Enteric Bacteria- anaerobes Flashcards

1
Q

anaerobe general characteristics

A
  • major contributors to gut microbiome
  • prevalent in oral cavity, skin, colon, and female genital tract
  • some clostridia found in soil and air as spores.
  • infections stink casued by metabolic end products of orgs which are mostly orgnaic acid. lack of putrid smell does NOT rule out anaerobic infection
  • special transport and culture required.
  • anerobes lack superoxide dismutase (SOD) and catalse which is why growth of anerobes is inhibited by oxygen. These enzymes eliminate toxic cmpds h202 and superoxide which are formed during production fo energy by the organism
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2
Q

general characteristics of bacteriodes fragilis

A
  • gram negative bacillus
  • predominant organism in the human colon and found in vagina of 60% of women
  • MCC of serious anaerobic infections
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3
Q

pathogenesis of Bacteroides fragilis?

A
  • infection arise from break in mucosal surface- predisposing factors: surgery, trauma, chronic disease
  • polysaccaride antiphagocytic capsule important virulence factor
  • host response to the capsule actually plays important role in abscess formation
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4
Q

clinical presentation of bacteroides fragilis?

A
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5
Q

dx and tx of bacteroides fragilis?

A
  • dx: anaerobic cultures
  • tx: resistent to penicilin. universally susceptible to metronidazole, carbamenems, combo beta lactam and betalactamase inhibitors.
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6
Q

prevotella melaninogencia general characteristics

A
  • gram neg coccobacillus
  • commonly found in oral cavity, gi tract, vagina and nasopharynx
  • opportunistic pathogen
  • clinical findings: oral/periodontal abscess, pulmonary abscess/empyemas, chronic otitis, sinusitis.
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7
Q

clostridium general characteristics

A
  • gram positive, spore forming rods
  • only anerorbic endospore forming bacteria (resistent to high heat and harsh environment)
  • exotoxins and secreted hydrolytic enzymes responsible for pathogenesis
  • found in colon and soil
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8
Q

c. perfringens general characteristics

A

boxcar gram + bacilli

  • found in soil and colon
  • clinical syndromes include gas gangrene, food poisoning (watery diarrhea-3rd most common foodborne illness in US)

* heat resistant spores survive cooking and can germinate in meats, poultry or gravy at lower temps

  • following genstions of large quantity of orgs, enterotoxin is produced in GI tract
  • oubreaks in PSYCH inpatient facilities
  • 8-16 hr incubation period w/ watery diarrhea and cramps. minimal vom. resolves in 24 hrs.
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9
Q

C. tetani general characteristics

A
  • spores found in soil, portal of entry in wound site (nail through foot), skin popping
  • neonatal tentanus major problem in devleoping countries- organisms enter through contaminated umbilicus or circumcision wound
  • pathogenesis: tetanus toxin- AB neurotoxin
  • enters at NMJ and is transported by motor neurons to ganglia
  • tonxin bind irreversibly to ganglioside receptors and block release of inhibitory NTs like glycine and GABA by cleaving on membrane proteins SNARE involved in neuroexocytosis.

–> disinhibition of neurons that modulate excitatory impulses from the motor cortex resulting in increased muscle tone, painful spasm, and widespread autonomic instability.

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10
Q

clinical presentation of tetanus?

A
  • strong muscle spasms or spastic paralysis
  • trismus (lock jaw) first
  • grimas known as risus sardonicus
  • exaggerated reflexes
  • opisthotonos- pronounced arching of back d/t spasm of the strong extensor muscles of the back
  • resp failure can occur
  • high mortality rate
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11
Q

tetanus tx?

A
  • wound debridement to eradicate spores
  • human tetanus immune globulin (HTIG) used to neutralize toxin
  • ab probably play a minor role but are recomended (DOC is metronidazole. pen is an acceptable alternative)
  • tetanus doesnt confer immunity following recovery - all pts with tetanus should receive active immunization with a total of 3 doses of tetanus toxoid spaced at least 2 weeks apart w/ the 1st dose given immediately at diagnosis.
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12
Q

what are the different forms of C. botulinum botulism?

A
  • foodborne (Classic) botulsim, veggies, home canned foods, fish
  • infant botulism (inhalation or ingestion of spores in carpet or raw honey)
  • wound botulism
  • inhalational- bioterrorism
  • Iatrogenic

72% infant in US

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13
Q

pathogenesis of C. botulinum?

A
  • AB toxins: 8 (A-H) antigenic types, most potent bacterial toxin, cleaves SNARE proteins and prevent release of Ach.
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14
Q

why are antibiotics NOT recommended for infant botulism or for adults with suspected GI botulism?

A

bc lysis of intraluminal c. botulinum could increase amt of toxin available for absorption

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15
Q

classic foodborne botulism clinical presentation and general characteristics?

A
  • spores resistant to heat, germinate after cooking and release toxin
  • subsequent heating will inactivate toxin (heat labile)
  • clinical presentation: acute assymetric DESCENDING flaccid paralysis. symptoms start 12-36 hrs after ingestion. Nausea, dry mouth, dysphagia, diarrhea, blurred vision

paralysis descends to resp muscles, trunk and extremeties.

**possible death via resp failure

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16
Q

infant botulism clinical presentation and characteristics?

A
  • floppy baby syndrome
  • infants 1 week to 12 months of age
  • infection first and then intoxication (inhale or ingest spores- environmental dust- orhoney)
  • presentation: constipation f/w weakness, feeding difficulties, descending global hypotonia, drooling, anorexia, irritability, weak cry.
17
Q

Tx of botulism?

A
  • mechanical ventilation
  • horse antitoxin for those over 1 year of age
  • human derived botulism globilim (BIG-IV) available for infants less than 1 year of age
  • ab therapy unproven by recommedned for WOUND botulism

DOC penicilin, metronidazole (not recommended for infant botulism bc of lysis)

**prevention: proper cooking and canning.

18
Q

H pylori gen characterisitcs

A
  • cause of ulcers
  • human to human by fecal-oral route or gastric secretions
  • associated with 95% duodenal ulcers and 70% of gastric ulcers
  • associated with gastric adenocarcinoma and lymphomas.
19
Q

H pylori virulence factors

A
  • slender curved gram negative rod

motile with polar flagella

microaerophillic

  • vacA- vaculolating cytotoxin
  • PAI- encoding type 3 secretion system
  • CAG-rearrange cytoskeleton
  • urease
20
Q

h pylori pathogenesis, dx, and tx?

A

pathogenesis: combination of cell destruction by VacA, Cag and immune response leads to ulcers
- diagnosis : endoscopy with biopsy and culture, stool antigen, urea breath test, serology
- tx: triple/quadruple therapy covered in GI lecture