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What are the 7 causes of inflammatory diarrhea?

- EHEC (enterohemorrhagic E. coli) 

- EIEC (enteroinvasive)

- Shigella 

- Salmonella: enterica and enteritidis 

- Campylobacter jejuni 

- Clostridium difficile 

- Yersinia enterocolitica 


What are the 6 causes of non-inflammatory diarrhea?

- ETEC (enterotoxigenic)

- EAEC (enteroaggregative)

- EPEC (enteropathogenic)

- Vibrio: cholera, parahemolyticus, and vulnificus 

- S. aureus 

- Bacillus cereus 


What are th 5 anaerobes?

- Bacteroides fragilis 

- Prevotella 

- Clostridium perfringens 

- Tetani

- Botulinum difficile 


What is the MCC of infectious diarrhea?

- 90% of infectious diarrheas are caused by VIRUSES


What should you think about when a pt presents with persistent diarrhea (>10-14d)? Chronic?

- PERSISTENT: more likely to be a parasite, rather than a bacterial or viral cause

- CHRONIC: start considering HIV status

1. Diarrhea is a big problem with AIDS pts: can get HIV-associated diarrhea w/or w/o other opportunistic infection

2. Mycobacterium avium intracellulare, CMV


What are the definitions of acute and chronic diarrhea?

- ACUTE: 3 or more loose stools/day lasting <2 wks

- CHRONIC: persists greater than 4 weeks


What is inflammatory diarrhea?

- BLOODY diarrhea, aka dysentery

1. WBCs and RBCs seen in stool

2. Fever is common

3. Small volume diarrhea

4. Colon is commonly affected, but not always just the colon


What is non-inflammatory diarrhea?

- WATERY diarrhea

1. No cells in stool

2. Usually afebrile

3. Large volume diarrhea

4. Small intestine is commonly affected


What are the general characteristics of Shigella, E. coli, and Salmonella?

- G(-), facultative, anaerobic rods 

1. Ferment glu w/acid production 

2. Oxidase (-) 

3. Reduce nitrates to nitrites (dipstick test) 

4. Motile (except Shigella) 

- Antigenic structures used in serotyping: H (flagellar) Ag's & O Ag's -> O-side chain (polysaccharide) of LPS

- E. coli are part of normal flora: most do NOT cause disease b/c lack pathogenicity associated island (PAI)


What are the 3 types, and transmission of Shigella?

- G(-), non-motile, non-lactose fermenting, does not produce H2S

1. S. dysenteriae: Central/S. America epidemics 

2. S. sonnei: 70% of US cases (mostly kids) 

3. S. flexneri: 2nd most comm in US (most comm worldwide)

- Highly transmissible (very low infectious dose) via fecal-oral or contaminated water/food 

1. Daycare centers, migrant workers, travelers to developing countries, nursing homes 

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What is the pathogenesis of Shigella?

- Resistant to acidic environment of stomach, and taken up by epithelial cells (M cells) in the intestine

- Proliferate IC, escape into lamina propria, and are phagocytosed by macros that then apoptose

- Inflam response damages epi and allows bac to gain access to colonic epi cells -> invasion

- Spreads into adjacent cells via bacterium-induced, membrane-bound protrusions from the surface of the host cell -> formation of these protrusions depends on cellular actin polymerization proteins called formins (F-actin polymerization b/c non-motile bac) 

1. Bacterium lyses membranes that surround it, freeing itself into the cytoplasm of the new cell 

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What are the clinical manifestations (and complications) of Shigella? Tx?

- CLINICAL: 1-wk incubation period 

1. Self-limited diarrhea, fever, & abdominal pain lasting about 1 week

2. Initially watery diarrhea, but progresses to dysentery (bloody) in 50%

3. Some adults will have a subacute course that lasts several weeks (less common)

- COMPLICATIONS: reactive arthritis, urethritis, conjunctivitis (Reiter’s)

1. Hemolytic uremic syndrome (HUS) may occur after infection with S. dysenteriae that produces Shiga toxin (AB toxin)

- TX: Ceftriaxone, Ciprofloxacin, Azithromycin -> AB's shorten the course and reduces duration of organism shedding in stools


What is unique about Enterohemorrhagic E. coli? Causes?

