Diarrhea Quiz Lectures Flashcards
secretory diarrhea
characterized as an infection of the proximal small bowel marked by watery diarrhea that does NOT contain fecal leukocytes. Viruses that cause gastroenteritis do not infect the colon
Rotavirus Clinical presentation:
gastroenteritis
Norwalk Virus (Norovirus) Clinical presentation:
gastroenteritis
Adenovirus Clinical presentation:
gastroenteritis (do not confuse with other serotypes of adenoviruses that cause respiratory tract infections)
Rotavirus Pathology:
transmitted via the fecal to oral route. After ingestion of the virus it travels in the GI tract (the virus particle is stable within the low pH of the gastrointestinal system) to eventually infect the villus cells of the proximal small intestine. Here the virus replicates within these cells eventually lysing these cells which leads to the impaired adsorption of carbohydrates and other nutrients. This can lead to vomiting followed by watery diarrhea.
Norwalk Virus (Norovirus) Pathology:
fecal to oral transmission usually through direct contact or through contaminated food and water. Causes a local infection and inflammation in the proximal small intestine.
Adenovirus Pathology:
fecal to oral transmission. Causes a local infection and inflammation in the proximal small intestine. If inhaled into the lungs some respiratory symptoms can be present.
Rotavirus Diagnosis:
stool specimen, serology for the virus. Electron microscopy and RT-PCR also possible.
Norwalk Virus (Norovirus) Diagnosis:
not typically done. When done it is through visualization of the virus in stool specimens or PCR/serology of stool and/or vomit specimens.
Adenovirus Diagnosis:
PCR detection of the viral genome within a stool sample
Rotavirus Treatment:
rehydration (supportive). There is a rotavirus vaccine (live oral attenuated).
Norwalk Virus (Norovirus) Treatment:
usually not required because it is self-limited. When done, treatment consists of rehydration (supportive) if there is severe fluid loss. Outbreaks can be minimized through proper food handling, clean water supplies, and hand washing.
Adenovirus Treatment:
self-limiting infection in immunocompetent individuals. Supportive care only.
Rotavirus
because rotaviruses cause no inflammation, diarrhea has no blood. Infection before 6 months of age is uncommon due to passive IgA immunity from the mother’s colostrum. However, by age 3, almost every individual worldwide (~95%) has been infected and develops lifelong immunity. Virus particle contains a double-layered capsid.
Norwalk Virus (Norovirus)
this virus is a major cause of group-related or institutional diarrhea.
Adenovirus
major cause of acute infantile gastroenteritis. These serotypes of adenoviruses rarely cause fever or respiratory tract symptoms.
bifidobacteria
are among the first colonizers in breast-fed infants
Staphylococcus aureus
Gram + Cocci Catalase + Coagulase + Also a common infectious agent of surgical wounds and cause of scalded skin syndrome
in food that sits around for a while
no need for antibiotics for a food borne infection
Bacillus cereus
Gram + Large Bacilli endospore-forming Facultative anaerobe Mostly motile β hemolytic Box-car shaped
Also frequently found on skin and is a threat in hospitals as it produces biofilms that adhere easily to invasive devices. This produces chronic persistent infection, as the biofilm can periodically release B. cereus into the bloodstream
B. Cereus spores are commonly found in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..
Spores can survive rice cooking process
Duration for both only about 24 hrs
Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen.
B. cereus in food and vomitus or feces of same serotype
Large numbers of B. cereus of serotype known to produce endotoxin
Only necessary when tracking outbreaks
Clostridium botulinum
Gram + Bacilli Spore-forming Obligate anaerobe Motile Spores or toxin are the important issues for transmission of botulism
Staphylococcus aureus Symptoms:
Symptoms:
nausea, vomiting, stomach cramps, and diarrhea for 1-3 days
Appear 1-7 hrs following ingestion of food
Self-limiting, once toxin is gone, illness is gone
Staphylococcus aureus diagnosis
Positive diagnosis:
Toxin-producing S. aureus can be identified in stool or vomit
Most conclusive test is the linking of an illness with a specific food, or in cases in which multiple vehicles exist, detection of pre-formed enterotoxin in food sample(s).
