Bad Bug Book Flashcards
Ciguatoxin: Organism and Toxin
Dinoflagellates (marine algae) in the genus Gambierdiscus occur in certain tropical and subtropical areas of the world.
These dinoflagellates elaborate ciguatoxins and/or precursors of the ciguatoxins called gambiertoxins.
These compounds are transmitted through the marine food web, they are concentrated and may be chemically altered. Ciguatoxins are not significantly affected by cooking or freezing
Ciguatoxin mortality
Mortality: There is a very low incidence of death, from respiratory and/or cardiovascular failure.
Ciguatoxin Toxic dose
Toxic dose: Not well established, and variable, since many different ciguatoxins, of different toxicities, may be present in a toxic fish.
Probably less than 100 nanograms (100 billionths of a gram) is adequate to cause illness.
Ciguatoxin Onset of symptoms
Onset: Usually within 6 hours after consumption of toxic fish
Ciguatoxin Illness / complications and Treatment
Illness / complications: Ciguatera in humans usually involves a combination of gastrointestinal, neurological, and, occasionally, cardiovascular disorders.
There is no reliable, proven treatment for the poison.
Ciguatoxin Symptoms
- Gastrointestinal symptoms include nausea, vomiting, and diarrhea.
- Neurological symptoms include perioral numbness and tingling (paresthesias), which may spread to the extremities; itching; arthralgia; myalgia; headache; acute sensitivity to temperature extremes; vertigo; and severe muscular weakness.
- Cardiovascular signs include arrhythmia, bradycardia or tachycardia, and hypotension.
Symptoms defined within these general categories vary with the geographic origin of toxic fish, and to some extent, with the species of fish.
Ciguatoxin Duration
Duration: Symptoms of poisoning often subside within several days of onset. However, in severe cases, the neurological symptoms may persist from weeks to months.
In a few isolated cases, neurological symptoms have persisted for several years, and, in other cases, patients who have recovered have experienced recurrence of neurological symptoms months to years afterwards. Such relapses are most often associated with consumption of fish (even non-toxic fish), alcohol, caffeine, or nuts.
Ciguatoxin Route of entry:
Route of entry: Oral.
Ciguatoxin Pathway
Pathway: Ciguatoxins are cyclic polyether compounds that bind to and activate voltage-sensitive sodium channels in excitable tissues.
Ciguatoxin Frequency in the US
The relative frequency of ciguatera fish poisoning in the United States is unknown;
current estimates of the worldwide occurrence range from 50,000 to 500,000 cases per year.
There is a concern that the incidence is largely under-reported.
Ciguatoxin Sources and Areas that are noted for toxic fish in or near U.S. waters
Marine finfish most commonly implicated in ciguatera fish poisoning include certain species of groupers, barracudas, snappers, jacks, mackerel, triggerfish, and others.
Many warm-water marine fish species in tropical and subtropical waters may harbor ciguatera toxins.The occurrence of toxic fish is sporadic, and not all fish of a given species or from a given locality will be toxic.
Areas that are noted for toxic fish in or near U.S. waters include South Florida, the Bahamas, the U.S. and British Virgin Islands, Puerto Rico, and Hawaii.
Ciguatoxin Diagnosis
Clinical testing procedures are not presently available for the diagnosis of ciguatera in humans.
Diagnosis is based entirely on signs, symptoms, and a history of having consumed fish from tropical or subtropical areas.
Ciguatoxin Target Populations
All humans are believed to be susceptible to ciguatera toxins. Populations in tropical / subtropical regions are most likely to be affected because of the frequency of exposure to toxic fish
Ciguatoxin Food Analysis
The ciguatera toxins can be recovered from toxic fish through time-consuming extraction and purification procedures.
The mouse bioassay historically has been the accepted method of establishing toxicity of suspect fish. It has now been largely supplanted by in vitro (e.g., the cytotoxicity assay) and instrumental (e.g., LC-MS/MS) methods
Ciguatoxin Examples of Outbreaks
Examples of Outbreaks
MMWR 58(11): 2007 – Seven cases of ciguatera caused by consumption of amberjack were investigated by the Food and Drug Protection Division of the North Carolina.
MMWR 47(33):1998 – This report summarizes an investigation of this outbreak by the Texas Department of Health (TDH), which indicated that 17 crew members experienced ciguatera fish poisoning resulting from eating a contaminated barracuda.
MMWR 42(21):1993 – Twenty cases of ciguatera fish poisoning from consumption of amberjack were reported to the Florida Department of Health and Rehabilitative Services (HRS) in August and September 1991.
Shellfish toxins currently regulated by the FDA
- Paralytic shellfish poisoning (PSP) ,
- Diarrhetic shellfish poisoning DSP,
- Neurotoxic shellfish poisoning (NSP),
- Amnesic shellfish poisoning (ASP),
- Azaspiracid shellfish poisoning (AZP)
Paralytic Shellfish Poisoning toxins
Paralytic shellfish poisoning (PSP) is caused by water-soluble alkaloid neurotoxins that are collectively referred to as saxitoxins or paralytic shellfish toxins (PSTs).
To date 57 analogs have been identified, although not all are always present, and they vary greatly in overall toxicity
Diarrhetic shellfish poisoning (DSP) toxins
Diarrhetic shellfish poisoning (DSP) is caused by a group of lipid-soluble polyether toxins that includes:
- okadaic acid,
- the dinophysistoxins, and
- a series of fatty acid esters of okadaic acid and the dinophysistoxins (collectively known as DSTs)
Neurotoxic shellfish poisoning (NSP) toxins
Neurotoxic shellfish poisoning (NSP) is caused by a group of lipid-soluble polyether toxins called brevetoxins.
NSP causing toxins in shellfish include intact algal brevetoxins and their metabolites (collectively known as NSTs).
Amnesic shellfish poisoning (ASP) toxins
Amnesic shellfish poisoning (ASP) is caused by the neurotoxin domoic acid (DA), a watersoluble, non-protein, excitatory amino acid.
Isomers of domoic acid have been reported, but are less toxic than domoic acid itself.
Azaspiracid shellfish poisoning (AZP)
Azaspiracid shellfish poisoning (AZP) is caused by the lipid-soluble toxin azaspiracid and several derivatives (AZAs).
To date, more than 30 AZA analogs have been identified, with three analogs routinely monitored in shellfish.
Paralytic Shellfish Poisoning Mortality:
Mortality: Death has been reported to occur as soon as 3 to 4 hours after the contaminated food has been consumed.
Paralytic Shellfish Poisoning Onset
Onset: Symptoms can generally occur within 30 minutes of consuming contaminated seafood, although reports have indicated that symptoms can even ensue within a few minutes, if high enough toxin concentrations are present
Paralytic Shellfish Poisoning Symptoms and course of illness / Treatment
Symptoms and course of illness: Effects of PSP are predominantly neurologic and include tingling of the lips, mouth, and tongue; numbness of extremities; paresthesias; weakness; ataxia; floating/dissociative feelings; nausea; shortness of breath; dizziness; vomiting; headache; and respiratory paralysis.
Medical treatment consists of providing respiratory support, and fluid therapy can be used to facilitate toxin excretion. For patients surviving 24 hours, with or without respiratory support, the prognosis is considered good, with no lasting side effects. In fatal cases, death is typically due to asphyxiation. In unusual cases, death may occur from cardiovascular collapse, despite respiratory support, because of the weak hypotensive action of the toxin.
Paralytic Shellfish Poisoning Food Sources:
Food Sources: PSP generally is associated with bivalves, such as mussels, clams, cockles, oysters, and scallops (excluding the scallop adductor muscle)
Diarrhetic Shellfish Poisoning Mortality
Mortality: This disease generally is not life-threatening
Diarrhetic Shellfish Poisoning Onset
Onset: Onset of the disease, depending on the dose of toxin ingested, may be as little as 30 minutes to 3 hours.
Diarrhetic Shellfish Poisoning Symptoms and course of illness:
Symptoms and course of illness: DSP is primarily observed as a generally mild gastrointestinal disorder; i.e., nausea, vomiting, diarrhea, and abdominal pain, accompanied by chills, headache, and fever.
Symptoms may last as long as 2 to 3 days, with no chronic effects.
Diarrhetic Shellfish Poisoning Food Sources
Food Sources: DSP generally is associated with mussels, oysters, and scallops
Neurotoxic Shellfish Poisoning Mortality
Mortality: No fatalities have been reported
Neurotoxic Shellfish Poisoning Onset
Onset: Onset of this disease occurs within a few minutes to a few hours
Neurotoxic Shellfish Poisoning Symptoms and course of illness
Symptoms and course of illness: Both gastrointestinal and neurologic symptoms characterize NSP, including tingling and numbness of lips, tongue, and throat; muscular aches; dizziness; diarrhea; and vomiting. Duration is fairly short, from a few hours to several days. Recovery is complete, with few after-effects.
Neurotoxic Shellfish Poisoning Food Sources
Food Sources: NSP generally is associated with oysters and clams harvested along the Florida coast and the Gulf of Mexico.
In 1992 / 1993, NSP was linked to shellfish harvested from New Zealand.
Amnesic Shellfish Poisoning Mortality
Mortality: All fatalities, to date, have involved elderly patients
Amnesic Shellfish Poisoning Onset
Onset: The toxicosis is characterized by onset of gastrointestinal symptoms within 24 hours; neurologic symptoms occur within 48 hours.
Amnesic Shellfish Poisoning Symptoms and course of illness:
Symptoms and course of illness:
Human clinical signs of domoic acid toxicity are reported as mild gastrointestinal symptoms (vomiting, diarrhea, abdominal pain), from an oral dose of 0.9-2.0 mg domoic acid (DA)/kg body weight.
Neurologic effects (confusion, short-term memory loss, disorientation, seizure, coma) are reported from an oral dose of 1.9-4.2 mg DA/kg body weight.
The toxicosis is particularly serious in elderly patients, and includes symptoms reminiscent of Alzheimer’s disease.
Amnesic Shellfish Poisoning Food Sources:
Food Sources: ASP generally is associated with mussels. Other taxa of interest include scallops, razor clams, market squid, and anchovy
Azaspiracid Shellfish Poisoning Mortality
Mortality: No known fatalities to date.
Azaspiracid Shellfish Poisoning Onset
Onset: Symptoms appear in humans within hours of eating AZA-contaminated shellfish.
Azaspiracid Shellfish Poisoning Symptoms and course of illness
Symptoms and course of illness: Symptoms are predominantly gastrointestinal disturbances resembling those of diarrhetic shellfish poisoning and include nausea, vomiting, stomach cramps, and diarrhea. Illness is self-limiting, with symptoms lasting 2 or 3 days
Azaspiracid Shellfish Poisoning Food Sources
Food Sources: AZAs have been detected in mussels, oysters, scallops, clams, cockles, and crabs
Diagnosis of shellfish poisoning
Diagnosis of shellfish poisoning is based entirely on observed symptomatology and recent dietary history
Frequency of shellfish poisoning
Good statistical data on the occurrence and severity of shellfish poisoning are largely unavailable, which undoubtedly reflects the inability to measure the true incidence of the disease. Cases are frequently misdiagnosed and, in general, infrequently reported. The proliferation (sometimes referred to as “blooms”) of the toxin-producing algae and subsequent toxin events or outbreaks of illness appear to be increasing around the world.