- Aka, STEC: Shiga toxin producing E. coli 

1. Produce Shiga-like toxins – clinical symptoms similar to Shigellosis (S. dysenteriae) 

2. Hemorrhagic colitis 

- Can’t ferment sorbitol (can be differentiated from other E. coli)

- Categorized as 0157:H7 and non-0157:H7 (both may cause severe illness)

- Caused by ingesting inadequately cooked meat (hamburgers), contaminated vegetables and milk; also human-to-human

1. Low infectious dose

2. Hospitalization required in 25-50% of patients


What are the 2 key pathogenetic mechs of EHEC?

- Locus of Enterocyte Effacement (LEE): 

1. PAI

2. Type III secretion system that delivers E. coli receptor to host cell

3. Pedestal formation 4 attachment -> attaching and effacing lesion

4. Responsible for the diarrhea

Shiga toxin acts by removing an adenine from large (28S) ribosomal RNA, stopping protein synthesis


What is the clinical presentation of EHEC?

- Little fever, acute onset cramps, + watery diarrhea

- Diarrhea becomes bloody (hemorrhagic colitis) w/in 24 hours, and lasts up to 8 days (quite a long time)

1. O157:H7 strains more likely to cause large outbreaks, bloody diarrhea, hemolytic uremic syndrome, and ischemic colitis


What 2 bacteria can cause HUS? How? Clinical manifestations?

- Shigella and more commonly, EHEC (6-9% of EHEC cases -> accounts for >90% of HUS in children)

1. One of the main causes of AKI in children <3

- HOW: shiga toxin absorbed from inflamed GI mucosa into circulation, and alters endo cell function of sm blood vessels and kidney epithelium -> platelet activation and aggregation + damaged RBC's that are lysed (schistocytes) 

- CLINICAL: microangiopathic hemolytic anemia and thrombocytopenia 5-10 days after onset of diarrhea

1. AKI w/dialysis required in >50% pts (most regain kidney function)

2. Neuro sxs (seizures, somnolence): 25%

3. Mortality rate of about 5%

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How is EHEC diagnosed and treated?

- DIAGNOSIS: Sorbitol-MacConkey agar

1. 0157:H7 strain does NOT ferment sorbitol:  colonies will be white/translucent (image)

2. Other EHEC/E. coli colonies will be red/pink

3. PCR or ELISA can detect Shiga toxin (in stool) 

- TX: supportive care + monitoring for complications

1. Avoid anti-diarrheals (INC risk of systemic cxs)

2. AB's are NOT beneficial, and may predispose to HUS by inducing more Shiga toxin release -> basically CONTRAINDICATED 

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How is EIEC transmitted? Pathogenesis?

- Similar to Shigella: causes similar disease

1. NO toxins produced 

- Transmitted via food/water and person-to-person contact 

- PATHOGENESIS: invades intestinal cell, multiplies IC, and extends into adjacent intestinal cells

- Most common in young children in developing countries


What are the basics of Salmonella? Subtypes?

- G(-) bacilli, non-lactose fermenting, produces H2S (unlike shigella)

- Salmonella enterica serotype Typhimurium (formerly S. typhi) and nontyphoid Salmonella

1. S. enterica is the causative agent of typhoid fever, and does NOT cause gastroenteritis

2. S. paratyphi is another species that can cause illness similar to Typhoid fever (also does NOT cause gastroenteritis)

3. Non-typhoid Salmonella, most commonly S. enteritidis, causes salmonellosis, a significant source of gastroenteritis from food poisoning


What are the sources of S. enteritidis?

- Dairy products

- Meat

- Poultry and eggs

- Pet turtles, lizards, other reptiles

- Human-to-human


What is the pathogenesis of S. enteritidis?

- Organisms attach to M cells, and are endocytosed through a complex pathway

1. Virulence genes encode a type III secretion system capable of transferring bacterial proteins into M cells and enterocytes

2. Bacterial proteins trigger endocytosis and allow bacterial growth within endosomes

- Bacteria cross basal membrane and enter lamina propria -> inflammatory response occurs

1. S. enteritidis also kills macrophages

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What is the clinical presentation of Salmonellosis? Dx?