Only necessary when tracking outbreaks
Bacillus cereus infection
Infection takes two forms:
Emetic (vomiting):
Diarrheal:
Duration for both only about 24 hrs
Bacillus cereus Emetic infection
Emetic (vomiting):
1 to 6 hours incubation
Nausea and vomiting
resembles the vomiting illness caused by Staphylococcus aureus enterotoxins
Caused by preformed enterotoxin that forms holes in membranes
Self limiting
Bacillus cereus Diarrheal infection
Diarrheal:
6-15 hours incubation
clinically similar to the symptoms of Clostridium perfringens infection
Watery diarrhea and abdominal cramps
Mechanism: Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanisms
This toxin is not likely pre-formed!
Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestine
Vulnerable populations might get sicker and require antibiotics
Poor outcomes for systemic infection
Bacillus cereus diagnosis
Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen.
B. cereus in food and vomitus or feces of same serotype
Large numbers of B. cereus of serotype known to produce endotoxin
Only necessary when tracking outbreaks
Botulism
Food borne botulism: ingesting toxin
Wound botulism: producing toxin
Infant botulism: ingested spores
Not really a GI illness, diarrhea not prominent
Botulism Diagnosis
Symptoms and history, results of physical exam indicate botulism
Tests to exclude other causes of the illness
Organism or toxin in stool sample only indirect evidence
Treatment for foodborne botulism
Ventilator if respiratory failure and paralysis
Antitoxin if paralysis is not yet complete
Remove contaminated food if still likely in gut
Botulism toxin
neurotoxin
irreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysis
Toxin is absorbed from GI tract to bloodstream
Symptoms, botulism
Toxin already produced, symptoms can begin when toxin hits GI tract
double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness
Symptoms, infant botulism
Incubation period, spores have to produce toxin-forming bacteria
lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone
Can lead to paralysis of respiratory system and other muscles
Clostridium perfringens
Gram + Bacilli Spore-forming Obligate anaerobe Non-motile
Enterotoxin binds to receptors in endothelial cell junctions, then generates pores in host mucosa cells.
“C. perfringens infection often occurs when foods are prepared in large quantities and kept warm for a long time before serving”
Clostridium perfringens Symptoms
Symptoms:
Diarrhea and abdominal cramps
Incubation 6 to 24 hours (typically 8-12)
Symptoms last for less than 24 hours
Usually NO fever or vomiting
The illness is not passed from one person to another
Clostridium perfringens Positive diagnosis
Positive diagnosis:
Detection of toxin or high amounts of bacteria in feces
C. perfringens normally present in the GI tract, the problem is when you ingest a C. perfringens load high enough to produce enough toxin to generate symptoms
Clostridium perfringens Treatment
Treatment:
Usually self-limiting, but more serious, longer-lasting cases in immunocompromised individuals should be treated to avoid complications
Campylobacter jejuni
Gram - Bacilli (Spirilli) microaerophilic Motile Cold sensitive (often leads to false negatives)
get it from poultry
One unique feature is that campylobacter cannot usually multiply in food.
Symptoms:
diarrhea, cramping, abdominal pain, and fever
2-5 day incubation
Symptoms can last a week
Can have vomiting, diarrhea can be bloody
Mechanism: Symptoms are an inflammatory response to cell invasion
Positive Diagnosis: stool culture
Possible complication: Guillain-Barré syndrome
Salmonella enterica
Gram - Bacilli Non spore forming H2S positive & lactose negative Motile, flagellated
Salmonellosis
Symptoms: diarrhea, fever, and abdominal cramps 12 hr to 3 day incubation Symptoms typically last 4 to 7 days Most persons recover without treatment Remember: reactive arthritis as a possible complication
Diagnosis: we know for sure with a stool culture
Treatment: Hydration. Antibiotics only necessary if infection spreads beyond gut
Vibrio parahaemolyticus
Gram (-) Vibrio (curved rod) facultative anaerobes Flagellated, motile Oxidase + water loving
Diagnosis: Vibrio may be isolated from cultures of stool, wound, or blood.
Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasis
sushi and shellfish
Vibrio parahaemolyticus Symptoms
Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting,
Symptoms last less than a week.
In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body
Listeria monocytogenes
Gram positive rod-shaped bacteria
Although a rare illness, a leading cause of death by foodborne illness
Gram (+) Bacillus Non-fastidious!!! Flagellated, motile Non spore forming Oxidase -
Diagnosis:
Stool sample ID inappropriate
Positive ID is the bacterium found in a normally sterile site
Immune cells spread Listeria to other organs
Trojan horse
Liver is a major target
milk, cheese, seafood, deli
Listeriosis
Mild GI infection for most
More vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTIC
Fever and muscle aches or stiff neck, or if you develop while pregnant: fever and chills
Meningitis and sepsis in vulnerable populations
Shigella
Gram (-) Bacillus Facultative anaerobe nonmotile (distinguishes from e. coli) Non spore forming Mainly lactose negative, H2S (-) (distinguishes from e. coli)
Shigella sonnei: most Shigella-caused GI illnesses
Shigella flexnori: causes bacillary dysentery
Shigella dysenteriae: rarest but most severe dysentery
invade through m cells
Since Shigella is invasive, if not treated it can spread beyond the GI tract and cause complications
Antibiotics for more severe cases, most usually resolve without antibiotics
Possible complication: hemolytic uremic syndrome (HUS)
What is dysentery
Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)
Shigella Transmission
Transmission: Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.
Shigella Symptoms:
Symptoms: diarrhea (often bloody) fever stomach cramps Symptoms start 1-2 days following exposure Usually resolves in 5 to 7 days.
E. coli
Gram (-) Bacillus Facultative anaerobe motile Non spore forming Mainly lactose positive
Diarrhea
Urinary tract infection
Neonatal sepsis
Gram-negative sepsis
ETEC
STEC
Treatment: antibiotics generally not recommended (decaying bacteria release toxins)
Tracking outbreaks: commercial PCR and antibody-based kits.
ETEC
Traveler’s Diarrhea, diarrhea in children
activates adenylate cyclase, end result water into lumen, NO bacterial penetration.
STEC
penetrates like Shigilla toxin. hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable
E. coli Symptoms:
profuse watery diarrhea and abdominal cramping
Can progress to bloody diarrhea for STEC
Fever, chills
Nausea with or without vomiting, loss of appetite
Less common: headache, muscle aches and bloating
Incubation:1-3 days ETEC, 3-8 for STEC
Illness typically lasts 3-4 days, less than 10.
cholera toxin
Activates adenylate cyclase
cAMP → Na+ absorption, Cl- excretion
Water moves into lumen
typhoid fever
Only fecal-oral contaminant, no other host, so water is a big source of contaminaton
Drinking water, unwashed fruits/veggies
Travelers are vulnerable
Vaccine available
Life-threatening illness
In GI tract and then to bloodstream
High fevers (103-104 °F)
Weakness and headache
Stomach pains, loss of appetite, diarrhea or constipation
Sometimes, a rash of flat, rose-colored spots
After symptoms clear, person could become a carrier
Antibiotic treatment is recommended
High inoculum organisms
Tens of thousands or more needed
Examples: Vibrio cholerae, C. perfringens
Clostridium difficile
Gram + Bacilli Spore-forming Obligate anaerobe Motile Makes exotoxins antibiotic diarrhea
Toxins produced by C. difficile result in apoptosis of the colonic epithelium, and in the case of pseudomembranous colitis, produce a mucosal surface exudate of necrotic epithelial cells, neutrophils, mucin, and fibrin.
Diagnosis is established by detecting toxin producing strains of C. difficile, typically with a stool PCR assay.
