Lecture 6 (GI)- Exam 2 Flashcards
Enterobacteriaceae – G- rods
* Normally found where?
* What are some bacteria that cause disease?(3)
* What are the opportunistic bacteria?(3)
- Normally found in intestinal flora
- Some cause disease: Salmonella, Shigella, Yersinia pestis
- Some are opportunistic: E. coli, K. pneumoniae, P. mirabilis
Enterobacteriaceae – G- rods
* What does E.coli cause? (4)
* What is it the MCC?
* What are the types of AGEs?
E. coli: Cause UTI’s, Neonatal Meningitis, Sepsis, AGE
* MCC of G- sepsis and responsible for 80% of UTI’s
* Types of AGE (see next slide)
* ETEC (Enterotoxigenic)
* EPEC (Enteropathogenic)
* EAEC (Enteroaggregative)
* EHEC (Enterohemorrhagic)
* EIEC (Enteroinvasive)
Types of AGE
* What is ETEC?
* What is EPEC?
- ETEC (Enterotoxigenic): Developing countries (traveler’s diarrhea, infant diarrhea). Consumption of fecally contaminated water or food produces secretory diarrhea. Can involve A-B enterotoxin that acts like cholera toxin (milder symptoms).
- EPEC (Enteropathogenic): Underdeveloped countries (infant diarrhea); can be spread from person-to-person (easily spread). Bacteria attachment to intestinal cells results in loss of microvilli, followed by cell death.
Types of AGE
* What is EAEC?
* What is EIEC?
- EAEC (Enteroaggregative): Developing countries (traveler’s diarrhea, infant diarrhea) with outbreaks also occurring in developed countries; associated with chronic diarrhea and growth retardation in children. Bacteria adhere to intestinal cells and aggregate, promote protective biofilm formation, and produce toxins.
- EIEC (Enteroinvasive): Rare in developed and uncommon in developing countries. Watery diarrhea. E. coli enters into cytoplasm of colonic epithelium.
Types of AGE
* What is EHEC? What does it contain?
EHEC (Enterohemorrhagic): Most common pathogenic E. coli strains in developed countries. Consumption of undercooked ground beef or other meat, water, unpasteurized milk or fruit juices, uncooked vegetables (spinach), and fruits. Person to person spread can also occur. Mild symptoms to hemorrhagic colitis (bloody diarrhea and severe abdominal pain; no fever; 50% with vomiting). More common in warm months and in children under 5.
* EHEC contain Shiga toxin. Complications include hemolytic uremic syndrome (kidney failure) in 5-10% of infected children, which is lethal in 3-5% of cases.
Salmonella enterica
* What type of bacteria?
* Replicate where? What can they do?
* Inflammatory response confines where and causes what?
Pathogenic (not part of normal flora), ~2000 serotypes
Replicate in Peyer’s patches, therefore can invade lymphatic and circulatory systems
* Inflammatory response confines infection to gastrointestinal tract and promotes fluid secretion
Salmonella enterica
* Transmitted how? Liked to what?
* What is an important exception? How is it transmitted?
* Who is it most risk?
All are transmitted via ingestion
* Linked to food consumption during outdoor gatherings (summer and fall in US): poultry, eggs, dairy products, or surfaces contaminated with these
Important exception: Salmonella enterica, serovar Typhi and Paratyphi can be transmitted person-to-person or via food or drinks contaminated by infected food handler
Very young (under 5 years) and elderly (over 60 years) are most at risk
Salmonella enterica
* What are the 3 distinct clinical syndromes?
Gastroenteritis, Septicemia, Enteric (Typhoid) fever
Salmonella enterica: Gastroenteritis
* When does it occur?
* What are the sxs? (7)
* Most common what?
* 30% of infected individuals develop what?
- 6 to 48 hours after contamination (can last 2-7 days)
- Nausea, vomiting, and may have either bloody or non-bloody diarrhea (may include fever, abdominal cramps, myalgias (muscle pain), and headache)
- Most common salmonellosis in US
- 30% of infected individuals develop septic arthritis months after infection
Salmonella enterica
* What are the septicemia sxs?
* Enteric (typhoid) fever: Similar to what? Exam may revel what?(5)
Septicemia
* Symptoms generally resemble those of septicemia by other Gram – rods
Enteric (Typhoid) fever
* Similar to gastroenteritis but can last up to 2 weeks.
* Exam may reveal distended abdomen, splenomegaly, abdominal tenderness, bradycardia. Rash (rose spots) commonly occur in 2nd week of disease
Salmonella enterica
* How do you dx and tx it?
Dx: Stool Culture
* Leukopenia is typical
Tx: Supportive (IVF’s).
Salmonella enterica
* What does abx cause? What are the exceptions?
* What are the options?
- ABX do not shorten, but actually extend disease duration
* Exception: those with bacteremia, immunocompromised, malnourished or severely ill - Options: Bactrim, Cipro, ceftriaxone
Shigella
* Subspecies of what? What are the reservoirs? Who does it affect a lot of?
* What does the shiga toxin cause?