- CLINICAL: incubation period 1-3 days

1. N/V, diarrhea (can be bloody), crampy abdominal pain + fever in 50%

2. Illness lasts 3-4 days

3. 5% devo invasive disease: bacteremia, endo-vascular infections, endocarditis, osteomyelitis (SICKLE CELL) -> predilection for aortic plaques, bone prostheses (likes to cling to, infect these)

a. Note: Shigella does NOT do this

4. Can also develop reactive arthritis

- DX: routine stool culture 


What is the tx for Salmonellosis? Who is it indicated for?

- Not required for healthy people between 2 and 50 years (self-limited, and will resolve on its own)

- Tx INDICATED FOR those at-risk of disseminated or invasive disease:

1. Immunocompetent patients w/severe infection requiring hospitalization

2. Those w/known or suspected atherosclerotic plaques and endovascular/bone prostheses

3. Immunocompromised (HIV, those on steroids or o/immunosuppressants), sickle cell disease

- TX: Flouroquinolones -> susceptibility testing should be performed


What is the causative agent of Typhoid fever? Transmission and epi?

- CAUSATIVE AGENT: S. enterica serotype Typhi

1. S. paratyphi can cause a similar illness

- Humans are sole reservoir; TRANSMISSION occurs person-to-person (fecal-oral, infected food handler) or via contaminated food/water

- EPI: more common in children and young adults than older patients

1. Most prevalent in impoverished, overcrowded areas with poor access to sanitation

2. 80% US cases in travelers to countries where typhoid fever is endemic (South-central Asia)

3. Outbreaks in the U.S. most often foodborne 


What is the pathogenesis of Typhoid fever?

- Orgs taken up by, invade M cells in sm intestine -> bacteria then engulfed by macros in lymphoid tissue 

- Can disseminate to lymph nodes and RES (reticuloendothelial system), then spread to blood

1. Sepsis can occur

- Proliferate in submucosa -> hypertrophy of Peyer’s patches due to influx of inflammatory cells

1. Hypertrophy + subsequent necrosis of sub-mucosal tissues can cause GI tract perforation 

- Chronic carriage can occur in the biliary tract

- NOTE: pts may devo "2o" bacteremia w/o/bugs due to micro or macro breach in intestinal mucosal barrier 

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What is the clinical presentation of Typhoid fever (by week)?

- Incubation period 5-21 days (variable)

- 1st wk of illness: rising fever/chills develop; pts are bacteremic, and relative bradycardia is possible

- 2nd wk: adominal pain + “rose spots” (faint salmon-colored macules on trunk/abdomen) may appear (see attached image)

3rd wk: hepatosplenomegaly, GI bleed, perforation, 2o bacteremia

1. Septic shock or altered mental status possible

- In the absence of death or severe complications, symptoms resolve over weeks to months

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How can Typhoid fever be dx'd? Tx'd? Prevented?

- DX: blood cultures (+) in 50-80% of pts, but may require several days (up to 5) of incubation

- TX: Ceftriaxone, Azithromycin, or Ciprofloxacin (unless the pt has been in an area with high rates of flouroquinolone resistance like South Asia)

- PREVENTION: vaccine


What are the basics of Campylobacter jejuni? Transmission?

- Thin, spiral shaped G(-) rods

1. C. coli is another species that can cause enterocolitis

- Most common bac enteric pathogen in developed countries (important cause of traveler’s diarrhea)

- TRANSMISSION: eating improperly cooked chicken; o/sources: unpasteurized milk, contaminated H2O

1. Reservoirs: sheep, cows, chickens, birds, dogs

2. Highly transmissible – very low ID

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What is the clinical presentation of C. jejuni?

- Incubation period 1 week

- Watery diarrhea (10+ BMs/day) that becomes bloody in 15% of adults and >50% of children

- Fever

- Crampy, periumbilical abdominal pain

- Self-limited over 3-7 days


What are the dx and tx for C. jejuni?

- DX: stool culture

- TX: only warranted for those with severe disease or at-risk of severe disease (bloody stools, high fever, worsening symptoms)

1. Azithromycin or Cipro are DOC; resistance rates to flouroquinolones are rising, however


What are the potential complications w/C. jejuni?