Target Populations of shellfish poisoning
All humans are susceptible to shellfish poisoning. A disproportionate number of shellfishpoisoning cases occur among (1) tourists or others who are not native to the location where the toxic shellfish are harvested and (2) fishermen and recreational harvesters. This may be due to disregard for either official quarantines or traditions of safe consumption
Food Analysis According to the 4th edition of the FDA Fish and Fisheries Products Hazards and Controls Guidance, regulatory action levels for the shellfish toxins are as follows
PSP – 0.8 ppm (80 μg/100 g) saxitoxin equivalents NSP – 0.8 ppm (20 mouse units/100 g) brevetoxin-2 equivalents DSP – 0.16 ppm total okadaic acid equivalents (i.e., combined free okadaic acid, dinophysistoxins, acyl-esters of okadaic acid and dinophysistoxins) ASP – 20 ppm domoic acid (except in the viscera of Dungeness crab, for which the action level is 30 ppm) AZP – 0.16 ppm azaspiracid 1 equivalent
shellfish poisoning Examples of Outbreaks
PSP – Despite widespread PSP closures, poisoning events still occur and are generally associated with recreational harvest. For example, in July 2007, a lobster fisherman harvested mussels from a floating barrel off Jonesport, ME (an area that was currently open to shellfish harvesting), and he and his family ate them for dinner. All four consumers became ill with PSP symptoms, and three of them were admitted to the hospital. It was apparent that the barrel of mussels had originated further up the coast in an area that had been banned to commercial harvest. DSP – Although there have been numerous outbreaks of diarrhetic shellfish poisoning around the world, until recently there were no confirmed cases of DSP in the U.S. that were due to domestically harvested shellfish. However, in 2008, a large portion of the Texas Gulf Coast was closed to the harvesting of oysters due to the presence of okadaic acid in excess of the FDA guidance level. Although no illnesses were reported, these were the first closures in the U.S. due to confirmed toxins. In 2011, approximately 60 illnesses occurred in British Columbia, Canada, and 3 illnesses occurred in Washington State due to consumption of DSP-contaminated mussels. Subsequent harvesting closures and product recalls were issued. NSP – Until NSP toxins were implicated in more than 180 human illnesses in New Zealand, in 1992/1993, NSP was considered to be an issue only in the U.S. Outbreaks of NSP are rare where programs for monitoring K. brevis blooms and shellfish toxicity are implemented. An NSP outbreak involving 48 individuals occurred in North Carolina, in 1987. A series of NSP cases occurred along the southwest coast of Florida, in 2006, after people consumed recreationallyharvested clams from waters unapproved for shellfish harvesting. ASP - The first human domoic acid poisoning events were reported in 1987, in Canada. While domoic acid exposure still exists, there have been no documented ASP cases since 1987, following implementation of effective seafood toxin-monitoring programs. AZP – There have been no confirmed cases of AZP in the U.S. from domestically harvested product. Examples from around the world include: (1) Several AZP intoxications (20 to 24) were reported in Ireland, in 1997, following consumption of mussels harvested from Arranmore Island. (2) An AZP outbreak involving 10 people was reported in Italy, after they consumed contaminated mussels produced in Clew Bay, Ireland. (3) In 1998, in France, 20 to 30 AZP illnesses were attributed to scallops that originated in Ireland. (4) In 2008, the first recognized outbreak of AZP in the U.S. was reported, but was associated with a mussel product imported from Ireland.
Scombrotoxin Toxin
Scombrotoxin is a combination of substances, histamine prominent among them. Histamine is produced during decomposition of fish, when decarboxylase enzymes made by bacteria that inhabit (but do not sicken) the fish interact with the fish’s naturally occurring histidine, resulting in histamine formation. Other vasoactive biogenic amines resulting from decomposition of the fish, such as putrescine and cadaverine, also are thought to be components of scombrotoxin. Time / temperature abuse of scombrotoxin-forming fish (e.g., tuna and mahi-mahi) create conditions that promote formation of the toxin. Scombrotoxin poisoning is closely linked to the accumulation of histamine in these fish.
Scombrotoxin FDA regulatory guidelines
FDA has established regulatory guidelines that consider fish containing histamine at 50 ppm or greater to be in a state of decomposition and fish containing histamine at 500 ppm or greater to be a public health hazard
Scombrotoxin Mortality
No deaths have been confirmed to have resulted from scombrotoxin poisoning.
Scombrotoxin Dose
Dose: In most cases, histamine levels in illness-causing (scombrotoxic) fish have exceeded 200 ppm, often above 500 ppm. However, there is some evidence that other biogenic amines also may play a role in the illness.
Scombrotoxin Onset
Onset: The onset of intoxication symptoms is rapid, ranging from minutes to a few hours after consumption.
Scombrotoxin Disease / complications:
Disease / complications: Severe reactions (e.g., cardiac and respiratory complications) occur rarely, but people with pre-existing conditions may be susceptible. People on certain medications, including the anti-tuberculosis drug isoniazid, are at increased risk for severe reactions
Scombrotoxin Symptoms
Symptoms: Symptoms of scombrotoxin poisoning include tingling or burning in or around the mouth or throat, rash or hives, drop in blood pressure, headache, dizziness, itching of the skin, nausea, vomiting, diarrhea, asthmatic-like constriction of air passage, heart palpitation, and respiratory distress
Scombrotoxin Duration
Duration: The duration of the illness is relatively short, with symptoms commonly lasting several hours, but, in some cases, adverse effects may persist for several days.
Scombrotoxin Route of entry:
Route of entry: Oral.
Scombrotoxin Pathway
Pathway: In humans, histamine exerts its effects on the cardiovascular system by causing blood-vessel dilation, which results in flushing, headache, and hypotension. It increases heart rate and contraction strength, leading to heart palpitations, and induces intestinal smooth-muscle contraction, causing abdominal cramps, vomiting, and diarrhea. Histamine also stimulates motor and sensory neurons, which may account for burning sensations and itching associated with scombrotoxin poisoning. Other biogenic amines, such as putrescine and cadaverine, may potentiate scombrotoxin poisoning by interfering with the enzymes necessary to metabolize histamine in the human body
Scombrotoxin Frequency
Scombrotoxin poisoning is one of the most common forms of fish poisoning in the United States. From 1990 to 2007, outbreaks of scombrotoxin poisoning numbered 379 and involved 1,726 people, per reports to the Centers for Disease Control and Prevention (CDC). However, the actual number of outbreaks is believed to be far greater than that reported
Scombrotoxin Sources
Fishery products that have been implicated in scombrotoxin poisoning include tuna, mahi-mahi, bluefish, sardines, mackerel, amberjack, anchovies, and others. Scombrotoxin-forming fish are commonly distributed as fresh, frozen, or processed products and may be consumed in a myriad of product forms. Distribution of the toxin within an individual fish or between cans in a case lot can be uneven, with some sections of a product capable of causing illnesses and others not. Cooking, canning, and freezing do not reduce the toxic effects. Common sensory examination by the consumer cannot ensure the absence or presence of the toxin. Chemical analysis is a reliable test for evaluating a suspect fishery product. Histamine also may be produced in other foods, such as cheese and sauerkraut, which also has resulted in toxic effects in humans
Scombrotoxin Diagnosis
Diagnosis of the illness is usually based on the patient’s symptoms, time of onset, and the effect of treatment with antihistamine medication. The suspected food should be collected; rapidly chilled or, preferably, frozen; and transported to the appropriate laboratory for histamine analyses. Elevated levels of histamine in food suspected of causing scombrotoxin poisoning aid in confirming a diagnosis.
Scombrotoxin Target Populations
All humans are susceptible to scombrotoxin poisoning; however, as noted, the commonly mild symptoms can be more severe for individuals taking some medications, such as the antituberculosis drug isoniazid. Because of the worldwide network for harvesting, processing, and distributing fishery products, the impact of the problem is not limited to specific geographic areas or consumption patterns
Scombrotoxin Food Analysis
The official method (AOAC 977.13) for histamine analysis in seafood employs a simple alcoholic extraction and quantitation by fluorescence spectroscopy. Putrescine and cadaverine can be analyzed by AOAC Official Method 996.07. Several other analytical procedures to quantify biogenic amines have been published in the literature
Tetrodotoxin Toxin
to be completed
Tetrodotoxin Mortality
Mortality: Death is from respiratory-muscle paralysis and usually occurs within 4 to 6 hours, with a known range of about 20 minutes to 8 hours
Tetrodotoxin Lethal dose:
Lethal dose: The minimum lethal dose in humans is estimated to be 2 to 3 mg (1/500 of a gram).
Tetrodotoxin Onset
Onset: The first symptom of intoxication is a slight numbness of the lips and tongue, typically appearing between 20 minutes to 3 hours after ingestion, depending on the ingested dose. With higher doses, symptoms can start within minutes.
Tetrodotoxin Illness / complications
Illness / complications: Tetrodotoxin acts on both the central and peripheral nervous systems. After the initial slight oral numbness, the next symptom is increasing paraesthesia in the face and extremities, which may be followed by sensations of lightness or floating. Headache, epigastric pain, nausea, diarrhea, and/or vomiting may occur. Occasionally, some reeling or difficulty in walking may occur. The second stage of the intoxication includes progressive paralysis. Many victims are unable to move; even sitting may be difficult. There is increasing respiratory distress. Speech is affected, and the victim usually exhibits dyspnea, cyanosis, and hypotension. Paralysis increases, and convulsions, mental impairment, and cardiac arrhythmia may occur. The victim, although completely paralyzed, may be conscious and, in some cases, completely lucid until shortly before death. There is no antidote for TTX poisoning, and treatment is symptomatic and supportive. Patients who receive ventilatory support recover fully, in most cases.
Tetrodotoxin Duration
Duration: It is generally considered that if victims survive the initial 24 hours, they are expected to recover fully. It is known that TTX is cleared from the human body relatively quickly (in days) through the urine. Other symptoms, such as muscle weakness, can persist longer. No chronic effects have been reported
Tetrodotoxin Route of entry:
Route of entry: Oral.
Tetrodotoxin Pathway
Pathway: Tetrodotoxin acts directly on voltage-activated sodium channels in nerve tissue. Toxin binding to the channel blocks the diffusion of sodium ions, preventing depolarization and propagation of action potentials. All of the observed toxicity is secondary to action-potential blockage.
Tetrodotoxin Frequency
Only a few cases of intoxication from TTX have been reported in the U.S., and only from consumption of pufferfish. In Japan, however, 1,032 cases of pufferfish poisoning (PFP) were reported from 1965 through 2007, with 211 fatalities. In 1983, the Japanese Ministry of Health, Labour, and Welfare enacted guidance for pufferfish harvest and consumption, thereby greatly reducing the number of illnesses and mortalities from commercial product. Between 2002 and 2006, however, 116 incidents of PFP, with 223 individuals intoxicated and 13 mortalities, were reported, suggesting that problems still occur. Most of these illnesses were from home-prepared meals made from recreationally harvested fish.
Tetrodotoxin Sources
As many as 19 species of pufferfish occur in U.S. waters, many of which contain TTX
strict regulations on importation of pufferfish into the U.S
Only muscle, skin, and testicles from a single species (Takifugu rubripes, a.k.a. tiger puffer or torafugu) are allowed entry into the U.S. from Japan. These products must be processed in a certified facility by trained personnel and certified as safe for consumption by the Japanese government. Any pufferfish products imported outside the guidelines of this agreement are subject to detention without physical examination, under FDA Import Alert #16-20. Due to the fact that imported pufferfish are limited to a single species (T. rubripes) processed and certified as safe prior to importation, the domestic puffer (sea squab) fishery targets a nontoxic species, and the U.S. does not import other species known to contain TTX (i.e. trumpet shells, xanthid crabs, etc.) for food. The FDA makes no recommendations for control of TTX in seafood in its Fish and Fisheries Products Hazards and Controls Guidance. However, due to recent issues with the illegal importation of misbranded Asian pufferfish and the recent appearance of saxitoxin in east-coast Florida southern pufferfish (Sphoeroides nephelus) – described in the sidebar below – FDA advises consumers who choose to consume pufferfish to consume only those from known safe sources.
