What are some examples of the antimicrobial defense mechanisms of the GI tract?
- 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
Describe characteristics of the normal flora of the gut
- 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
Describe when the normal gut flora is established, how it is disrupted, and describe its composition
- 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
What are the antimicrobial products of the different parts of the digestive system?
- 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
Why are newborns especially susceptible to GI disease?
- 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
Which parts of the newborn GI tract is most vulnerable to disease?
mid-jejunum and distal ileum
Describe gingivitis and periodontitis
- 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
Describe the 3 stages of the Gingivitis Index (GI)
- Marginal gingivitis with minimal inflammation and edema at free gingiva
- No bleeding on probing
- Moderate gingivitis with a wider band of inflammation
- Bleeding on probing
- Advanced gingivitis with inflammation clinically reaching mucogingival junction, usually with ulcerations
- Periodontitis usually also present
How do you score and treat gingivitis and periodontitis?
What do the ADVC guidelines for gingivitis and periodontitis say about the use of systemic antibiotics?
- 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
Antibiotics should never be considered as what?
- Monotherapy for treatment of oral infections
- Preventative management of oral conditions
What are some of the systemic manifestations of dental infections?
- 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
What are some primary causes for glossitis?
- 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.
- Candida spp.
Describe Feline lymphocytic plasmacytic ulceroproliferative gingivostomatitis (aka chronic faucitis, caudal stomatitis)
- 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
What are the primary pathogens causing stomatitis? What about dental enamel hypoplasia?
Describe the characterisitcs of GI infections
- 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
What are the major clinical signs of microbial infections of the intestines?
- Vomiting
- diarrhea
- incr frequency, fluidity, and volume
- Severity, duration, characteristics of diarrhea vary depending on infectious agents
How do you differentiate between small and large bowel diarrhea?
- 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
What are the staples of therapy for diarrhea?
- Fluids: IV, SQ, oral
- Electrolyte replacement
- Maintenance of acid/base balance
- Control of discomfort
- Motility-modifying drugs
When should antimicrobial therapy be utilized in treating diarrhea?
- 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
What is the exception to the rule of antibiotic use for GI infections?
- Neonates with diarrhea
- they deteriorate rapidly before your culture and sensitivity results return
What is the treatment protocol for neonates with suspected septicemia or endotoxemia secondary to a GI infection?
- 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
What are the causes of infectious pancreatitis and pancreatic abscesses?
- 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
What are the routes of infection for hepatobiliary infections?
- Portal vein
- hepatic artery
- ascending via biliary system
- contagious spread from adjacent sites of infection
- Viruses, as part of systemic dz