- MCC of Guillain Barre syndrome, but devo in only 0.1% or less of those infected w/C. jejuni 

1. Molecular mimicry: serum Ab's to C. jejuni LPS cross-react with peripheral & CNS gangliosides

2. Ascending paralysis that begins 1-2 weeks post-GI infection

- Erythema nodosum: inflam condition w/inflam of fat cells under skin -> tender, red nodules or lumps that are usually seen on both shins (attached image)

- Reactive arthritis (used to be called Reiter’s): more common with HLA-B27 phenotype

1. Can also be seen with Salmonella, Shigella, and Yersinia

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Yersinia enterocolitica

- G(-) coccobacilli w/bipolar staining (more common in Europe)

1. Infection preferentially involves ileum, right colon, appendix

2. Multiplies in lymphoid tissue -> regional lymph node and Peyer's patch hyperplasia

- SOURCES: pork, raw milk, contaminated water, pet feces

- CLINICAL: abdominal pain is main feature (Peyer's patch, mesenteric lymph node hyperplasia can mimic acute appendicitis in teens/young adults; RLQ pain)

1. N/V common, and fever/diarrhea can occur

2. Extraintestinal sxs frequent: pharyngitis, arthralgia, erythema nodosum (image attached)

- DX: stool culture

- TX: most cases do not warrant treatment

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What is C. diff? Transmission and epi?

- Anaerobic, spore-forming G(+) rod

- Carried in GI tract in 3% of pop and 30% of pts in the hospital

- TRANSMISSION: fecal-oral 

1. Hands of hospital personnel are important intermediaries

- EPI: most comm nosocomial cause of diarrhea and most common cause of antibiotic-associated diarrhea

- NOTE: may be hard to get under control and pts can have serious disease


What is the pathogenesis of C. diff?

- AB's suppress normal flora, allowing C. diff to multiply and produce exotoxins A and B

1. Exotoxins A and B cause glucosylation of small GTPases like Rho, involved in cytoskeleton structure and signal transduction

•Toxin A (enterotoxin) disrupts colonic mucosal cell adherence to colonic basement membrane and damages villous tips; inflammation leads to fluid secretion

•Toxin B (cytotoxin) causes depolymerization of actin, resulting in loss of cytoskeletal integrity, apoptosis and death of enterocytes

•Both toxins (A>B) stimulate monocytes and macrophages, which release IL-8 resulting in tissue infiltration with neutrophils; both cause disruption of epithelial tight junctions

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What is the clinical presentation of C. diff?

- Watery diarrhea is the cardinal symptom, but can progress to bloody diarrhea 

1. SPECTRUM of manifestations incl. carrier state to fulminant disease with toxic megacolon

- C diff associated diarrhea (CDAD) w/colitis: watery diarrhea (10-15 BM/day), mild lower abdominal pain and cramping, low grade fever, leukocytosis

- Pseudomembranous colitis: present similarly + sigmoidoscopy shows pseudomembranes (adherent layer of inflam cells + debris at sites of colonic muscle injury)

- Fulminant colitis: severe disease (severe abdominal pain, abdominal distention, fever, hypovolemia)

1. Toxic megacolon: colonic dilatation >7 cm with severe systemic toxicity

- Hypervirulent strains emerging: more severe, lower clinical cure rates, higher relapse rates (NAP-1/027)


What are the risk factors for C. diff?

- Advanced age

- Hospitalization

- Antibiotic treatment



How is C. diff dx'd?

- PCR can detect A & B toxins -> highly sensitive and specific

EIA for A & B toxins: high false (-) rate (75% sens)

Cell culture cytotoxicity assay: gold standard

1. Stool sample is added to a monolayer of cultured cells -> if C diff toxin is present, exerts cytopathic effect in tissue culture

2. Labor intensive: takes 2 days


How is C. diff treated?

- Metronidazole usually 1st line usually

1. If severe, PO Vancomycin indicated as 1st line 

- 1st recurrence: Metronidazole; 2nd recurrence: PO Vancomycin extended course

- Fidaxomycin new, and superior clinical response + less recurrences compared head-to-head with Vanc

- Fecal transplants hot new thing


What is this? Associated infection?