Tetrodotoxin Diagnosis
The diagnosis of PFP is based on the observed symptomatology and recent dietary history. A case definition is available from the Centers for Disease Control and Prevention.
Tetrodotoxin Target populations
All humans are susceptible to TTX poisoning. This toxicosis may be avoided by not consuming pufferfish or other animal species containing TTX. In the U.S., most other animal species known to contain TTX are not usually consumed by humans. Poisoning from TTX is of major public health concern primarily in Japan and other Indo-Pacific countries, where “fugu” is a traditional delicacy. In Japan, it is prepared and sold in special restaurants, where trained and licensed individuals carefully remove the viscera to reduce the danger of poisoning. Due to its import restrictions and high value, there is potential for intentional mislabeling and illegal importation, particularly of prepared, frozen fish products. Several firms have been placed on the FDA Import Alert list for species misbranding and illegal importation of pufferfish.
Tetrodotoxin Food Analysis
The mouse bioassay for paralytic shellfish poisoning (PSP) can be used to monitor TTX in seafood products. An HPLC method with post-column reaction with alkali and fluorescence has been developed to determine TTX and its associated toxins. The alkali degradation products can also be confirmed as their trimethylsilyl derivatives, by gas chromatography. Mass spectrometry methods have been developed and show good sensitivity and selectivity. Antibody- and receptorbased methods are also available. To date, none of these chemical methods have been validated for regulatory compliance.
Tetrodotoxin Examples of Outbreaks
On April 29, 1996, three cases of TTX poisoning occurred among chefs in California who shared contaminated fugu (pufferfish) brought from Japan by a co-worker as a prepackaged, ready-toeat product. The quantity eaten by each person was minimal, ranging from approximately ¼ to 1½ oz. Onset of symptoms began approximately 3 to 20 minutes after ingestion, and all three chefs were transported by ambulance to a local emergency department. Three deaths were reported in Italy, in 1977, following consumption of frozen pufferfish imported from Taiwan and mislabeled as angler fish. In 2007, it was reported that fish sellers in Thailand were selling meat from a highly poisonous species of pufferfish labeled as salmon. This practice led to the death of 15 people over a 3-year period. In 2007, four separate incidents of TTX poisoning occurred in California, Illinois, and New Jersey, all linked to the pufferfish species L. lunaris imported from China, illegally invoiced as monkfish to avoid import restrictions. For several of the poisonings, the product in question was being sold as “bok,” a Korean term for pufferfish. The sidebar below describes 28 cases of PFP, from consumption of southern pufferfish, (Sphoeroides nephelus) that occurred on the U.S. east coast between 2002 to 2004, believed to be due not to TTX, but from accumulation of saxitoxins
Aflatoxins Toxin
The aflatoxins (AFs) are mycotoxins produced by certain fungi and can cause serious illness in animals and humans. The four major aflatoxins are AFB1, AFB2, AFG1, and AFG2. In adverse weather or under poor storage conditions, these toxins are produced mainly by certain strains of Aspergillus flavus and A. parasiticus in a broad range of agricultural commodities, such as corn and nuts
Aflatoxin in milk, origin and limit.
aflatoxin M1 (AFM1), is produced by mammals after consumption of feed (or food) contaminated by AFB1. Cows are able to convert AFB1 into AFM1 and transmit it through their milk. Although AFM1 in milk is, by far, not as hazardous as the parent compound, a limit of 0.5 parts per billion is applied, largely because milk tends to constitute a large part of the diet of infants and children
Aflatoxins major target organ
liver
most potent known natural carcinogen
AFB1
Aflatoxins Mortality
Documented epidemics of AF poisoning in the following countries illustrate mortality rates from outbreaks: - In northwest India, in 1974, there were 108 fatalities from 397 illnesses. AF levels of 0.25 to 15 mg/kg were found in corn. - In 1982, in Kenya, there were 20 hospital admissions, with a 60% mortality rate, with AF intake at 38 µg/kg of body weight. - In 1988, in Malaysia, 13 Chinese children died of acute hepatic encephalopathy after eating Chinese noodles. Aflatoxins were confirmed in postmortem samples from the patients. - In 2004 and 2005, one of the largest aflatoxicosis outbreaks on record occurred in rural Kenya, resulting in illness in 317 people, 125 of whom died. AFcontaminated homegrown maize with an average concentration of 354 ng/g was the source of the outbreak
Aflatoxins Toxic dose
The toxic level of AF in humans is largely unknown. In one example, a laboratory worker who intentionally ingested AFB1 at 12 µg/kg body weight for 2 days developed a rash, nausea, and headache, but recovered without ill effect. In a 14-year follow-up of the worker, a physical examination and blood chemistry, including tests for liver function, were normal. In animals, the effects of AFs on health depend on the species of the animal, level and duration of exposure, and nutritional status. Among various animals, median lethal dose (i.e., LD50) values obtained with single doses showed wide variation, ranging from 0.3 mg/kg body weight in rabbits to 18 mg/kg body weight in rats.
Aflatoxins carcinogenic impact
AFs have been found to be moderately to highly toxic and carcinogenic in almost every animal species tested, including monkeys, although AFs do not affect all animals equally. The main factor in tolerance relates to the nature of the digestive system. Ruminants are more tolerant, and swine, chickens, ducks, and ducklings (and pet and wild birds) are more sensitive. Other factors contributing to differences in animal susceptibility to AFs include breed variety, nutrition, sex, age, environmental stress, and presence of other disease agents
Aflatoxins Onset
Onset: Not applicable.
Aflatoxins Illness / complications: From acute exposure
From acute exposure: Acute exposure to high doses of AFs can result in aflatoxicosis, with the target organ being the liver, leading to serious liver damage. AFs inhibit the normal functions of the liver, including carbohydrate and lipid metabolism and protein synthesis
Aflatoxins Illness / complications: From chronic exposure at sublethal doses
From chronic exposure at sublethal doses: cancer, impaired protein formation, impaired blood coagulation, toxic hepatitis, and probable immunosuppression. In animals, AFs may cause, in addition, reduced weight gain and reduced feed-conversion efficiency AFB1 is the most potent known natural carcinogen and is the most abundant of the AFs.
Aflatoxins Symptoms
Symptoms: The disruption and inhibition of carbohydrate and lipid metabolism and protein synthesis associated with aflatoxicosis can lead to hemorrhaging, jaundice, premature cell death, and tissue necrosis in liver and, possibly, other organs. Other general symptoms include edema of the lower extremities, abdominal pain, and vomiting.
Aflatoxins Route of entry
Route of entry: Oral.
Aflatoxins Pathway
Pathway: There is sufficient evidence that AFB1 can interact with DNA, producing damage. If the DNA is not repaired, a mutation can occur that may initiate the cascade of events required to produce cancer. After activation by cytochrome P450 monooxygenases, AFB1 is metabolized to form a highly reactive metabolite, AFB1-exo-8,9-epoxide. The exo-epoxide binds to the guanine moiety of DNA at the N7 position, forming trans-8,9-dihydro-8-(N7-guanyl)-9 hydoxyAFB1 adducts, which can rearrange and form a stable adduct. This can be measured in tumor tissues. AFB1-DNA adducts can result in GC-to-AT transversions. This specific mutation at codon 249 of the p53 tumor suppressor gene may be important in the development of HCC. Studies of liver-cancer patients in Southeast Asia and subSaharan Africa, where AF contamination in foods was high, have shown that a mutation in the p53 at codon 249 is associated with a G-to-T transversion. Biomarkers continue to serve as important tools in the epidemiology of HCC
Aflatoxins Frequency
In 2004, according to the Worldwide Regulations for Mycotoxins 2003, a Compendium published by the Food and Agriculture Organization, more than 76 countries have legislated limits on aflatoxins, ranging from 0 to 35 ng/g. Subsequently, in developed countries, AF contamination has rarely occurred in foods at levels that cause acute aflatoxicosis in humans. AF acute and chronic exposures are more likely to occur in developing countries where no regulatory limits, poor agricultural practices in food handling and storage, malnutrition, and disease are problems. Aflatoxicosis in humans has been reported in many countries, including India, China, Thailand, Ghana, Kenya, Nigeria, Sierra Leone, and Sudan. Human epidemiologic studies were initiated, in 1966, in Africa. To date, in the U.S., no human aflatoxicosis outbreak has been reported; however, dogs died in an outbreak, in 1998. In 2005, a number of dogs and cats died from eating aflatoxincontaminated pet food.
Aflatoxins Sources
In the U.S., AFs are commonly found in corn (maize), sorghum, rice, cottonseed, peanuts, tree nuts, copra, cocoa beans, figs, ginger, and nutmeg. AFM1 may be found in milk and dairy products. Aflatoxin M1 also may be found in human breast milk, as has been the case in Ghana, Kenya, Nigeria, Sudan, Thailand, and other countries, from a mother’s chronic exposure to dietary AFs.
Aflatoxins Diagnosis
People who have aflatoxicosis might exhibit the following characteristics. Liver damage may be evidenced by jaundice and its characteristic yellowing of tissues. Gall bladder may become swollen. Immunosuppression may provide an opportunity for secondary infections. Vitamin K functions may decrease. High levels of AFB1-albumin adducts may be present in plasma. AF exposure can be monitored through the use of biomarkers that detect the presence of AF metabolites in blood, milk, and urine, and excreted DNA adducts and blood-protein adducts. AFB1-albumin adducts can be measured in blood; AFM1 and AFB1-DNA adduct (AFB1-guanine adduct) can be detected in the urine of people consuming sufficient amounts of AFB1
Aflatoxins Target Populations
Human susceptibility to AFs can vary with sex, age, health, nutrition, environmental stress, and level and duration of exposure. In many cases, exposure is due to consumption of a single, affected dietary staple. Also see “Frequency” section, above.
Aflatoxins Food Analysis sampling
A bulk sample must be taken following a sampling plan, so that it is accurately representative of the toxin levels present throughout the lot. A subsample is removed from the bulk sample and subjected to sample preparation. The subsample is comminuted with proper grinding and mixing mills. The sample preparation variability decreases with decreasing particle size. A test sample is removed from the properly comminuted sample for analysis.
Two important aspects that can affect sampling variability of Aflatoxins in food
Two important aspects that can affect sampling variability include the sample-selection procedure and the distribution among contaminated particles within a lot. Using proper sampling equipment and procedures can reduce the effects of sample selection. Increasing sample size can reduce the effects of the distribution of contaminated particles within a lot.
Aflatoxins Food Analysis Analytical methods
Analytical methods can be divided into quantitative or semiquantitative assays and rapid screening tests. Sample cleanup is a time-consuming step and usually consists of extraction with solvent, liquid-liquid partition, and/or chromatographic separation and determination. Thin-layer chromatography (TLC) is among the most widely-used analytical methods. This simple and inexpensive technique is especially useful for AF analysis in developing countries, screening purposes, and multi-mycotoxin analysis. Since the late 1970s, AF-specific antibodies have been developed. The antibody development has led to the development of enzyme-linked immunosorbent assays (ELISAs) for AFs. The ELISAs are mainly used in screening methods. With advances in instrumentation, chromatographic methods for AFs have expanded from TLC to high-performance liquid chromatography (LC) with fluorescence detection. Hyphenated methods, such as LC/mass spectrometry (MS) or LC/MS-MS, have also been developed for AF quantitation and confirmation of identities.
