Dysentery-diarrhea c blood and pus
Mechanisms of diarrhea
1. Increased fluid (secretory)
2. Decreased absorption
3. Increased transit
Functional-only during day
Secretory which is due to poor electrolyte absorption does not stop with fasting
Osmotic will stop with fasting
Bentyl 20 mg PO QID or 20 mg IM (not IV) Q4-6
Glycopyrrolate 1-2 mg PO Bid/Tid or 0.2 mg IV/IM Tid/Qid
osmotic diarrhea can be assessed by a stool osmotic gap >50 between measured and calculated (Stool Osm=2(Na+K))
WHO solution for oral hydration
3/4 tsp salt
1 tsp baking soda
1 cup of orange juice
4 tbl sugar
4 cups of water
(fluids must contain sugar)
D5 ½ NS c ½-1 amp bicarb and 20 meq KCl
Use Pepto, but not if ASA allergic
If cramps, try donnatol and 25 mg demorol
Get fecal wbc-if postive, get cx (pt can call for results and then get abx)
Cipro 500 BID x 5 days (if you use abx, then can give immodium as well)
Treat c bulk laxatives (yes laxatives in diarrhea they will absorb moisture reducing sx) Metamucil 1 tbl QID or
Then Kaopectate 1 tbl QID or Pepto 2 tbl q 30 minutes until no sx or 8 doses
Food Poisoning (Non-Sea Food)
most common bacterial
incubation 1-7 days, 24-72 hours most common
can progress to Guillane Barre
Bleed 60-90% of the time. ABX (Erythro or Cipro)
2nd most common bacterial food poisoning
S. typhimurium and S. enteriditis
Sx 6-48 hours after ingestion
Treat infants, elderly, compromised with cipro in adults, amp in kiddies
think underlying disease if healthy patient gets this infection
requires very small inoculum. Large WBCs
can have neuro symptoms, especially in kids
CBC with L shift and incredible number of bands
Can result in reiter’s, hus, pneumonitis
terminal ileum, mimics appendicitis. Can last 2 weeks. No ABX
Vibrio parahaemolyticus and vulnificus
Treatment of V. vulnificus consists of doxycycline, a third generation cephalosporin, and an aminoglycoside
E. Coli O157:H7
small # WBCs, hemolytic-uremic syndrome and TTP
Can be normal flora in healthy cattle
Fever is often absent, looks more like a LGIB than gastroenteritis
Syndrome of Toxemia, not bacteremia. Shiga Toxin
Pathophys is platelet-thrombin clots in arteries leading to ischemia
Normal stool culturing will not pick up, must ask for specifically
Antibiotics are not helpful
Contaminated food does not taste off
. Healthcare providers should specifically request testing for Shiga toxin producing E. coli (STEC) in patients being evaluated for bloody diarrhea or hemolytic uremic syndrome (HUS). The medium of choice for isolation is sorbitol-MacConkey (SMAC) agar. . Immediately report all suspected and confirmed cases of STEC infection or HUS to the New York City Department of Health and Mental Hygiene (DOHMH). . Send suspect and culture confirmed STEC (including E. coli O157:H7) isolates to the Public Health Laboratory (PHL) for confirmation, serotyping, and pulsed-field gel electrophoresis (PFGE).
can last up to 10 weeks. From brackish water (wells and springs) USE ABX
acts by toxin effect on CNS, not in GI
heat stable toxin, usually onset of sx is 6 hrs post-ingestion
vomiting c mild diarrhea
caused by spore formation of bacteria in gi tract which then causes release of enterotoxin
heat resistant spores, meat or poultry
6-24 hrs post-ingestion
vomiting is rare, severe watery diarrhea
can rarely cause necrotizing enterocolitis (can be fatal)
- is from heat stable toxin, usually fried rice
- Sx 2-3 hrs post-ingestion, 25% will have diarrhea as well. Lasts less than 10 hrs
- heat labile toxin from meat and vegetables
- 20% will have vomiting as well
- 6-14 hrs post ingestion
Sea Food Poisoning
Dark flesh fish-tuna, mahi-mahi, blue fish, bonito
heat stable toxin, saurine, a histamine-like toxin. Histidine on the fish’s skin is converted to histamine by surface bacteria.