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- Pseudomembranes (on sigmoidoscopy) 

- C. diff 


What do you see here? Associated infection?

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- Colonic dilatation 

- C. diff 

- NOTE: toxic megacolon possible too (see attached)

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How do ppl get ETEC? Clinical presentation?

- Enterotoxigenic E. coli: contaminated food/water

1. Major cause of traveler’s diarrhea

- Clinical presentation:

1. Watery diarrhea, ranges from mild to severe

2. Duration of 1-5 days


What is the pathogenesis of ETEC?

- Produces heat-labile (LT) and heat-stable toxin (ST)

1. LT: like Cholera toxin; stimulates adenylate cyclase and INC IC cAMP, leading to secretion of Cl- from intestinal crypt cells + INH of absorption of NaCl at villous tips = secretion of free water into intestinal lumen (watery diarrhea)

2. ST: activates enterocyte cyclic GMP, also leading to stimulation of Cl- secretion and INH of NaCl absorption -> end result again secretion of free water into intestinal lumen


What is EPEC? Epi and pathogenesis?

- Enteropathogenic E. coli: most commonly assoc. with illness in children <6 months to 2 years of age in developing countries (diarrhea has been described in adults, though uncommon)

1. Profuse, watery diarrhea; can be severe, with vomiting and dehydration

- PATHOGENESIS: characterized by ability to produce attaching and effacing lesions and formation of pedestal like structures (LEE; attached image)

1. No Shiga toxin produced

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What is the epi of EAEC?

- Enteroaggregative E. coli: cause of diarrhea in kids and adults in both developed and developing countries (uncommon in adults)

1. Also can affect HIV+ patients in developing countries (and probably developed countries)

2. Can cause traveler’s diarrhea

- Pathogenesis not well understood


What are some other E. coli infections?

- Hospital-acquired infections: in many hospital labs, E. coli is the most commonly isolated organism

1. Sepsis

- Neonatal meningitis: encapsulated strains (K1-Ag)

- Uropathogenic E. coli (UPEC): cause 90% of urinary tract infections (UTI)

1. More common in females than males

2. Symptoms: freq, dysuria, pyuria, suprapubic pain, cloudy urine, cramping, afebrile or low-grade fever

2. Diagnosis: bacteria in urine

a. >105 per ml in females

b. >103 per ml in males

3. Virulence factors: P fimbriae (also called PAP pili), and a capsule (K antigen)


What are the Vibrio basics? Types?

- Curved (comma-shaped), G(-) rods

- Motile, polar flagellum; oxidase positive

- Commonly found in saltwater, disease in warm months

- Significant human pathogens:

1. V. cholerae

2. V. parahaemolyticus

3. V. vulnificus

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Transmission and epi of V. cholerae?

- TRANSMISSION: primarily via fecally contaminated drinking water, and less often food 

1. Natural/man-made disasters (Haiti earthquake)

2. Other factors predisposing to epidemics: poor sanitation, malnutrition, overcrowding, inadequate medical services

3. Humans are carriers and envo reservoirs; main animal reservoirs marine shellfish (eating without adequate cooking can cause disease)

- EPI: endemic in Asia, Africa, S. America, Indian subcontinent

1. Marked seasonal variation in incidence in most climates b/c rapid growth in warmer temps

2. >200 serogroups based on the O antigen, but O1 and O139 responsible for epidemic and pandemic cholera

a. O1 has 2 biotypes: E1 Tor and Classic

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What is the pathogenesis of V. cholerae?

- Dependent on colonization of small intestine and secretion of AB toxin -> lg #s of bac must be ingested for colonization to occur (sensitive to stomach acid; high infectious dose)

- Adherence to cells of brush border of gut related to secretion of bacterial enzyme mucinase that dissolves glycoprotein covering the intestinal cells

- Multiplies and secretes cholera toxin –> AB toxin

1. 5 B (binding) subunits: binds to ganglioside receptor on the surface of the enterocyte 

2. 1 A (active) subunit: inserted into cytosol and catalyzes add'n of ADP-ribose to Gs (stimulatory G) protein, causing persistent stimulation of adenylate cyclase 

a. cAMP overproduced, activates cAMP-dependent protein kinase that phosphorylates ion transporters in cell mem, leading to loss of water and ions

b. Watery efflux enters the lumen of the gut and massive watery diarrhea ensues

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What is the clinical presentation of V. cholerae?