Gempylotoxin Toxin
Gempylotoxin is an indigestible wax, composed of C32, C34, C36, and C38 fatty acid esters, with the main component C34H66O2 (Ukishima, et al.), generally found in the fish escolar (Lepidocybium flavobrunneum) and its relative oilfish (Ruvettus pretiosus), sometimes called cocco. escolar’s muscle contained about 20% lipid, and 88.8% consisted of wax. The wax was composed of C32, C34, C36 and C38 compounds, and the main component was C34H66O2. The alcohol components were mainly C16:0 and C18:1, as well as those of sperm whale (Physeter catodon) wax. The fatty acid components were mainly C18:1 and smaller amounts of highly unsaturated fatty acids.
Gempylotoxin Disease
Humans can’t digest this wax, which, in some people, acts as a purgative if consumed. The resulting illness is called gempylid fish poisoning or gempylotoxism
Gempylotoxin Mortality
Mortality: None known.
Gempylotoxin Onset
Onset: Symptoms have been reported to start between 1 and 90 hours after the fish is consumed, with a median onset of 2.5 hours
Gempylotoxin Symptoms
Symptoms: Diarrhea, often consisting of an oily orange or brownish-green discharge (keriorrhoea), without major fluid loss; abdominal cramps; nausea; headache; and vomiting
Gempylotoxin Duration
Duration: Symptoms usually abate within 1 to 2 days.
Gempylotoxin Route of entry:
Route of entry: Oral.
Gempylotoxin Frequency
Cases may occur sporadically (i.e., in isolation from one another) or in clusters, usually when the fish is eaten in group settings
Gempylotoxin Sources
Symptoms usually are associated with ingestion of escolar (Lepidocybium flavobrunneum) or oilfish (Ruvettus pretiosus). Other products have been implicated in illness (including butterfish, rudderfish, walu, white tuna, and Taiwanese seabass). In most cases, these products were actually escolar or oilfish, but were marketed under inappropriate local or vernacular names, such as those used where the species was harvested (e.g. walu, butterfish). Species substitution or misbranding occurs when a deceptive and misleading name is used (e.g., white tuna or Taiwanese seabass). The FDA maintains a guide to acceptable market names for food fish sold in interstate commerce (The Seafood List), to avoid this confusion among consumers and resulting inadvertent illness. Additional deep-sea fish species, such as orange roughy (Hoplostethus atlanticus) and oreo dory (Allocyttus spp., Pseudocyttus spp., Oreosoma spp., and Neocyttus spp.), are known to contain lesser amounts of the same indigestible wax esters.
Gempylotoxin Diagnosis
Diagnosis is per symptoms, particularly of oily, orange or greenish-brown diarrhea, and history of having consumed this type of fish
Gempylotoxin Target Populations
Not everyone who eats the fish becomes ill to the same extent. Level of illness may be related to the quantity eaten.
Gempylotoxin Examples of Outbreaks
An outbreak that occurred in New South Wales, in October 2001, provides an example. Of 44 people who attended a conference at which lunch was served, 22 became ill, with a median postlunch incubation period of 2.5 hours. Among those, all of the 17 who met the case definition had eaten fish for lunch; none of the attendees who did not become ill had eaten fish. Eighty percent of the people who became ill had diarrhea, often oily; half had abdominal cramps and almost half had nausea; more than one-third had a headache; and one-quarter had vomiting. Analysis of the oil in the fish that had been served for lunch was consistent with escolar.
Examples of DNA barcoding’s utility (fish)
After a fish is turned into fillets or steaks, it can be very hard to determine exactly what species it is. FDA scientists are now using DNA barcoding to find out. DNA barcoding uses genetic material in fish to identify them. This method of definitive identification helps the FDA enforce policies on proper labeling of escolar and other fish (Gempylotoxin ) Pufferfish can be poisonous, depending on the type of pufferfish and the parts that are eaten (tetrodotoxin)
Phytohaemagglutinin (kidney bean lectin)
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Pyrrolizidine Toxin
Pyrrolizidine alkaloids are a large class of naturally occurring alkaloids containing pyrrolizidine rings. More than 600 pyrrolizidine alkaloids are known. They are widely distributed in the plant kingdom, particularly in the Boraginaceae, Compositae, and Leguminosae families. Some of these alkaloids cause illness in humans and other animals.
Pyrrolizidine Toxin
Pyrrolizidine alkaloids are a large class of naturally occurring alkaloids containing pyrrolizidine rings. More than 600 pyrrolizidine alkaloids are known. They are widely distributed in the plant kingdom, particularly in the Boraginaceae, Compositae, and Leguminosae families. Some of these alkaloids cause illness in humans and other animals.
Pyrrolizidine Mortality
Mortality: Possible, when liver or lung damage is extensive.
Pyrrolizidine Toxicity dose
Toxicity dose: Variable among different pyrrolizidine alkaloids.
Pyrrolizidine Illness / complications
Illness / complications: Most cases of pyrrolizidine alkaloid toxicity result in moderate to severe liver damage. In some cases, the lungs are affected; pulmonary edema and pleural effusions have been observed. Lung damage may be prominent and has been fatal. Chronic illness from ingestion of small amounts of the alkaloids over a long period proceeds through fibrosis of the liver to cirrhosis. The carcinogenic potential of some pyrrolizidine alkaloids has been proven in rodents, and the National Toxicology Program recently has accepted riddelliine as a human carcinogen.
Pyrrolizidine Symptoms
Symptoms: Gastrointestinal symptoms usually are the first sign of intoxication. They consist predominantly of abdominal pain, with vomiting, and development of ascites. Other early clinical signs include nausea and acute upper gastric pain, acute abdominal distension with prominent dilated veins on the abdominal wall, fever, and biochemical evidence of liver dysfunction. Jaundice may be present.
Pyrrolizidine Duration
Duration: Death may ensue from 2 weeks to more than 2 years after poisoning, but patients may recover almost completely if the alkaloid intake is discontinued and the liver damage has not been too severe.
Pyrrolizidine Route of entry:
Route of entry: Oral.
Pyrrolizidine Pathway
Pathway: Mediated by cytochrome P450
Pyrrolizidine Frequency
Worldwide, reports of pyrrolizidine alkaloid intoxication are associated mainly with consumption of dietary supplements containing pyrrolizidine alkaloids and grains contaminated with weeds that contain pyrrolizidine alkaloids. Although the occurrence has been rare, there have been periodic reports of pyrrolizidine alkaloid intoxication in the United States, mainly due to consumption of herbal teas and dietary supplements that contained pyrrolizidine alkaloids; mainly the herb comfrey (Symphytum spp.).
Pyrrolizidine Frequency
Worldwide, reports of pyrrolizidine alkaloid intoxication are associated mainly with consumption of dietary supplements containing pyrrolizidine alkaloids and grains contaminated with weeds that contain pyrrolizidine alkaloids. Although the occurrence has been rare, there have been periodic reports of pyrrolizidine alkaloid intoxication in the United States, mainly due to consumption of herbal teas and dietary supplements that contained pyrrolizidine alkaloids; mainly the herb comfrey (Symphytum spp.).
Pyrrolizidine Diagnosis
Diagnosis of poisoning from pyrrolizidine alkaloids often is difficult, since they usually are excreted within 24 hours, while symptoms of the poisoning might not appear until days or weeks after the toxins were ingested. Key clinical features of the veno-occlusive disease that typically is indicative of pyrrolizidine alkaloids may include hyperbilirubinemia, painful hepatomegaly, and fluid retention. Diagnosis usually is made on the basis of symptoms and on patients’ reports of having ingested substances associated with pyrrolizidine alkaloids.
Pyrrolizidine Target Populations
All humans are believed to be susceptible to the hepatotoxic pyrrolizidine alkaloids. Males are more susceptible than females, and fetuses and children show the highest sensitivity. Home remedies and consumption of herbal teas in large quantities can be a risk factor and are the most likely causes of alkaloid poisonings in the U.S. In 2001, FDA advised all dietary supplement manufacturers to remove from the market products that contained comfrey and were intended for internal use.
Pyrrolizidine Food Analysis
The pyrrolizidine alkaloids can be isolated from the suspect commodity by any of several standard alkaloid extraction procedures. The toxins are identified by thin-layer chromatography. The pyrrolizidine ring is first oxidized to a pyrrole, followed by spraying with Ehrlich reagent, which gives a characteristic purple spot. A colorimetric test employing Ehrich reagent also can be used to detect most common pyrrolizidine alkaloids, except the otonecine-type. Liquid and gas-liquid chromatography, in conjunction with mass spectrometric methods, also are available for identifying the alkaloids in trace amounts.
Pyrrolizidine Examples of outbreaks
Intoxication reported from Afghanistan’s Gulran province in 2008. List of Morbidity and Mortality Weekly Reports, from the Centers for Disease Control and Prevention, relating to this toxin.
Venomous Fish: Venomous Species
from primitive cartilaginous fish, such as stingrays, to more advanced, bony fish such as scorpionfish, stonefish, weeverfish, blennies, and, as noted, lionfish. Venom injections from certain stonefish species (Synanceja horrida, S. trachynis, and S. verrucosa) are the most notorious among venomous fish, and have been responsible for numerous deaths from incidents in coastal Indo-Pacific waters.
Venomous Fish: habitats,
Venomous fish are found in diverse habitats, from freshwater streams to coral reefs to the open ocean. The greatest variety is found in the waters surrounding Indo-Pacific island countries, eastern and southern Africa, Australia, Polynesia, the Philippines, Indonesia, and southern Japan. Most venomous fish inhabit shallow, inshore waters among coral reefs and rocks. They generally swim slowly and are non-migratory, and tend either to be brightly colored or to blend in with their environments. Stonefish, as their name suggests, are well camouflaged in their native habitat, and most lethal envenomations have occurred through accidental contact (i.e., being stepped on) by recreational divers and fishermen
Venomous Fish: Fish Venom
Fish venoms are complex mixtures of proteins and enzymes, each with its own biological activity, most of which have yet to be isolated and characterized. Studies have shown that many fish venoms are chemically and pharmacologically similar. Fish venoms are known to have cardiovascular, neuromuscular, inflammatory, and cytolytic properties. No fish venom mixtures have been fully characterized, and only a few components (e.g. stonustoxin, a lethal compound from the stonefish Synanceja horrida, which causes severe hypotension) have been purified and studied in detail. Although fish venoms are believed to be unstable and heat labile, no thorough studies have been performed on the potency of venom components after fish harvest or death.
Venomous Fish: Venom Apparatus in Fish
Fish venom is produced in specialized glands associated with distinct venom-delivery structures. Most of these structures are spines located on the dorsal (back), pectoral, pelvic, anal, caudal (tail) or opercular (cheek) surfaces. The venom-producing glands are usually located in a groove on the surface or at the base of the spine. The size and complexity of this glandular tissue varies by species. Unlike other venomous creatures, such as spiders, wasps, and snakes, in which venom can be actively injected through a bite or sting, fish venom is delivered involuntarily when a spine pierces the tissue of the victim, leading to rupture of the spine’s sheath, and venom passes into the puncture wound.