Giardia lamblia
Also most common intestinal parasite in US
Giardiasis (aka Beaver Fever) is the foe of backpackers/hikers
Symptoms for 1-2 weeks or more, may seem to resolve and then come back
Mechanism: presence of parasite causes loss of epithelial absorptive surface area.
Trophozoites: Attachment but not penetration
Foul-smelling diarrhea
Filter water in areas where Giardia cysts are likely to exist. Water does not need to be contaminated with human sewage. Wildlife can deposit cysts.
Cryptosporidium parvum
Often seen when a sanitation system fails
Pool/waterpark chlorination/UV treatment
Storms or issues with drinking water
Diarrhea symptoms for 1-2 weeks to ~30 days, may seem to resolve and then come back
Mechanism: Absorption impaired and secretion enhanced when intestinal epithelial cells are infected by Cryptosporidium
“Crypto” is opportunistic
HIV/Immunocompromised individuals
Chronic Diarrhea/fluid loss
Can be fatal
Watery, frequent, non-bloody stool
Disrupts epithelial microvilli, slides into host
cells, enveloping itself in the host cell membrane
Oocysts to sporozoites and back
Coccidia subclass
Entamoeba histolytica
Amebiasis
More prevalent in tropical/subtropical climates
Only 10-20% of infected individuals will become ill (CDC)
Of US population, male homosexuals most vulnerable
Bloody, mucus-ey loose stool
Relatively mild symptoms but
Can invade the liver and form an abcess
X-ray/ultrasound to detect abscess or tissue damage
Cysts in stool sample. Must differentiate from non-pathogenic entamoeba, takes a specialist.
cytotoxic
Metronidazole, Tinidazole
Tissue antiparasitic- low concentration in intestine, oral dose almost completely absorbed with high bioavailability
Despite this, it is the drug of choice to treat symptomatic Giardia infection, even though organism that does not penetrate the epithelium!!
Reminder: all about metronidazole/Tinidazole in lectures relating to treatment of H. pylori
Disulfiram reaction, avoid alcohol
Disturb normal GI flora
breaks down into toxic metabolites, damages DNA
Nitazoxanide
Mechanism: Interferes with pyruvate::ferredoxin oxidoreductase enzyme dependent electron transfer, essential to anaerobic energy metabolism protein
Selectivity: Species difference in electron transfer
Distribution: Rapidly metabolized to tizoxanide. Parent compound is not detected in plasma. Moderately absorbed (33%), primarily luminal.
For Crypto, used in combination with retroviral therapy for AIDS patients if at all, because of ineffectiveness
Iodoquinol
Mechanism: Unknown
Toxicity:
loss of visual acuity
Use with caution in patients with thyroid disease – its use interferes with certain thyroid tests
Distribution: only 10% of the drug is absorbed so it works locally on the protozoa including cysts in the GI tract, luminal antiparasitic (amebicide)
Paromomycin
Mechanism: Aminoglycoside- targets 30S subunit ribosome
Toxicity: Diarrhea, other GI effects including issues with intestinal flora because it has activity against some bacteria.
Distribution: Luminal antiparasitic- Minimal absorption after oral administration
Ototoxicity, nephrotoxicity
TMP-SMX
Spectrum: Broad spectrum, many bacteria, but also effective against apicomplexans including Toxoplasma and Cystoisospora (formerly Isospora), and Cyclospora
hits folic acid system
Enterobius vermicularis
Staple-sized worms
pinworms
Worldwide distribution, most common helminth infection in US
Prevalence can reach 50% in children, caregivers of infected children, and institutionalized individuals.
Symptom: perianal pruritis
Acquired by ingestion of pinworm eggs
Eggs can remain viable on surfaces for 2-3 weeks
Necator americanus/Ancylostoma duodenale
Pruritic Papular Erythematous Rash
Hookworms are bloodsuckers…
Major symptom is iron-deficiency anemia
¼ ml/day/worm
Strongolides stercoralis
Autoinfection possible, especially with Immunosuppressed individuals
Stomach and GI complaints
Respiratory
dry cough
throat irritation
Skin
an itchy, red rash that occurs where the worm entered the skin
recurrent raised red rash typically along the thighs and buttocks.
