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Clinical Microbio > GI Pathogens > Flashcards

GI Pathogens Flashcards

1
Q

What are some examples of the antimicrobial defense mechanisms of the GI tract?

A
  • Microbial flora
    • Gram pos aerobes & anaerobes
  • Gastric acidity
    • inactivates some viruses, cidal for some enterics
  • Peristalsis
    • removes nonadherent bacteria, primarily in SI, limits size of population of pathogens, distributes normal flora
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2
Q

Describe characteristics of the normal flora of the gut

A
  • Complex ecosystem
  • important for protection vs. pathogens AND physiological health
    • Intestinal villi formation
    • synthesis of nutrients (Vit K)
    • degradation of secreted glycoproteins to help establish functional mucus consistency
    • Decrease & regulate inflammation
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3
Q

Describe when the normal gut flora is established, how it is disrupted, and describe its composition

A
  • Established after birth - influenced by diet/age, niche specific colonization
  • Disrupted by antimicrobial treatment
  • Composition - most (99.9%) obligate anaerobes, produce fatty acids that inhibit pathogens
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4
Q

What are the antimicrobial products of the different parts of the digestive system?

A
  • Mouth/oral cavity: saliva (Ig, complement, lysozyme, lactoferrin, peroxidases, defensins)
  • Intestines: bile salts, alpha/beta defensins (Paneth cells)
  • Pancreas: Lactoferrin, peroxidases
  • Colostrum: Ig, lactoferrin, lysozyme
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5
Q

Why are newborns especially susceptible to GI disease?

A
  • Immunologically naive
  • developmental/environmental signals drive changes of intestinal epithelium postnatally
  • neonatal intestinal mucosa characterized by:
    • Low levels of epithelial cell proliferation
    • absence of crypts and crypt-based Paneth cells
  • Lack of established normal flora
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6
Q

Which parts of the newborn GI tract is most vulnerable to disease?

A

mid-jejunum and distal ileum

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7
Q

Describe gingivitis and periodontitis

A
  • Infections caused by bacteria in biofilm (dental plaque) on oral surfaces
    • ​affects 80% of dogs and 70% of cats by 3 yo
  • Gingivitis = reversible stage of periodontal disease
  • Periodontitis = more severe
    • untreated = pain, tooth loss, systemic dz
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8
Q

Describe the 3 stages of the Gingivitis Index (GI)

A
  1. Marginal gingivitis with minimal inflammation and edema at free gingiva
    • No bleeding on probing
  2. Moderate gingivitis with a wider band of inflammation
    • Bleeding on probing
  3. ​Advanced gingivitis with inflammation clinically reaching mucogingival junction, usually with ulcerations
    • ​​Periodontitis usually also present
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9
Q

How do you score and treat gingivitis and periodontitis?

A
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10
Q

What do the ADVC guidelines for gingivitis and periodontitis say about the use of systemic antibiotics?

A
  • Should base abx selection on published MIC of known oral pathogens
  • pre-treatment w/ abx may improve health of infected oral tissues
  • Bacteremia is a recognized sequels to dental scaling & other oral procedures
    • ​healthy animals overcome this w/o use of systemic abx
  • Systemic abx recommended if animal:
    • Is immunocompromised
    • has underlying systemic dz
    • has oral infection present
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11
Q

Antibiotics should never be considered as what?

A
  • Monotherapy for treatment of oral infections
  • Preventative management of oral conditions
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12
Q

What are some of the systemic manifestations of dental infections?

A
  • Ophthalmic
    • orbital cellulitis, periodical abscesses, conjunctival signs, nasolacrimal signs, neuro-ophthalmologic signs, uveitis, endophthalmitis
  • Septicemia
    • ​bacterial endocarditits, localized embolic tissue infections
  • Degenerative mitral valve dz
  • Incr pathology of liver, kidney
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13
Q

What are some primary causes for glossitis?