Venomous Fish: Symptoms
In terms of envenomation by puncture, the severity of symptoms depends on the fish species, amount of venom delivered, and age and health status of the victim. The most common symptom associated with envenomation by puncture is acute, localized pain disproportionate to the size or severity of the wound. This symptom reaches its greatest intensity within 60 to 90 minutes and, if untreated, can last 8 to 12 hours. In addition to the localized symptoms and complications associated with the puncture wound itself, systemic symptoms occur in a limited number of victims. They include dizziness, nausea or vomiting, difficulty breathing, chest pain, abdominal pain, hypotension, and generalized weakness. Stonefish envenomations appear to be the most potent and may result in death from hypotension, arrhythmia, and/or pulmonary edema. A secondary consequence of handling fish with venomous spines is bacterial infection of the wound, particularly from species with barbed spines (e.g. catfish, stingrays) that can break off and become embedded in the victim. Medical attention should be sought in cases in which the spines cannot be removed or systemic symptoms persist.
Venomous Fish: Treatment
The most common and effective treatment for acute pain from fish envenomation is immersion of the affected area in hot (45 C, not boiling) water for as long as is tolerable by the patient. Tetanus or antibiotic treatment may be administered by a health professional, if secondary infection of the wound is suspected. For severe cases of stonefish envenomation, commercial antivenom is available. In laboratory studies, this product has been shown to be effective in reducing the potency of several scorpionfish venoms, including those from the devil stinger (Inimicus japonicus), lionfish (Pterois volitans, P. lunulata, and P. antennata), and zebra turkeyfish (Dendrochirus zebra).
Phytohaemagglutinin (kidney bean lectin): Protein / Toxin
Lectins are widely occurring, sugar-binding proteins that perform a variety of biological functions in plants and animals, including humans, but some of them may become toxic at high levels. Besides inducing mitosis, lectins are known for their ability to agglutinate many mammalian red blood cell types, alter cell-membrane transport systems, alter cell permeability to proteins, and generally interfere with cellular metabolism. Among the lectins known to have toxic effects is phytohaemagglutinin, which occurs at relatively high levels in the seeds of legumes (e.g., beans). The role of this compound in defense against plant pests and pathogens has been established. This hemagglutinin also is used in research; for example, to trigger DNA and RNA synthesis in T lymphocytes, in vitro. PHAs are used to test competence of cell-mediated immunity; for example, in patients with chronic viral infections.
Phytohaemagglutinin (kidney bean lectin): Mortality:
Not reported
Phytohaemagglutinin (kidney bean lectin); Toxic dose:
Toxic dose: As few as four or five raw beans can trigger symptoms.
Phytohaemagglutinin (kidney bean lectin) Onset
Onset: Usually begins with extreme nausea and vomiting within 1 to 3 hours of ingestion of the product, with diarrhea developing later within that timeframe.
Phytohaemagglutinin (kidney bean lectin); Illness / complications:
Illness / complications: Upper and lower gastrointestinal illness. Vomiting may become severe.
Phytohaemagglutinin (kidney bean lectin); Symptoms
Symptoms: In addition to vomiting and diarrhea, abdominal pain has been reported by some people.
Phytohaemagglutinin (kidney bean lectin); Duration
Duration: Recovery usually is rapid, within 3 to 4 hours after onset of symptoms, and spontaneous, although some cases have required hospitalization
Phytohaemagglutinin (kidney bean lectin); Route of entry:
Route of entry: Oral (consumption of uncooked or undercooked kidney beans).
Phytohaemagglutinin (kidney bean lectin); Pathway
Pathway: The mechanism and pathway of toxicity is not known, but oral ingestion of lectins is known to reduce intestinal absorption and cause weight loss, growth retardation, and diarrhea in several animal species.
Phytohaemagglutinin (kidney bean lectin); Frequency
This syndrome has occurred in the United Kingdom with some regularity. Seven outbreaks occurred in the U.K. between 1976 and 1979. Two more incidents were reported by the Public Health Laboratory Services (PHLS), of Colindale, U.K., in the summer of 1988. Reports of this syndrome in the United States are anecdotal and have not been formally published
Phytohaemagglutinin (kidney bean lectin); Sources
Phytohaemagglutinin, the presumed toxic agent, is found in many species of beans, but is in highest concentration in red kidney beans (Phaseolus vulgaris). The unit of toxin measure is the hemagglutinating unit (hau). Raw kidney beans contain from 20,000 to 70,000 hau, while fully cooked beans contain from 200 to 400 hau. White kidney beans, another variety of Phaseolus vulgaris, contain about one-third the amount of toxin as the red variety; broad beans (Vicia faba) contain 5% to 10% the amount that red kidney beans contain. The syndrome usually is caused by ingestion of raw, soaked kidney beans, either alone or in salads or casseroles. Several outbreaks have been associated with beans cooked in slow cookers (i.e., countertop appliances that cook foods at low temperatures for several hours) or in casseroles that had not reached an internal temperature high enough to destroy the glycoprotein lectin.
Phytohaemagglutinin (kidney bean lectin); Cooking temperatures
PHA is destroyed by adequate cooking. Some variation in toxin stability has been found at different temperatures. However, Bender and Readi found that boiling the beans for 10 minutes (100 C) completely destroyed the toxin. Consumers should boil the beans for at least 30 minutes to ensure that the product reaches sufficient temperature, for a sufficient amount of time, to completely destroy the toxin. Slow cookers should not be used to cook these beans or dishes that contain them. Studies of casseroles cooked in slow cookers revealed that the food often reached internal temperatures of only 75 C or less, which is inadequate for destruction of the toxin.
Phytohaemagglutinin (kidney bean lectin); Diagnosis
Diagnosis is made on the basis of symptoms, food history, and exclusion of other rapid-onset food-poisoning agents (e.g., Bacillus cereus, Staphylococcus aureus, arsenic, mercury, lead, and cyanide).
Phytohaemagglutinin (kidney bean lectin); Target Populations
All people, regardless of age or gender, appear to be equally susceptible; the severity is related to the dose ingested. In the seven outbreaks mentioned below, the attack rate was 100%.
Phytohaemagglutinin (kidney bean lectin); Food Analysis
The difficulty in food analysis is that this syndrome is not well known in the medical community. Other possible causes, such as Bacillus cereus, staphylococcal food poisoning, and chemical toxicity, must first be eliminated. If beans were a component of the suspect meal, analysis is quite simple, based on hemagglutination of red blood cells (hau).
Salmonella species and subspecies
The genus Salmonella is divided into two species that can cause illness in humans: S. enterica S. bongori Salmonella enterica, which is of the greatest public health concern, is comprised of six subspecies: S. enterica subsp. enterica (I) S. enterica subsp. salamae (II) S. enterica subsp. arizonae (IIIa) S. enterica subsp. diarizonae (IIIb) S. enterica subsp. houtenae (IV) S. enterica subsp. indica (VI) Salmonella is further subdivided into serotypes, based on the Kaufmann-White typing scheme first published in 1934, which differentiates Salmonella strains by their surface and flagellar antigenic properties
Salmonella characteristics
Salmonella is a motile, non-sporeforming, Gramnegative, rod-shaped bacterium in the family Enterobacteriaceae and the tribe Salmonellae. Non-motile variants include S. Gallinarum and S. Pullorum
Salmonella can cause two types of illness,:
Salmonella can cause two types of illness, depending on the serotype: (1) nontyphoidal salmonellosis and (2) typhoid fever, both of which are described below. The symptoms of nontyphoidal salmonellosis can be quite unpleasant, but this illness is generally self-limiting among healthy people with intact immune systems (although it can cause lifethreatening illness even in healthy people). Typhoid fever is more serious and has a higher mortality rate than does nontyphoidal salmonellosis.
Nontyphoidal Salmonellosis serotypes
Caused by serotypes other than S. Typhi and S. Paratyphi A ((Note that species names are italicized, but serotype names are not.)
Nontyphoidal Salmonellosis Mortality
Mortality: Generally less than 1%; however, S. Enteritidis has a 3.6% mortality rate in outbreaks in nursing homes and hospitals, with the elderly being particularly affected.
Nontyphoidal Salmonellosis Onset
Onset: 6 to 72 hours after exposure.
Nontyphoidal Salmonellosis Infective dose:
Infective dose: As low as one cell, depending on age and health of host and strain differences among members of the genus.
Nontyphoidal Salmonellosis Symptoms
Symptoms: Nausea, vomiting, abdominal cramps, diarrhea, fever, headache
Nontyphoidal Salmonellosis Duration
Duration: Symptoms generally last 4 to 7 days, with acute symptoms usually lasting 1 to 2 days or longer, depending on host factors, the dose ingested, and strain characteristics
Nontyphoidal Salmonellosis Complications
Complications: (1) Dehydration and electrolyte imbalance may occur as a result of diarrhea and vomiting. This can lead to death in the very young, the elderly, and the immunocompromised, if not treated promptly. (2) In 2% of culture-proven cases, reactive arthritis (i.e., arthritis from an immune reaction to the infection – an autoimmune response – rather than directly from the infection itself) may follow 3 to 4 weeks after the onset of acute symptoms. Indications of reactive arthritis may include, for example, joint inflammation, urethritis, uveitis, and/or conjunctivitis. (3) Nontyphoidal Salmonella can sometimes escape from the gastrointestinal tract into the body and cause blood poisoning (septicemia) or infect the blood, internal organs, and/or joints (bacteremia). S. Dublin is sometimes associated with this complication.
Nontyphoidal Salmonellosis Route of entry:
Route of entry: oral (e.g., ingestion of contaminated food, fecal particles, or contaminated water).
Nontyphoidal Salmonellosis Pathway
Pathway: Penetration and passage of Salmonella organisms from gut lumen into epithelium of small intestine, where inflammation occurs. There is evidence that enterotoxin may be produced, perhaps within enterocytes.
Typhoid Fever serotypes
Caused by serotypes S. Typhi and S. Paratyphi A, both of which are found only in humans
Typhoid Fever Mortality
Mortality: Untreated, as high as 10%.
Typhoid Fever Onset
Onset: Generally 1 to 3 weeks, but may be as long as 2 months after exposure.
Typhoid Fever Infective dose
Infective dose: Fewer than 1,000 cells
Typhoid Fever Symptoms
Symptoms: High fever, from 103° to 104°F; lethargy; gastrointestinal symptoms, including abdominal pains and diarrhea or constipation; headache; achiness; loss of appetite. A rash of flat, rose-colored spots sometimes occurs.
Typhoid Fever Duration
Duration: Generally 2 to 4 weeks.
Typhoid Fever Illness / Complications
Illness / Complications: Septicemia, with colonization of other tissues and organs; e.g., may lead to endocarditis. Septic arthritis may occur, in which the infection directly affects the joints and may be difficult to treat. Chronic infection of the gallbladder may occur, which may cause the infected person to become a carrier
Typhoid Fever Route of entry:
Route of entry: Oral (e.g., ingestion of contaminated food, fecal particles, or contaminated water).
Typhoid Fever Pathway
Pathway: Penetration and passage of typhoid Salmonella organisms from gut lumen into epithelium of small intestine and into the bloodstream (i.e., septicemia), which may carry the organisms to other sites in the body, where inflammation occurs. There is evidence that enterotoxin may be produced, perhaps within enterocytes.
