominant organisms in the human colon (1011/g of feces) and found in vagina of 60% of women
T or F: Bacteroides fragilis is the the 2nd most common cause of serious anaerobic infections.
FALSE, it is the #1 cause of serious anaerobic infections in humans
Bacteriodes fragilis
• Major Virulence factor
• What role does this play in the formation of abscesses?
Polysaccharide capsule antiphagocytic important virulence factor
Host response to the capsule actually plays important role in abscess formation
What are the common predisposing factors to infection by bacteriodes fragilis?
Pathogenesis
Infections usually arise from a break in a mucosal surface
• Predisposing factors: surgery, trauma, chronic disease
What clinical finding are typical in a B. fragilis infection?
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
T or F: B. fragilis can have an enterotoxin that causes diarrhea.
True, some strains are associated with enterotoxin
Bacteroides fragilis
• Diagnosis
• Treatment
Diagnosis
Anaerobic cultures
Treatment
Resistant to Penicillin.
Universally susceptible to metronidazole, carbapenems, combination beta-lactam and beta-lactamase inhibitors (PIP/TAZO, AMOXI/CLAV)
Prevotella melaninogenica
• Gram Stain and Structure
• Typical Location
• Type of Pathogen
Gram negative coccobacillus
Commonly found in the oral cavity, also GI tract, vagina, nasopharynx
Opportunistic pathogen
Prevotella melaninogenica
• Types of opportunistic infections it can cause?
Clinical findings
• Oral/periodontal abscesses
• Pulmonary abscesses/empyemas
• Chronic otitis
• Sinusitis
Clostridium spp.
• what staining and structural features are common to all types?
Gram positive, spore-forming rods
The only anaerobic endospore-forming bacteria
• Resistant to high heat
• Resistant to harsh environment
Clostrium spp.
• what is key to the pathogenesis of this species?
• where are they found?
Exotoxins and secreted hydrolytic enzymes responsible for pathogenesis
Found in the colon and soil (spores)
Clostridium perfringins
• Describe the pathogenesis of food poisoning caused by this bug.
• how long before disease onset?
• how long before resolution?
- 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 (not preformed)
- 8-16 hour incubation period characterized by watery diarrhea with cramps; minimal vomiting. Resolves in 24 hours.
How clostridium tetani typically introduced into a wound?
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
How does the Tetanus (metalloprotease) toxin work?
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
How do patients infected by Tetanus often present clinically?
• what is often the first presenting symptom?
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
Clostridium Tetanae
• how would you treat this infection?
- 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 - Tetanus Vaccine at the time of diagnosis and 2 more doses after
T or F: Tetanus vaccine is not necessary in people who have been infected with the actual bug.
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
How is botulism typically acquired?
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
What is the most common type of botulism?
Infant > Food > Wound
What should you NOT give in the treatment of botulism?
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
How does botulism toxin work?
Pathogenesis
AB toxins
8 (A-H) antigenic types
Most potent bacterial toxin
Cleave SNARE proteins and prevent release of acetylcholine
What is the clinical presentation of botulism acquired by eating contaminated food?
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
What causes floppy baby syndrome?
• who do we see this in?
C. botulinum causes botulism - we see this in children 1 wk to 12 mo old.
How do kids most often get infected with C. botulinum?
• how does it present?
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
What is the treatment for botulism infections?
• how does this differ on the basis of age?
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.
Why are antibiotic contraindicated in infantile botulism?
Not recommended for infant botulism because lysis of intraluminal C. botulinum could increase the amount of toxin available for absorption
How can botulism be prevented?
Prevention
Proper cooking/canning
H. pylori
• Structure, Staining, Metabolism, Motility
Slender, curved gram negative rods
Motile with polar flagella
Microaerophilic
H. pylori
• what factors allow it to cause ulcers?
VacA: vaculolating cytotoxin
Cag: rearranges cytoskeleton (Cag = cytoskeleton associated gene)
H. pylori
• is Urease positive
• Has a PAI encoding a type III secretion system
H. pylori
• is Urease positive
• Has a PAI encoding a type III secretion system