A
  • Primary noninfectious causes: physical injury, metabolic conditions, autoimmune dz
  • Viral
    • CDV, canine/feline calicivirus, canine parvo
  • Bacterial, fungal, protozoa
    • Suppurative or granulomatous lesions (Histoplasma capsulatum)
  • Secondary infections
    • Candida spp.
      ​
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14
Q

Describe Feline lymphocytic plasmacytic ulceroproliferative gingivostomatitis (aka chronic faucitis, caudal stomatitis)

A
  • Multifactorial dz
  • Infectious agents: FeLV, FIV, FHV-1, Bartonella
    • ​direct causation not determined
  • C/S: vesicular, ulcerative, proliferative lesion in mucosa
  • Tx: aggressive oral health measures; extraction and tissue debridement if refractory
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15
Q

What are the primary pathogens causing stomatitis? What about dental enamel hypoplasia?

A
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16
Q

Describe the characterisitcs of GI infections

A
  • Spread by direct contact or fecal-oral route
  • many pathogens part of normal intestinal flora and disease develops after stress/disruption
  • definitive etiologic dx: demonstrate pathogen in tract or feces
17
Q

What are the major clinical signs of microbial infections of the intestines?

A
  • Vomiting
  • diarrhea
    • incr frequency, fluidity, and volume
  • Severity, duration, characteristics of diarrhea vary depending on infectious agents
18
Q

How do you differentiate between small and large bowel diarrhea?

A
  • Small bowel diarrhea: infrequent passage of large amounts of fluid feces
  • Large bowel diarrhea: frequent passage of small amounts of fluid feces, sometimes with mucus or blood
19
Q

What are the staples of therapy for diarrhea?

A
  • Fluids: IV, SQ, oral
  • Electrolyte replacement
  • Maintenance of acid/base balance
  • Control of discomfort
  • Motility-modifying drugs
20
Q

When should antimicrobial therapy be utilized in treating diarrhea?

A
  • If vomiting and diarrhea are accompanied by signs of systemic dz
    • ​e.g. Fever, lethargy, impending shock, presence of leukopenia or leukocytosis with marked left shift
    • absorption of microbes or toxins has occurred
  • If using abx, select drugs that target pathogenic species while sparing commensals
21
Q

What is the exception to the rule of antibiotic use for GI infections?

A
  • Neonates with diarrhea
    • ​they deteriorate rapidly before your culture and sensitivity results return
22
Q

What is the treatment protocol for neonates with suspected septicemia or endotoxemia secondary to a GI infection?

A
  • treat w/ systemic antimicrobials AND an NSAID
  • Initiate broad-spectrum abx:
    • Fluoroquinolones, penicillin, or cephalosporin + aminoglycoside, ampicillin, amoxicillin, tetracyclines, potentiated sulfas, chloramphenicol, florfenicol
    • In septic animals, GI absorption is likely altered —> parenteral administration preferred
23
Q

What are the causes of infectious pancreatitis and pancreatic abscesses?

A
  • Bacterial contamination secondary to acute pancreatitis
    • hematogenous, duodenal reflux, contamination from biliary tree, bacterial translocation from lower bowel via portal circulation
    • primary bacterial peritonitis is uncommon, secondary peritonitis d/t leakage from GI tract much more common
24
Q

What are the routes of infection for hepatobiliary infections?

A
  • Portal vein
  • hepatic artery
  • ascending via biliary system
  • contagious spread from adjacent sites of infection
  • Viruses, as part of systemic dz
25
Q

What are the causative bacterial agents of suppurative hepatobiliary infections?

A
26
Q

Name the common viral agents that result in GI infections in dogs

A
27
Q

Name the common viral agents that result in GI infections in cats

A
28
Q

Name the common bacterial agents that result in GI infections in dogs

A
29
Q

Name the common bacterial agents that result in GI infections in cats

A
30
Q

Name the common fungal and algal agents that result in GI infections in dogs

A

Clinical Microbio (11 decks)

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