Salmonellosis Frequency of Disease
Annually in the United States: Nontyphoidal salmonellosis – A recent report from the Centers for Disease Control and Prevention (CDC) estimates that 1,027,561 cases of domestically acquired nontyphoidal salmonellosis occur annually in the U.S., when under-reporting and under-diagnosis are taken into account. Typhoid fever – In terms of domestically acquired S. enterica serotype Typhi, the same CDC report estimated that a mean of 1,821 cases occur annually in the U.S. Additional cases in the U.S. are associated with foreign travel. The report estimates that 433 cases of typhoid fever in the U.S., overall (i.e., whether or not they are domestically acquired), are culture-confirmed. The last case of a foodborne, noncarrier-based typhoid outbreak in the U.S. was in 1999 and was associated with the tropical fruit mamey.
Salmonellosis Sources
Salmonella is widely dispersed in nature. It can colonize the intestinal tracts of vertebrates, including livestock, wildlife, domestic pets, and humans, and may also live in environments such as pond-water sediment. It is spread through the fecal-oral route and through contact with contaminated water. It may, for example, contaminate meat, farm-irrigation water (thus contaminating produce in the field), soil and insects, factory equipment, hands, and kitchen surfaces and utensils. Since S. Typhi and S. Paratyphi A are found only in human hosts, the usual sources of these organisms in the environment are drinking and/or irrigation water contaminated by untreated sewage. It is highly recommended that only potable water and cooked vegetables be consumed in areas where these organisms are endemic.
Salmonella species that can be found inside the egg
Various Salmonella species have long been isolated from the outside of egg shells, but S. Enteritidis can be present inside the egg. This and other information strongly suggest vertical transmission; i.e., deposition of the organism on the albumen (egg white) side of the yolk-sack membrane (vitelline membrane) by an infected hen, prior to shell formation.
Salmonellosis Diagnosis
Serological identification of cultural isolates from stool. Genetic identification of approximately 100 Salmonella serotypes from pure culture is now possible, but the remaining 2,400-plus serotypes can be identified only through traditional serotyping.
Salmonellosis Target Populations
Anyone, of any age, may become infected with Salmonella. Particularly vulnerable are people with weak immune systems, such as the very young and the elderly, people with HIV or chronic illnesses, and people on some medications; for example, chemotherapy for cancer or the immunosuppressive drugs used to treat some types of arthritis. People with HIV are estimated to have salmonellosis at least 20 times more than does the general population and tend to have recurrent episodes.
Salmonellosis Food Analysis
Isolation and detection methods have been developed for many foods having prior history of Salmonella contamination. Conventional culture and identification methods may require 4 to 6 days for presumptive results. To screen foods, several rapid methods are available, which require 1 to 2 days. These rapid methods include antibody and molecular (DNA or RNA) based assays, but in most cases, require a cultural means to confirm the presence of Salmonella, for regulatory purposes.
Campylobacter jejuni organism
Campylobacter jejuni is a nonsporeforming, Gram-negative rod with a curved- to S-shaped morphology. Many strains display motility, which is associated with the presence of a flagellum at one or both of the polar ends of this bacterium. Members of the Campylobacter genus are microaerophilic; i.e., they grow at lower-thanatmospheric oxygen concentrations. Most grow optimally at oxygen concentrations from 3% to 5%. Thus, these bacteria generally are fairly fragile in the ambient environment and somewhat difficult to culture in the laboratory. Additional conditions to which C. jejuni are susceptible include drying, heating, freezing, disinfectants, and acidic conditions.
Campylobacter species that can cause foodborne diseases in humans
Campylobacter jejuni (80% of Campylobacter infections), C. coli and C. fetus. C. coli and C. jejuni cause similar disease symptoms. C. fetus infections often are associated with animal contact or consumption of contaminated foods and beverages and are especially problematic for fetuses and neonates, in whom the mortality rate may be up to 70%
Campylobacteriosis Mortality
The CDC attributes an estimated 76 deaths in the United States, per year, to campylobacteriosis.
Campylobacteriosis Infective dose:
Infective dose: In general, the minimum number of ingested Campylobacter cells that can cause infection is thought to be about 10,000. However, in trials, as few as 500 ingested Campylobacter cells led to disease in volunteers. Differences in infectious dose likely can be attributed to several factors, such as the type of contaminated food consumed and the general health of the exposed person.
Campylobacteriosis Onset
Onset: The incubation period, from time of exposure to onset of symptoms, generally is 2 to 5 days.
Campylobacteriosis Disease / complications:
Disease / complications: The disease caused by C. jejuni infections is called campylobacteriosis. The most common manifestation of campylobacteriosis is selflimiting gastroenteritis, termed “Campylobacter enteritis,” without need for antimicrobial therapy. When antimicrobial therapy is indicated, erythromycin or ciprofloxacin are most commonly prescribed. A small percentage of patients develop complications that may be severe. These include bacteremia and infection of various organ systems, such as meningitis, hepatitis, cholecystitis, and pancreatitis. An estimated 1.5 cases of bacteremia occur for every 1,000 case of gastroenteritis. Infections also may lead, although rarely, to miscarriage or neonatal sepsis. Autoimmune disorders are another potential long-term complication associated with campylobacteriosis; for example, Guillain-Barré syndrome (GBS). One case of GBS is estimated to develop per 2,000 C. jejuni infections, typically 2 to 3 weeks post infection. Not all cases of GBS appear to be associated with campylobacteriosis, but it is the factor most commonly identified prior to development of GBS. Various studies have shown that up to 40% of GBS patients first had Campylobacter infection. It is believed that antigens present on C. jejuni are similar to those in certain nervous tissues in humans, leading to the autoimmune reaction. Reactive arthritis is another potential long-term autoimmune complication. It can be triggered by various kinds of infections and occurs in about 2% of C. jejuni gastroenteritis cases. Hemolytic uremic syndrome and recurrent colitis following C. jejuni infection also have been documented.
Campylobacteriosis Symptoms
Symptoms: Fever, diarrhea, abdominal cramps, and vomiting are the major symptoms. The stool may be watery or sticky and may contain blood (sometimes occult – not discernible to the naked eye) and fecal leukocytes (white cells). Other symptoms often present include abdominal pain, nausea, headache, and muscle pain.
Campylobacteriosis Duration
Duration: Most cases of campylobacteriosis are self-limiting. The disease typically lasts from 2 to 10 days.
Campylobacteriosis Route of entry
Route of entry: Oral.
Campylobacteriosis Pathway
Pathway: The mechanisms of pathogenesis by C. jejuni are not well understood and usually vary based on the virulence genes present in a particular strain. In general, C. jejuni cause infections by invading and colonizing the human gastrointestinal tract. Motility appears to be an important factor in C. jejuni pathogenesis, enabling the bacterium to invade the human intestinal mucosa. The mechanisms by which cellular invasion by C. jejuni cause the observed symptoms remain a mystery. In genomesequencing studies, researchers were not able to identify the presence of toxin genes that likely contribute to diarrhea and other common symptoms.
Campylobacteriosis Frequency
Campylobacter species are believed to be the third leading cause of domestically acquired bacterial foodborne illness in the United States, with an estimated 845,024 cases occurring annually, according to a 2011 Centers for Disease Control and Prevention (CDC) report. According to data from FoodNet, the incidence of cases of campylobacteriosis reported to the CDC in 2008 was 12.68 per 100,000 individuals, which is a decrease of 32% over the last decade. For each reported case of campylobacteriosis, it is estimated that 30 cases are unreported.
Campylobacteriosis Sources
Major food sources linked to C. jejuni infections include improperly handled or undercooked poultry products, unpasteurized (“raw”) milk and cheeses made from unpasteurized milk, and contaminated water. Campylobacter infection in humans has been linked to handling and eating raw or undercooked meat and poultry, whether fresh or frozen. Avoiding cross contamination of uncooked items from raw meat and poultry products, thorough cooking, pasteurization of milk and dairy products, and water disinfection are effective ways to limit food- and water-borne exposure to Campylobacter. Reduction of risk from contaminated poultry products can be achieved through good hygienic practices by manufacturers and consumers.
Campylobacteriosis Diagnosis
Special incubation conditions are required for isolation and growth of C. jejuni cells, since the organism is microaerophilic. Samples from stool or rectal swabs are inoculated directly onto selective media, or they can be enriched to increase recovery. To limit growth of competing organisms, media used for cultivation usually are supplemented with blood and antimicrobial agents. The cultures are incubated at 42ºC, under microaerophilic conditions (5% oxygen and 5% to 10% carbon dioxide), for optimal recovery
Campylobacteriosis Target Populations
Children younger than 5 years old and young adults 15 to 29 years old are the populations in whom C. jejuni gastroenteritis most commonly is detected. The highest incidence of infection is among infants 6 to 12 months old. C. jejuni bacteremia may also affect pregnant women, leading to infection of the fetus, which can lead to miscarriage or stillbirth. The incidence of infection is estimated to be 40-fold greater in people with HIV/AIDS, compared with others in the same age group.
Campylobacteriosis Food Analysis
Isolation of C. jejuni from food is difficult, because the bacteria are usually present in very low numbers. For isolation from most food products, samples are rinsed and the rinsate is collected and subjected to pre-enrichment and enrichment steps, followed by isolation of C. jejuni from the agar medium
Yersinia spp characteristics
The Yersinia genus has 11 species; 4 are pathogenic, but only Y. enterocolitica and Y. pseudotuberculosis cause gastroenteritis. Y. enterocolitica and Y. pseudotuberculosis are small, rod-shaped, Gram-negative bacteria. The former is often isolated from clinical specimens, such as wounds, feces, sputum, and mesenteric lymph nodes. However, it is not part of the normal human flora. Y. pseudotuberculosis has been isolated from diseased human appendix. Both pathogens are transmitted through the fecal-oral route. Y. enterocolitica is psychrotrophic (i.e., a microorganism that grows well at low temperature) and has the ability to grow at temperatures below 4°C. The doubling time, at 30°C, is 34 min; at 22°C, is 1 hr; and at 7°C, is 5 hrs. It can withstand freezing and can survive in frozen foods for extended periods. In fact, Y. enterocolitica has survived better in artificially contaminated food stored at room and refrigeration temperatures than at an intermediate temperature. It persists longer in cooked foods than in raw foods, due to increased nutrient availability Y. enterocolitica has between 10% and 30% DNA homology with the Enterobacteriaceae family and is 50% related to Y. pseudotuberculosis and Y. pestis. Genetic analysis of Y. pestis revealed it to be a clone of Y. pseudotuberculosis, which evolved sometime between 1,500 to 20,000 years ago
Yersinia enterocolitica Mortality
Mortality: Fatalities are extremely rare.
Yersinia enterocolitica Infective dose
Infective dose: The medium infective dose for humans is not known, but is estimated to be between 104 to 106 organisms. The infective dose and clinical presentation of symptoms may depend on pathogen (strain-dependent) and host factors. For example, in some cases, in people with gastric hypoacidity, the infective dose may be lower.
Yersinia enterocolitica Onset
Onset: Incubation times from 1 to 11 days have been observed, but occasionally last for several months.