- Incubation period 1-3 days

- Watery diarrhea in large volumes: up to 20 L/day

1. No RBCs or WBCs in stool

- Rice water stools: watery stool w/flecks of mucous and often has a fishy odor -> very large # of orgs in the stool

1. Vomiting and dehydration common

2. Abdominal pain usually absent

- DEHYDRATION: loss of fluid and electrolytes leads to cardiac and renal failure

1. Acidosis and hypokalemia also occur b/c loss of bicarb and K in the stool 

- 40% mortality rate without treatment 

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How is V. cholerae diagnosed? Tx?

- DX: most cases dx'd based on clinical suspicion

1. Organism can be isolated from stool using selective media like: Thiosulfate citrate bile sucrose (TCBS) agar, Taurocholate tellurite gelatin agar (TTGA), or MacConkey agar (colonies will be colorless)

- TX: mainstay is aggressive volume repletion 

1. AB's adjunctive therapy for pts w/cholera and moderate-severe vol depletion: Tetracycline, Erythromycin, Azithromycin, Ciprofloxacin 

2. Reduced osmolar ORS DEC stool output, vomiting, and need for supplemental IV fluids 

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How can V. cholerae be prevented?

- Clean water supply, appropriate sanitation

1. About 760 million people still lack access to clean water sources

- WHO recommends oral cholera vaccine in cholera control programs in endemic areas: Asia, Africa, S. America, Indian subcontinent

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V. parahaemolyticus: epi, clinical, dx, tx

- Marine organism transmitted by ingesting raw or undercooked seafood, especially shellfish (oysters).

- Major cause of diarrhea in Japan (raw fish eaten in large quantities)

1. Relatively rare in US, but can be seen in the Gulf and Pacific Coasts in warm months

- CLINICAL: incubation period about 1 day

1. Mild to severe WATERY diarrhea, N/V, fever, abdominal cramps

2. Self-limited of about 3 days’ duration

3. Bacteremia can occur in those w/underlying conditions, such as liver disease

4. Also causes wound infections: assoc with marine recreational activities and handling of seafood (generally mild, but can get severe cellulitis in those with liver disease, diabetes, alcoholism, etc.)

- DX: culture

- TX: volume repletion

1. AB's in severe cases: Doxycycline


V. vulnificus: epi, clinical, dx, tx

- Marine organism; most common foodborne illness in Japan

- CLINICAL: diarrhea, severe skin and soft tissue infections (see attached image)

1. Shellfish handlers who often sustain hand wounds are at risk of skin infection

2. Can cause rapidly fatal septicemia in immuno-compromised pts who eat raw shellfish w/org

a. Pts most at-risk are those w/underlying liver disease, alcohol abuse, and some chronic disease (diabetes, rheumatoid arthritis) -> 39% mortality rate, and bullous skin lesions are characteristic

- DX: culture

- TX: Doxy + Cefotaxime or Ceftriaxone

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Bacillus cereus: epi, transmission, clinical presentation

- Spore-forming, G+ bacilli abundant in soil, fresh H2O

- Can survive in envo for extended periods and withstand extremes of temp; can also survive in food processing environments

1. Has been recovered from rice, dairy products, spices, bean sprouts; fried rice important cause of emetic-type food poisoning 

- 2 enterotoxins: diarrheal enterotoxin & emetic toxin

- CLINICAL: diarrheal or emetic syndrome

1. Diarrheal syndrome: abdominal cramps, copious diarrhea, 8-16 hours after ingestion, resolves within 24 hours; vomiting uncommon

1. Emetic syndrome: caused by direct ingestion of the toxin cereulide (heat stable); abdominal cramps, N/V (diarrhea in 1/3 of people) w/onset in 1-5 hours of ingestion, resolve in 6-24 hours

a. Rice dishes: cooling fried rice dishes overnight at room temperature, then reheating the next day 

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S. aureus: toxin, transmission, clinical presentation

- Enterotoxin is heat-stable: acts as a superantigen within the GI tract to stimulate release of IL-1 and IL-2

- Consumption of foods prepared by a food handler like dairy, produce, meats, eggs, and salads (potato salad at a picnic)

1. Food handler contaminates the product

2. Food left at room temp and orgs multiply and can produce substantial quantity of toxin

- Symptoms begin within 1-6 hours of ingestion with N/V and abdominal cramps

1. Fever and/or diarrhea in a minority of patients

- Lasts 24 hours or less, but can be longer


Briefly describe the gut microbiome.