Can be prevented by proper refrigeration which keeps surface bacteria counts low.
metallic, peppery taste when eating the fish
resembles histamine intoxication-face flushing, urticaria, diarrhea, dry mouth, n/v
Sx 30 minutes post-ingestion
Give Antihistamines (H1 and H2)
Diff Dx of Flushing: anaphylaxis, scombroid, ethanol/disulfiram rxn, ethanol in Asians (low aldehyde dehyd.), Niacin
Ciguatoxin (Ciguatera Syndrome)
Half of all fish food poisoning (most common in USA)
Tropical Regions from 35N to 35S latitude
Neurotoxin made by plankton then consumed by fish
Most commonly implicated is the Barracuda, higher up on the food chain is highest concentration: sea bass, grouper
Colorless, odorless, tasteless
Not inactivated by cooking, freezing, drying or smoking
Blocks sodium membrane permeability????
2 to 30 hour incubation, usually 5-6 hours
Begins c GI Sx: N/V/D
Progresses to neuromuscular/sensory: myalgias, paresthesias (perioral and extremity), Burning of hands and feet, pruritis, Vertigo, CN abnormality
Sensory Reversal: Hot feels cold and vice versa
Sensation of looseness of teeth
Dysuria or dyspareunia if have sex with infected man
Worsened c consumption of nuts or alcohol
Can see bradycardia or hypotension from induced vagal tone
GI symptoms abate 24-48 hrs but other symptoms can last days-weeks
Mannitol 1 g/kg over 30 min, though 1 recent study showed no benefit over NS (Neurology 58:873, March 2002) or antihistamines may have a role
Can also try amitriptyline 25 mg PO bid
Ciguatera fish poisoning occurs when fish is eaten that contain toxins produced by a dinoflagellate microalgae called Gambierdiscus toxicus. The toxin accumulates in fish that feed on algae. These small fish are the major food source for larger fish, the toxin becoming more concentrated in the fatty tissue, flesh and viscera in the larger fish. The fish most commonly involved in poisonings include barracuda, red snapper, amberjack, grouper, surgeon fish, sea bass, parrot fish, hogfish, kingfish, sturgeon, and dolphin. In the U.S., poisonings occur most frequently in the warm waters of Hawaii, Florida, Puerto Rico, U.S. Virgin Islands and other tropical territories; however, some fish migrate as far as South Carolina and Texas where cases have been reported. Scientists theorize that with increasing water temperatures and changes in fish migration patterns, the presence of G. toxicus will possibly increase in the Gulf of Mexico and southern Atlantic coastline. Cases reported in Maryland are usually people returning from visits to endemic areas. Fish shipped from southern waters to other areas have also resulted in poisonings. The appearance, taste and smell of contaminated fish are not altered. The toxin is not diminished by cooking or freezing. In a series of 12,890 cases, the onset of clinical effects was within 24 hours in 96% of patients, within 12 hours in 77%, and within 6 hours in 52%. Paresthesias and myalgias of the mouth, tongue and extremities, as well as abdominal pain, nausea, vomiting, and profuse watery diarrhea are characteristic of ciguatera poisoning. Other effects may include muscle weakness, diaphoresis, pruritus, headache, watery eyes, blurred vision, metallic taste and chills. The sensation of burning when in contact with cold objects has been described. Bradycardia, hypotension, hypothermia and respiratory depression may develop in severe cases; however, ciguatera has a very low mortality rate (<0.5%). Gastrointestinal symptoms usually subside within 24-48 hours but neurologic and cardiovascular symptoms persist for days to weeks. Treatment consists of supportive care. Activated charcoal may be beneficial in the rare case when a patient presents very early after the ingestion, but most patients do not realize that they have eaten contaminated fish until symptoms develop. Patients should be counseled to avoid alcohol and exercising for several months as they may exacerbate the neurologic symptoms. (Lisa Booze MD Poisons)
Fugu is the Japanese term for certain types of fish, such as puffer fish, balloon fish, and blowfish, whose flesh contains tetrodotoxin, the same potent paralytic neurotoxin found in blue ringed octopus saliva and certain newts.