Trichuris trichiura
Diagnosis:
Eggs in feces have a characteristic barrel-shaped appearance
Finger clubbing best indicator of
severity of infestation
Bloody diarrhea = iron
deficiency anemia
Heavy cases:
Frequent, painful stools with mucus, water and blood, tenesmus
Rectal prolapseAscaris lumbricoides
Disease: ascariasis
Disease: IF symptoms are experienced, abdominal discomfort
If a severe case, intestinal blockages
Ultrasonography and radiology to determine
Has a lung stage of life cycle, may cause cough
Diagnosis: eggs w/thick shells
Albendazole and Mebendazole
Broad-spectrum benzimidazole drugs
Roundworms and tapeworms
Distribution: Limited oral absorption, albendazole is better absorbed if targeting tissue-migrating larvae is important
Broad-spectrum benzimidazole drugs
Mechanism: Binds to parasite β-tubulin and inhibits the formation of microtubules
Death can take several days, for some helminths more than one dose may be necessary
Specificity: differences in tubulin
Toxicity:
Systemic toxic affects on liver/bone marrow rare
Abdominal pain, nausea, dizziness, headache
Embryotoxic and teratogenic in pregnant rats
Evidence suggests safe for use in children when warranted
Pyrantel pamoate and Levamisole
Mechanism:
Levamisole selectively opens a restricted subgroup of nematode acetylcholine receptor (AChR) ion channels in nematode nerve and muscle. depolarization entry of calcium through the opened channels, and an increase in sarcoplasmic calcium, producing spastic muscle contraction the parasite is then unable to maintain its location (often in the intestine) and is then swept away, effecting the cure.
Toxicity: Causes nausea, vomiting, diarrhea
Distribution: Poorly absorbed
Ivermectin
Mechanism: Binds to glutamate-gated chloride channels in invertebrate nerve and muscle cells, causing deactivation of channel: worm paralysis and death by starvation
Resistance: efflux transporters
Toxicity:
Generally well-tolerated
Itching, swollen lymph glands and rarely dizziness
Inflammatory reaction due to death of adult worms
Specificity: This type of channel restricted to phyla Nematoda and Arthropoda. in humans are only in the CNS , Doesn’t cross blood-brain barrier
Spectrum: Nematodes- Ascaris, Strongyloides and Onchocerca
Initial upper GI bleed management
Remember ABC’s
Airway?
CPR?
IV access
At least 2 large bore IVs
Infusion
Crystalloid
Blood products
Varices
Presentation: Dramatic bleeding, usually hematemesis
Causes: Portal hypertension
Associated with: Liver disease/cirrhosis
Treatment: Octreotide or Vasopressin Proton Pump inhibitor Non-selective Beta-blocker Variceal band ligation
Responsible for tolerance
Treg cells
NSAIDs and Peptic Ulcer Disease
Direct injury effects
Systemic effects
COX inhibition and prostaglandin production
Prostaglandins in the gut regulate mucus secretion and basal bicarbonate secretion
Prostaglandins are trophic for gastric epithelia and play role in feedback inhibition of gastric acid secretion
COX-2 selective inhibitors still pose risk for PUD
Intraepithelial Barrier
Intraepithelial Lymphocytes (IEL) promote barrier repair and are rapidly recruited Majority of IELs express CD8 (recognize MHC class I Ag) Two types of TCR αβ, thymus derived γδ, non-thymic derived 15% of small intestine IEL 40% of colonic IEL Produce keratinocyte growth factor
Lamina Propria
Reservoir to 70-80% total lymphocytes Predominate T cells are CD4, recognize MHC class II Ag
M Cells
Some bacteria and viruses cross the epithelial barrier via M Cells