- Each individual harbors at least 160 different gut microbes

1. 57 shared by 90% of Europeans

2. 75 shared by 50%

3. Two phyla account for 90% of the species

- Evidence that our core gut microbiome influences our body weight, CV health and tendency to develop of type II diabetes

- Anaerobes (Bacteroides, Clostridia) are major contributors to the gut microbiome


What are the unique features of anaerobic infections?

- Lack SOD (superoxide dismutase) and catalase, so their growth is INH by O-> these enzymes eliminate the toxic compounds H2O2 and superoxide that are formed during production of energy by the organism

- Anaerobic infections STINK: odor caused by metabolic end-products (mostly organic acids)

1. Lack of putrid smell does NOT rule out anaerobic infection

- Special transport and culture required

- Anaerobic flora cause disease (abscesses) when introduced into normally sterile sites or when balance of orgs upset and pathogenic orgs overgrow

1. Species found in abscesses often reflect the normal flora in that site 

2. Anaerobic infections often polymicrobial (mixed anaerobic + facultative aerobic bacteria)

- Environmental anaerobes also cause disease: tetanus, botulism, gas gangrene


What is Bacteroides fragilis? Pathogenesis?

- G(-) bacillus: predominant orgs in human colon (1011/g of feces) + found in vagina of 60% of women

1. MCC of serious anaerobic infections

- PATHOGENESIS: usually arises from a break in a mucosal surface -> predisposing factors: surgery, trauma, chronic disease

1. Polysaccharide anti-phagocytic capsule important virulence factor

2. Host response to the capsule actually plays important role in abscess formation

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What clinical findings are assoc w/Bacteroides fragilis?

- Most frequently cause intra-abdominal infections, e.g., abscesses or peritonitis

- Pelvic or peri-rectal abscesses, bacteremia, infected decubitus ulcers can occur

- In general, causes disease below the diaphragm (lung abscess being the exception -> found in 25%)

- Enterotoxin producing strain can cause diarrhea


How is Bacteroides fragilis diagnosed and treated?

- DX: anaerobic cultures

- TX: resistant to Penicillin, but universally susceptible to metronidazole, carbapenems, combination beta-lactam and beta-lactamase inhibitors 


What is going on here? Describe the pathogen and other possible clinical findings.

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Prevatella melaninogenica: formerly Bacteroides melaninogenicus

- G(-) coccobacillus commonly found in oral cavity, GI tract, vagina, nasopharynx

- Opportunistic pathogen

- CLINICAL FINDINGS: oral/periodontal abscesses

1. Pulmonary abscesses/empyemas

2. Chronic otitis

3. Sinusitis: image on front of card 


What are the unique features of Clostridium?

- G(+), spore-forming rods

- The only anaerobic, endospore-forming bacteria

1. Resistant to high heat

2. Resistant to harsh environment

- Exotoxins and secreted hydrolytic enzymes responsible for pathogenesis

- Found in the colon and soil (spores)


What clinical syndromes are assoc w/C. perfringens?

- Large, “boxcar” G(+) bacilli found in soil and colon

- CLINICAL SYNDROMES: gas gangrene and food poisoning

1. 3rd most common foodborne illness in the U.S. -> watery diarrhea

2. Heat-resistant spores survive cooking, then spores can germinate in foods such as meats, poultry or gravy at lower temps

3. Following ingestion of large quantity of organisms, enterotoxin produced in the GI tract

4. Outbreaks in psych inpatient facilities 

5. 8-16 hr incubation period with watery diarrhea + cramps + minimal vomiting; resolves in 24 hrs


How is C. tetani transmitted? Pathogenesis?