Subspecies of E. coli (EHEC), humans are only reservoirs
* 60% of cases affect children (hygiene and immune strength)
Shiga toxin of S. dysenteriae damages intestinal epithelium and may cause hemolytic uremic syndrome (kidney failure).
Shigella
* Shigellosis includes what sxs?timing?
Shigellosis includes abdominal cramps, diarrhea, fever, and bloody stools 1 to 3 days after ingestion
* Profuse watery diarrhea at beginning leading to lower cramps, tenesmus (straining to defecate), abundant pus and blood in stool
Shigella
* How do you dx and tx it?
- Dx: Stool Culture
- Tx: Self-limited infection but antibiotics help prevent spread to others (Azithromycin, Cipro, Ceftriaxone)
Yersinia
* What does it cause?
* Y. entercolitica and Y. pseudotuberculosis (rodents, pigs, rabits) are primarily what?
* Enterocolitis develops when?
Y. pestis (rats) causes highly fatal systemic disease via flea vector (causes plague)
Y. entercolitica and Y. pseudotuberculosis (rodents, pigs, rabits) are primarily enteric
* Enterocolitis develops 4-6 days after ingestion of contaminated food and water
Yersinia
* What are the sxs?
* How do you dx and tx it?
- Expect fever, abdominal pain, and diarrhea, which is often bloody
- Dx: Stool or blood culture
- Tx: Streptomycin or Doxycycline or Bactrim
Vibrio
* Flourish where?
* What does V. cholerae produce?
* When do you clinical see it? timing?
* What are the sxs?
Flourish in waters with shellfish (oysters, clams, mussels)
V. cholerae produces cholera toxin (induces severe secretory diarrhea)
* At height of disease, adult may lose up to 1 L of fluid/hour.
Clinically see 2 to 3 day onset from exposure. Diarrheal stool becomes “rice-water” stool: colorless, odorless, speckled with mucus.
* 60% mortality unless treated (replace lost fluids and electrolytes)
Vibrio:
* How do you dx it? What is the prevention?
* How do you tx it?
Dx: Stool culture or PCR
* Prevention – a vaccine exists, short-lived, limited protection and expensive
Tx: Ciprofloxacin Or Doxycycline or Azithromycin AND Fluids Replacement
* Antimicrobials will shorten course – but are indicated only in Severe form of Cholera and pregnant patients or those with HIV.
CAD
Campylobacter
* Campylobacter jejuni is the most common cause of what? Distant cousin of what?
* What is the epidemiology?
- Campylobacter jejuni is the most common cause of gastroenteritis in the U.S. stemming from contaminated poultry, milk or water.
- H. pylori is a distant cousin
- Epidemiology – one of the most widespread infectious diseases globally. Annual US #>845,000 at a cost ~1.7 billion dollars
Campylobacter
* What do you clinical see?
* How do you dx it?
- Clinically see enteritis 2-5 days following ingestion, i.e. diarrhea, malaise, relapsing remitting fever, and abdominal pain. Stools may be bloody.
- Dx: Stool Culture
Campylobacter
* What is the txt?
Tx: Self limiting, supportive management advised. Severe disease treated with erythromycin
* Alt: either Azithromycin 1 gram as a single dose or Cipro 500mg BID x 3 days (27% resistance in U.S.)
Enterococcus and other G+ Cocci
* Related to what?
* Commonnly colonizes where?
* Can proliferate when?
- Related to streptococcus (Known as Group D Strep)
- Commonly colonizes intestinal tract
- Can proliferate when patient is on broad spectrum ABX, and is one of the more common nosocomial bugs
Enterococcus and other G+ Cocci
* Clinically causes what? (3)
* Dx?
* How do you tx it?
Clinically cause UTI’s, peritonitis and endocarditis
Dx via Culture
Tx: Aminoglycoside (Gent) + Cell Wall ABX (Ampicillin or Vanc) OR Linezolid OR Cipro
* 25% have resistance to aminoglycosides
* E. faecium resistant to Ampicillin and Vanc
Bacillus Species: Bacillus antracis and cereus
* What is the morphology?
* GI effects due to what?
* What are the sxs?(7)
- Gram + rods releasing both edema and lethal toxins
- GI effects due to ingestion, mortality nearly 100%
- Ulcers in mouth or esophagus with regional LAD, edema and sepsis, N/V, malaise etc.
Bacillus Species: Bacillus antracis and cereus
* B.cereus most commonly found where? Diarrheal form found where?
* Dx?
* How do you tx it?
- B. cereus most commonly found in rice, causes emetic form
- Diarrheal form found in meat and vegetables
- Dx: Culture or PCR
- Tx: Cipro + PCN or Doxycycline
- PCN is not effective
Listeria monocytogenes
* Wide range of what?
* What is the mortality rate? With what?
* Replicated where?
- Wide range of growth (1 to 45 °C)
- Mortality rate 20-30% with contaminated or unpasteurized milk products or unwashed veggies
- Replicate within the cell. Not just the body, so hard to target
Listeria monocytogenes
* Disease is restricted to who? (4)
* What are the sxs?