Yersinia enterocolitica Illness / complications
Illness / complications: In some patients, complications arise due to the strain type causing the initial infection and specific human immunologic leukocyte antigen, HLA-B27. These sequelae include reactive arthritis; glomerulonephritis; endocarditis; erythema nodosum (which occurs predominantly in women); uveitis; thyroid disorders, such as Graves’ disease; hyperthyroidism; nontoxic goiter; and Hashimoto’s thyroiditis. Y. enterocolitica has been associated with reactive arthritis, which may occur even in the absence of obvious symptoms. The frequency of such postenteritis arthritic conditions is about 2% to 3%. In Japan, Y. pseudotuberculosis was implicated in the etiology of Kawasaki’s disease. Another complication is bacteremia, which raises the possibility of disease dissemination. However, this is rare. Performance of unnecessary appendectomies also may be considered a major complication of yersiniosis, as one of the main symptoms of the disease is abdominal pain in the lower right quadrant. Treatment includes supportive care, since the gastroenteritis is self-limiting. If septicemia or other invasive diseases occur, antibiotic therapy with gentamicin or cefotaxime (doxycycline and ciprofloxacin) typically are administered.
Yersinia enterocolitica Symptoms
Symptoms: Infection with Y. enterocolitica manifests as nonspecific, self-limiting diarrhea, but may cause a variety of autoimmune complications, as noted above. Most symptomatic infections occur in children younger than 5 years old. Yersiniosis in these children is frequently characterized as gastroenteritis, with diarrhea and/or vomiting; however, fever and abdominal pain are the hallmark symptoms. A small proportion of children (less than 10%) produce bloody stools. Children usually complain of abdominal pain and headache and sore throat at the onset of the illness. Yersinia infections mimic appendicitis and mesenteric lymphadenitis, but the bacteria may also cause infection in other sites, such as wounds, joints, and the urinary tract.
Yersinia enterocolitica Duration
Duration: The illness might last from a few days to 3 weeks, unless it becomes chronic enterocolitis, in which case it might continue for several months
Yersinia enterocolitica Pathway
Pathway: As zoonotic pathogens, Y. enterocolitica and Y. pseudotuberculosis enter the gastrointestinal tract after ingestion of contaminated food or water. Gastric acid is a significant barrier to infection. The infective dose might be lower among people with gastric hypoacidity. Both pathogens harbor plasmid (pYV)-encoded virulence genes that affect pathogenesis. These include an outer-membrane protein, YadA (Yersinia adhesion A), and the genetic suite comprising the type III secretory system. This process usually is facilitated by Yops proteins, which contribute to the ability of Y. enterocolitica cells to resist phagocytosis by causing disruption (cytotoxic changes) of mammalian (human) cells.
Yersinia enterocolitica Frequency
Yersiniosis is far more common in Northern Europe, Scandinavia, and Japan than in the United States. It does not occur frequently and tends to be associated with improper food-processing techniques. Y. enterocolitica is a more frequent cause of yersiniosis than is Y. pseudotuberculosis, and cases have been reported on all continents. Different biotypes of Y. enterocolitica have been associated with infections around the world, with the most common biotype being 4/O:3. Information on Y. pseudotuberculosis is not as well defined and, as such, is reported less frequently than is Y. enterocolitica.
Yersinia enterocolitica Sources
Strains of Y. enterocolitica can be found in meats (pork, beef, lamb, etc.), oysters, fish, crabs, and raw milk. However, the prevalence of this organism in soil, water, and animals, such as beavers, pigs, and squirrels, offers many opportunities for Yersinia to enter the food supply. For example, poor sanitation and improper sterilization techniques by food handlers, including improper storage, may be a source of contamination. Raw or undercooked pork products have drawn much attention as a source of Y. enterocolitica, and Y. pseudotuberculosis, particularly since Y. enterocolitica has been associated with pigs.
Yersinia enterocolitica Diagnosis
Yersiniosis may be misdiagnosed as Crohn’s disease (regional enteritis) or appendicitis. Diagnosis of yersiniosis begins with isolation of the organism from the human host’s feces, blood, or vomit, and sometimes at the time of appendectomy. Confirmation occurs with the isolation, as well as biochemical and serological identification, of Y. enterocolitica from both the human host and the ingested food. Diarrhea occurs in about 80% of cases; abdominal pain and fever are the most reliable symptoms. Y. enterocolitica or Y. pseudotuberculosis in patients with acute gastroenteritis can be readily isolated via conventional bacteriological media designed to isolate Yersinia. It is much more challenging to isolate these pathogens in asymptomatic carriers or from foods. Since many Y. enterocolitica isolated from non-human sources are not considered pathogenic, it is imperative to distinguish these isolates from pathogenic Yersinia species. Molecular-based assays, particularly PCR methods, have been developed to target Y. enterocolitica and can be used to rapidly confirm the pathogenicity of the isolate. Several PCR primer sets are directed to either plasmid-borne genes, e.g., virF or yadA, or chromosomally located loci, such as ail. Serology is used to identify the biotype (based on biochemical analysis) and serogroup (O-antigen). Sera from acute or convalescent patients are titered against the suspect serotype of Yersinia spp.
Yersinia enterocolitica Target populations
The most susceptible populations for the main disease and potential complications are the very young (< 10 years), the debilitated, the very old, and people undergoing immunosuppressive therapy. Those most susceptible to post-enteritis arthritis are people with the antigen HLA-B27 (or related antigens, such as B7).
Yersinia enterocolitica Food Analysis
The isolation method is relatively easy to perform, but in some instances, cold enrichment (25 g sample of the food mixed with 225 ml of Peptone Sorbitol bile broth for 10 days at 10°C) may be required. Y. enterocolitica can be presumptively identified in 36 to 48 hours using biochemical testing or API 20E or Vitek GNI. The genes encoding for invasion of mammalian cells are located on the chromosome, while a 70 kb plasmid, present in almost all pathogenic Yersinia species, encodes most of the other virulence-associated phenotypes. PCR-based assays have been developed to target virulence genes on both the chromosome and plasmid.
Yersinia enterocolitica Examples of Outbreaks
To date (book: 2012), no foodborne outbreaks caused by Y. pseudotuberculosis have been reported in the U.S., but human infections transmitted via contaminated water and foods have been reported in Japan (Fukushima et al. 1988) and Finland (Jalava et al. 2004). Y. pseudotuberculosis has been implicated in a number of food-related outbreaks, but the number of foodborne outbreaks from Y. enterocolitica is higher.
Shigella species
Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae
Shigellae Organism characteristics
Shigellae are Gram-negative, non-motile, non-sporeforming, rod-shaped bacteria. Shigella species, which include Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae, are highly infectious agents. Some strains produce enterotoxins and Shiga toxin. The latter is very similar to the toxins produced by E. coli O157:H7. Humans are the only host of Shigella, but it has also been isolated from higher primates. The organism is frequently found in water polluted with human feces. In terms of survival, shigellae are very sensitive to environmental conditions and die rapidly. They are heat sensitive and do not survive pasteurization and cooking temperatures. In terms of growth, shigellae are not particularly fastidious in their requirements and, in most cases, the organisms are routinely cultivated in the laboratory, on artificial media. However, as noted in subsequent sections, the relative difficulty of cultivating this organism is dependent, in part, on the amount of time within which stool or food samples are collected and processed. Shigella species are tolerant to low pH and are able to transit the harsh environment of the stomach. These pathogens are able to survive and, in some cases, grow in foods with low pH, such as some fruits and vegetables. They are able to survive on produce commodities packaged under vacuum or modified atmosphere and can also survive in water, with a slight decrease in numbers.
illness caused by Shigella
The illness caused by Shigella is shigellosis (also called bacillary dysentery), in which diarrhea may range from watery stool to severe, life-threatening dysentery. All Shigella spp. can cause acute, bloody diarrhea. Shigella spp. can spread rapidly through a population, particularly in crowded and unsanitary conditions.
Shigella species that causes the most severe disease and the mildest form of shigellosis
S. dysenteriae type 1 causes the most severe disease and is the only serotype that produces the Shiga toxin, which may be partially responsible for cases in which hemolytic uremic syndrome (HUS) develops. S. sonnei produces the mildest form of shigellosis; usually watery diarrhea. S. flexneri and S. boydii infections can be either mild or severe.
Shigellosis (also called bacillary dysentery) Mortality
Mortality: In otherwise healthy people, the disease usually is self-limiting, although some strains are associated with fatality rates as high as 10-15%. (See Illness / complications section, below.)
Shigellosis (also called bacillary dysentery) Infective dose
Infective dose: As few as 10 to 200 cells can cause disease, depending on the age and condition of the host
Shigellosis (also called bacillary dysentery) Onset
Onset: Eight to 50 hours.
Shigellosis (also called bacillary dysentery) Illness / complications
Illness / complications: In otherwise healthy people, the disease usually consists of selflimiting diarrhea (often bloody), fever, and stomach cramps. Severe cases, which tend to occur primarily in immunocompromised or elderly people and young children, are associated with mucosal ulceration, rectal bleeding, and potentially drastic dehydration. Potential sequelae of shigellosis include reactive arthritis and hemolytic uremic syndrome.
Shigellosis (also called bacillary dysentery) Symptoms
Symptoms: May include abdominal pain; cramps; diarrhea; fever; vomiting; blood, pus, or mucus in stools; tenesmus (straining during bowel movements).
Shigellosis (also called bacillary dysentery) Duration
Duration: Uncomplicated cases usually resolve in 5 to 7 days. Most of the time, the illness is self-limiting. In some circumstances, antibiotics are given; usually trimethoprim-sulfamethoxazole, ceftriaxone, or ciprofloxacin.
Shigellosis (also called bacillary dysentery) Route of entry
Route of entry: The fecal-oral route is the primary means of human-to-human transmission of Shigella. With regard to foods, contamination is often due to an infected food handler with poor personal hygiene.
Shigellosis (also called bacillary dysentery) Pathway
Pathway: The disease is caused when Shigella cells attach to, and penetrate, colonic epithelial cells of the intestinal mucosa. After invasion, they multiply intracellularly and spread to contiguous epithelial cells, resulting in tissue destruction. As noted, some strains produce enterotoxin and Shiga toxin similar to those produced by E. coli O157:H7
Shigellosis (also called bacillary dysentery) Frequency
A recent Centers for Disease Control and Prevention (CDC) report on domestically acquired foodborne illnesses in the United States revealed that about 15,000 laboratory-confirmed isolates are reported each year, with estimates of actual occurrence ranging from 24,511 to 374,789 cases (average of 131,243). About 31% of these are estimated to be foodborne. Estimates of foodborne illness episodes (mean) caused by 31 pathogens placed Shigella as the sixth most frequent cause (after norovirus, Salmonella species, Clostridium perfringens, Campylobacter, and Staphylococcus aureus, in that order).
Shigellosis (also called bacillary dysentery) seasonality
Episodes of shigellosis appear to follow seasonal variations. In developed countries, the highest incidences generally occur during the warmer months of the year.
Shigellosis (also called bacillary dysentery) Sources
Most cases of shigellosis are caused by ingestion of fecally contaminated food or water. In the case of food, the major factor for contamination often is poor personal hygiene among food handlers. From infected carriers, this pathogen can spread by several routes, including food, fingers, feces, flies, and fomites. Shigella is commonly transmitted by foods consumed raw; for example, lettuce, or as nonprocessed ingredients, such as those in a five-layer bean dip. Salads (potato, tuna, shrimp, macaroni, and chicken), milk and dairy products, and poultry also are among the foods that have been associated with shigellosis.
Shigellosis (also called bacillary dysentery) Diagnosis
Diagnosis is by serological or molecular identification of cultures isolated from stool. Shigella may be more difficult to cultivate if stool samples are not processed within a few hours.