- TRANSMISSION: spores found in soil, and portal of entry usually a wound site (e.g., nail penetrates foot)

1. Also can be introduced during “skin-popping”

2. Neonatal tetanus a major problem in developing countries -> org enters through contaminated umbilicus or circumcision wound

- PATHOGENESIS: tetanus toxin (tetanospasmin), an AB neurotoxin (metalloprotease)

1. Enters at NM junction and is transported by motor neurons (via retrograde axonal transport) to ganglia in brain and spinal cord 

2. Toxin binds tightly and irreversibly to ganglioside receptors and blocks release of INH neurotransmitters (glycine and GABA) by its cleaving action on membrane proteins (SNARE) involved in neuro-exocytosis

3. Net effect is disINH of neurons that modulate excitatory impulses from motor cortex, resulting in INC muscle tone, painful spasms, widespread autonomic instability 

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What is the clinical presentation of tetanus?

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- 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

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What is the treatment for tetanus?

- Wound debridement to eradicate spores

- Human tetanus immune globulin (HTIG) used to neutralize the toxin

- AB's probably play minor role, but universally recommended -> DOC Metronidazole; Penicillin is an acceptable alternative

- Tetanus does NOT confer immunity after recovery from acute illness

1. All pts should receive active immunization with 3 doses of tetanus toxoid spaced at least 2 wks apart and 1st dose given immediately at dx


What are the 5 different manifestations of C. botulinum?

- Causes botulism of different forms:

1. Foodborne (classic) botulism: home-canned foods like fruits, vegetables; and fish 

2. Infant botulism: inhalation or ingestion of spores in carpet or raw honey 

3. Wound botulism: rise in incidence in CA due to black tar heroin users 

4. Inhalational: would be an act of bioterrorism

5. Iatrogenic

- 110 cases/year reported in the U.S.: 72% infant, 25% foodborne, 3% wound


How is foodborne botulism transmitted? Clinical presentation?

- Spores resistant to heat; germinate after cooking and release toxin

1. Subsequent heating will inactivate toxin (heat-labile)

- CLINICAL: acute, symmetric descending flaccid paralysis

1. Symptoms begin 12-36 hours post-ingestion

2. Nausea, dry mouth, dysphagia, diarrhea, blurred vision

3. Paralysis descends to respiratory muscles, trunk and extremities -> possible death by respiratory failure

- NOTE: AB's NOT recommended for infant botulism or adults w/suspected GI botulism bc lysis of intra-luminal bac could INC toxin available for absorption


How is infant botulism transmitted? Clinical presentation?

- “Floppy baby syndrome:" infants 1 wk-12 mos

- Infection first, then intoxication: inhale or ingest spores (environmental dust) or honey

- CLINICAL: presentation and severity variable

1. Constipation followed by weakness, feeding difficulties, descending global hypotonia, drooling, anorexia, irritability, weak cry


What is the treatment for botulism? Prevention?

- TX: mechanical ventilation

1. Horse anti-toxin for those over 1 year of age

2. Human-derived botulism immune globulin (BIG-IV) for infants <1 year of age

3. AB therapy unproven, but recommended for WOUND botulism only (DOC penicillin, but metronidazole a possible alternative)

a. Not recommended for infant botulism bc lysis of intraluminal bac could increase the amount of toxin available for absorption

- PREVENTION: proper cooking/canning


What is H. pylori? Clinical importance? Virulence factors?

- Cause of ulcers that is spread human-to-human by fecal-oral route or gastric secretions

1. Associated with 95% of duodenal ulcers and 70% of gastric ulcers

2. Also assoc with gastric adenocarcinomas and lymphomas

- Slender, curved G(-) rods that are motile with polar flagella and microaerophilic

1. VacA: vacuolating cytotoxin

2. PAI encoding Type III secretion system

3. Cag: rearranges cytoskeleton

4. Urease

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What is the pathogenesis of H. pylori?

- Combination of cell destruction leads to ulcers via: 

1. VacA: vacuolating cytotoxin

2. Cag: rearranges cytoskeleton

3. Immune response

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How is H. pylori dx'd and tx'd?

- DX: endoscopy with biopsy and culture

1. Stool antigen

2. Urea breath test

3. Serology

- TX: triple/quadruple therapy covered in GI lecture