Disease restricted to neonates (in-utero acquired), elderly, pregnant women, and patients with defective cellular immunity.
* Neonates: Meningitis
* Pregnant/Elderly: Severe flu-like symptoms/meningitis/bacteremia
Listeria monocytogenes
* How do you dx and tx it?
- Dx: CSF gram-stain will be negative, PCR is diagnostic
- Tx: Gentamicin + penicillin or ampicillin
Fecal Incontinence
* What is it?
* Most stem from what? (2)
* In some causes, what can contribute? (3)
* What are some other risk factors?(3)
Involuntary passage of stool due to lack of sphincter control
* Most stem from CNS or peripheral nerve destruction (MS)
* In some cases, hemorrhoids and rectal prolapse can contribute as well as use of laxatives or parasitic conditions
* Other risk factors are vaginal or cesarean delivery or anal trauma
Fecal Incontinence
* What is passive and urge incontinence?
* What is fecal seepage?
- Passive incontinence: Passive discharge of fecal material without any awareness; indicates neurological disease, impaired anorectal reflexes or sphincter dysfunction
- Urge incontinence: Inability to retain stool despite active attempts with preserved sensation; indicates sphincter dysfunction or inability of the rectum to hold stool
- Fecal seepage: Undesired leakage of stool often after abowel movement with normal continence
Fecal Incontinence
* What do you need to do for exam?
- Inspect for abnormalities and perform detailed neurological and rectal exam
- May use anal wink reflex, assess tone by having patient contract the sphincter
Fecal Incontinence: Dx
* Focus to r/o what?
* If incontinence without diarrhea, what should be performed?
* What is reserved for refractory or pre-operative assessment
- Focus to r/o infection, osmolality, steatorrhea of pancreatic insufficiency
- If incontinence without diarrhea, anorectal manometry with endoscopic ultrasound should be performed
- Defecography reserved for refractory or pre-operative assessment
Fecal Incontinence
* What are the supportive measures?
* What can do for medical management? (3)
* What can also be done?
Supportive measures: avoidance of provocations and treat underlying cause (if known)
Medical management
* Bulking agents (methycellulose)
* Loperamide or diphenoxylate
* If both urinary and fecal incontinece, amitriptyline is helpful
Biofeedback and surgery
Malabsorption
* Impaired what?
Impaired mucosal absorption of nutrients
Malabsorption
* What are the the phases that impairment can occur? (3)
- Luminal Phase: Nutrients are hydrolyzed and solubilized
- Mucosal Phase: Further break down of nutrients at the cell membrane and transported to the cell
- Transport Phase: Nutrients are transported to the vascular or lymphatic circulation
Luminal phase:
* What are the reduced nutrient availability causes?
* What are the defective nutrient hydrolysis causes? (3)
Reduced nutrient availability
* Cofactor deficiency (Pernicious Anemia) – intrinsic factor
* Nutrient consumption (Bacterial Overgrowth Syndrome) – not moving stuff well.
Defective nutrient hydrolysis
* Lipase
* Enzyme deficiency
* Improper mixing or rapid transit
Luminal phase:
* What is the impaired fat solubilization causes (5)
- Reduced bile salt
- Impaired bile salt secretion
- Bile salt inactivation
- Impaired CCK release
- Increased bile salt losses
Mucosal Phase
* WHat are the causes? (3)
- Extensive mucosal loss
- Diffuse mucosal disease
- Enterocyte defects
What are the mucosal phase enterocyte defects? (4)
- Microvillous inclusion disease
- Brush border hydrolase deficiency
- Transport defects
- Epithelial processing
What does this show?
KUB: Pancreatic Calcifications in Chronic Pancreatitis
Only in chronic. In Acute KUB is nl.
Celiac Sprue: presention
* What is happening with GI?
* Skin?
* Blood?
- Crampy abdominal pain, diarrhea, flatulence, bloating, weight loss, steatorrhea.
- Dermatitis Herpetiformis – blistering, pruritic skin rash (Gluten rash)
- Iron deficiency anemia
What happens to the mucosa in celiac sprue?
- Characterized by villous atrophy & crypt hyperplasia in proximal small bowel (right image)
- Blunting & flattening of villi with celiac disease, & in severe cases a loss of villi with flattening of mucosa
What is the difference between Marasmus vs Kwashiorkor
Marasmus: Caused primarily by a severe deficiency in total calorie intake (both protein and energy). It’s a result of prolonged starvation or insufficient intake of all nutrients.
Kwashiorkor: Primarily caused by severe protein deficiency despite an adequate intake of calories. It typically occurs when a child is weaned off breast milk onto a diet high in carbohydrates but low in protein.
Riboflavin (B2) Deficiency
* What are the sxs?
Angular stomatitis and chelitis
Vitamin A Deficiency
* What happens to Bowels?
* What are the sxs?
Typically malabsorptive
* Steatorrhea
Symptoms
* Night Blindness
* Follicular Hyperkeratosis
Vitamin D Deficiency
* What are two diseases that can occur?
- Rickets
- Osteomalacia