Highest concentration is in ovaries>skin>liver>intestine.
Eating these fish will lead to at least some degree of poisoning.
Cooking does not destroy the toxin.
Toxins effects are caused by the blockage of sodium channels
After eating the fish there may be a delay of 30 minutes or so before onset of first symptoms, usually tingling around the lips. This may be followed by dysarthria, dysphagia, drooling and diplopia. Pupils may become fixed, dilated, which in tetrodotoxin poisoning, is not indicative of cerebral injury. Next limb weakness will occur, followed by respiratory paralysis, hypoxia, coma and death. Hypotension may occur in the later stages.
First, insure the ABCs. The second priority is to remove remaining unabsorbed food from the stomach, to prevent further toxin reaching the circulation. If still within 1-3 hours after the fish meal, Lavage and then give AC
Complete paralysis will require mechanical ventilation, but this is often short lived, being required only for a few hours, rarely a few days. Hypotension may respond to IV fluid loads, but pressors may be required in some cases.
Probably the etiology of the Haitian zombie syndrome
Most common during red tide months (months without r in them) when dinoflagellates are most prevalent (shellfish fish feed on them)
Caused by dinoflagellate toxin saxitoxin
GI symptoms 30 min 5 hours post ingestion
Paresthesias of face and hands then weakness and paralysis
mussels and scallops
Brevitoxin, can be aerosolized by tides and cause respiratory distress in beach goers
Paresthesias, ataxia, and gi symptoms, neurological dysfunction, such as paresthesias, reversal of hot and cold sensations, ataxia, depression of cardiovascular and respiratory function, and such GI symptoms as nausea, vomiting, and diarrhea.
Domoic acid. Causes headaches, seizures, hemiparesis, memory loss, and altered mental status
Okadiac Acid and Dinophysis Toxin. Diarrhea, nausea, cramps, and vomiting
Onset ~3 hours, can last for days
symptoms consist of severe headache and paresthesia followed by paralysis. Palytoxin is a coronary vasoconstrictor. Ischemia is widespread, causing anoxia in major organs. Palytoxin may cause symptoms similar to ciguatera, as well as intense muscle contractions and rhabdomyolysis.
ABX, especially clinda, pseudomembrane. If treating recurrence, give saccharomyces boulardi (yeast)
from shellfish, give Pepto
Infection begins with the ingestion of oocysts from fecal/oral contamination. 7-10 day incubation, then diarrhea with low grade fever, nausea, and crampy abdominal pain. Rarely is there blood or leukocytes in the stool. Can also cause acalculous cholecystitis. Mainstay of treatment is supportive care.
from beaver crap. Also c travel to Russia (the Trotskys),
Giardia Lamblia is a single celled parasite that lives in intestines of animals and humans.
Infection begins with the ingestion of cysts from contaminated food or water or fecal/oral contamination.
Diarrhea, sometimes with periods of constipation. Stool is frequently heme negative and can be without white cells as well. There are stool antigen studies, or stool can be examine for trophozoites.
Flagyl (remember disulfiram effects) 250 TID for 7 days. For pregnant women, use paromomycin or flagyl can be used in the second or third trimesters.
must get serologic testing before giving steroids. Flagyl
pinworm, tape test, make butt itch so babes put fingers in mouth. Vermoxx 2 doses 2 weeks apart
Need to quarantine for 3 days after last loose stools or get cx.
Pepto for prevention 2 tabs QID
Prophylaxis Cipro 500 mg QD
Best treatment for food poisoning, tank them up with IV fluids
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