Shigellosis (also called bacillary dysentery) Target Populations
All people are susceptible to shigellosis, to some degree, but children 1 to 4 years old, the elderly, and the immunocompromised are most at risk. Shigellosis is very common among people with AIDS and AIDS-related complex
Shigellosis (also called bacillary dysentery) Food Analysis
Shigellae remain a challenge to isolate from foods. A molecular-based method (PCR) that targets a multi-copy virulence gene has been developed and implemented by FDA. Improvements in the bacterial isolation method continue and should be available in the near future. The window for collecting and processing Shigella from foods, for cultivation, may be days (rather than hours, as is the case with stool), depending on the food matrix and storage conditions; e.g., temperature. Shigella species can be outgrown by the resident bacterial populations found in foods, which may reflect the usual low numbers of the organism present in foods and, in some foods, a very large number of non-Shigella bacteria. Another factor that reduces the chance of isolating Shigella from foods may be the physiological state of the pathogen at the time of analysis. Environmental conditions could affect its ability to either grow or survive in any food matrix.
Vibrio parahaemolyticus Organism characteristics
Vibrio parahaemolyticus m is a Gram-negative, curve-shaped rod frequently isolated from the estuarine and marine environments of the United States and other tropical-to-temperate coastal areas, worldwide. Optimal temperatures for V. parahaemolyticus are 20°C to 35°C; it can grow at temperatures up to 41°C. It is slowly inactivated at temperatures <10°C (minimum growth temperature), and cultures should never be stored in refrigerators. V. parahaemolyticus is halophilic; the highest abundance in oysters is at 23 ppt salt. It is lysed almost immediately in freshwater; thus, it is not usually transmitted via the fecal-oral route. At least 0.5% NaCl is required in all media, and 2% NaCl is optimal. Like other vibrios, V. parahaemolyticus is highly susceptible to low pH, freezing, and cooking. Most strains of V. parahaemolyticus produce a capsule, but all strains can be killed by common disinfectants, such as bleach and alcohol.
Vibrio parahaemolyticus Mortality
Mortality: Death occurs in approximately 2% of gastroenteritis and 20% to 30% of septicemia cases.
Vibrio parahaemolyticus Infective dose:
Infective dose: The FDA V. parahaemolyticus Risk Assessment states that the ID50 (median infective dose) is 100 million organisms. However, evidence from an outbreak in 2004 suggests an infectious dose >1,000-fold less than in the FDA risk assessment.
Vibrio parahaemolyticus Onset
Onset: The incubation period is 4 to 90 hours after ingestion of the organism, with a mean of 17 hours
Vibrio parahaemolyticus Illness / complications
Illness / complications: V. parahaemolyticus-associated gastroenteritis is the name of the infection caused by consumption of this organism. It is usually mild or moderate. Diarrhea caused by this organism is usually self-limiting, with less than 40% of reported cases requiring hospitalization and/or antibiotic treatment. Although the illness is generally mild or moderate, V. parahaemolyticus can also cause septicemia in susceptible people. Those at risk include people with diabetes, liver disease, kidney disease, cancer, AIDS, or other illnesses that result in an immunocompromised state, and those on immunosuppressive medications. In addition to the foodborne gastrointestinal illness, this organism also can cause wound infections. This occurs either through exposure of a pre-existing wound to contaminated marine or estuarine water or through wounds incurred while handling fish, shellfish, or crustaceans.
Vibrio parahaemolyticus Symptoms
Symptoms: Diarrhea, abdominal cramps, nausea, vomiting, fever, and bloody diarrhea may be associated with gastroenteritis infections caused by this organism.
Vibrio parahaemolyticus Duration
Duration: The median duration of the illness is 2 to 6 days.
Vibrio parahaemolyticus Route of entry:
Route of entry: Oral (in the case of foodborne, gastroenteritis infections. As noted, wound infections also can occur through direct exposure).
Vibrio parahaemolyticus Pathway
Pathway: The complete pathway by which V. parahaemolyticus causes disease remains unclear. However, it is known that TDH is a pore-forming toxin that lyses red blood cells and can attack intestinal cells, disrupting the electrolyte balance. The mechanism of TRH toxin is similar to TDH, disrupting electrolyte flux in intestinal cells
Vibrio parahaemolyticus Frequency
The Centers for Disease Control and Prevention (CDC) estimates that about 45,000 illnesses from V. parahaemolyticus occur each year, in the United States, and that about 86% of them are foodborne. A correlation exists between probability of infection and warmer months, when water temperatures are greater than 15°C (59°F). CDC estimates that only 1 in 20 cases of V. parahaemolyticus are reported, and it is likely that hospitalization and death are rare among unreported cases.
Vibrio parahaemolyticus Sources
In the U.S., infections with this organism generally are associated with consumption of raw or improperly cooked oysters. Other seafood products, including finfish, squid, octopus, lobster, shrimp, crab, and clams, have been linked to V. parahaemolyticus illnesses, more frequently in Asian countries. . Improper refrigeration of seafood products contaminated with this organism will allow its proliferation, which increases the possibility of infection.
Vibrio parahaemolyticus Diagnosis
Diagnosis is made by culturing the organism from a person’s stool, wound, or blood (in septicemia cases).
Vibrio parahaemolyticus Target Populations
Anyone who eats raw or improperly cooked seafood products is susceptible to infection by this organism. People with compromised immune systems are at greater risk of septicemia and death
Vibrio parahaemolyticus Food Analysis
Many food isolates are non-pathogenic; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a DNA probe and/or a PCR procedure for identification of genes responsible for TDH and TRH production. Additionally, there are more recent molecular methods available for virulence characterization, many of which can be applied directly to seafood products, to screen for the presence of pathogenic organisms prior to isolation.
Vibrio parahaemolyticus Examples of Outbreaks
Shellfish were linked to 177 cases in New York, Oregon, and Washington, in 2006. In 2004, in Alaska, 62 cases were linked to consumption of raw oysters
Coxiella burnetii 1. Organism characteristics
Coxiella burnetii, a Gram-negative, obligate intracellular bacterium, is the causative agent of Q fever. Coxiella are noted for their resistance to extremely harsh physical conditions, such as heat, low and high pH, and desiccation, due to a tough, spore-like stage. These cells may survive for long periods in the environment and in contaminated foods, such as unpasteurized milk. Due to C. burnetii’s ability to be disseminated via aerosols and its low infective dose, the Centers for Disease Control and Prevention (CDC) have declared it a Category B potential bioterrorism agent. Coxiella burnetii has long been considered the most heat-resistant non-spore-forming pathogen found in milk, making it the benchmark organism for determining proper pasteurization conditions
Acute Q Fever Mortality
Mortality: < 1%
Acute Q Fever Infective dose
Infective dose: Presumed to be fewer than 10 bacteria.
Acute Q Fever Onset
Onset: May occur as soon as 2 weeks after exposure; average time to symptoms is 20 days.
Acute Q Fever Illness / complications
Illness / complications: The infection sometimes is asymptomatic. Symptomatic individuals with acute Q fever experience a flu-like disease. Infections generally are easy to resolve with antibiotic treatment. Complications that may occur in more serious cases include pneumonia, hepatitis, and myocarditis.
Acute Q Fever Symptoms
Symptoms: Symptoms may vary considerably among individuals, but commonly include very high fever (105°F); severe headaches; muscle aches; chills; profuse sweating; nausea, vomiting, and/or diarrhea; a dry cough; and abdominal and/or chest pain.
Acute Q Fever Duration
Duration: The fever usually lasts 1 to 2 weeks and generally is self-limiting.
Acute Q Fever Route of entry:
Route of entry: Transmission of C. burnetti is primarily through inhalation of aerosolized bacteria, although transmission via ingestion of contaminated unpasteurized (“raw”) milk or dairy products or via tick bite also is possible.
Acute Q Fever Pathway
Pathway: Once the bacteria enter host cells, the bacteria multiply in protective vacuoles before lysing the host cells and spreading to other, non-infected cells.
Chronic Q Fever Mortality
Mortality: If untreated, may be > 60%
Chronic Q Fever Onset
Onset: Chronic Q fever may develop 6 weeks to years after the acute illness.
Chronic Q Fever Illness / complications:
Illness / complications: Less than 5% of infected patients will exhibit chronic Q fever. This more severe disease typically occurs in patients who are already compromised due to pregnancy, heart-valve disease, or other illness. A majority of cases involve endocarditis, but may also include hepatitis, encephalitis, pericarditis, meningitis, or pneumonia
Chronic Q Fever Symptoms
Symptoms: Symptoms depend on the tissue affected; e.g., symptoms of endocarditis, hepatitis, encephalitis, pericarditis, meningitis, or pneumonia
Chronic Q Fever Duration
Duration: Although often curable with extended (> 18 months) antibiotic treatment, 50% of patients are prone to relapses.
Q Fever Frequency
Since first becoming a reportable disease, the number of Q fever cases has steadily increased, from 17 cases with onset in 2000 to more than 160 cases with onset in 2007. In 2008, after CDC began recording cases based on type of Q fever, 132 cases, total, were reported, consisting of 117 acute and 15 chronic cases. Since that time, 90 to 110 acute and 20 to 25 chronic cases of Q fever have been reported each year.
Q Fever Sources
C. burnetii is found nearly worldwide and is excreted in the urine, milk, feces, and birth products of its various hosts, which include humans, cattle, sheep, goats, reptiles, and birds. Ticks also are a reservoir and may transmit the bacteria directly, via bite, or indirectly, via infected feces. Inhalation of aerosolized bacteria is the most common route of transmission, although transfer also may occur through ingestion of contaminated unpasteurized milk or dairy products and, as noted, via ticks.
Q Fever Diagnosis
Q fever clinical diagnosis is difficult, due to the many different diseases it mimics. However, polymerase chain reaction (PCR) can be used for early detection of the disease when more conventional antibody tests are not useful. After full development of the disease, less-sensitive serological tests, such as an indirect immunofluorescence assay (IFA) against C. burnetiispecific antibodies, are capable of confirming the diagnosis.
Q Fever Target populations
Q fever is associated most with occupations in the livestock industry, especially where aerosolization of livestock birth products may be common. Q fever is more common in males than in females and in adults more than in children, probably due to the occupational characteristics of livestock workers. The average age of affected individuals is 45 to 50 years old. Women are at risk of miscarriage if infected
Q Fever Food Analysis
The FDA-mandated level of pasteurization for milk sold in interstate commerce is lethal to C. burnetii, essentially obviating the need to detect the organism in this product. Were analysis for C. burnetii necessary, a live animal host or tissue culture would be required for propagation of the organism.
Q Fever Examples of Recent Outbreaks
In July, 2011, three women, in Michigan (ages 30 to 40), were diagnosed with acute Q fever after drinking unpasteurized raw milk obtained as part of a herd-share arrangement. In April 2011, in Washington state, an outbreak involving six illnesses occurred, presumed to have been caused by inhalation of barnyard dust particles contaminated by infected goats. Some of these goats were sold and were suspected of being the source of a Montana outbreak that included six cases. An extremely large outbreak in the Netherlands caused nearly 4,000 illnesses over a 4-year span, starting in 2007. In this case, dairy goats and sheep appeared to be the sources of the outbreak, with 30 farms experiencing extremely high livestock abortion rates
Brucella species 1. Organism
Brucella spp. are small, Gram-negative, short, non-sporeforming coccobacilli. Members of the genus Brucella, of which there are six recognized species, belong to a class of Proteobacteria known as Alphaproteobacteria. Diverse groups of organisms comprise this class, including symbionts and plant pathogens, intracellular animal pathogens, and environmentally ubiquitous bacteria. Strictly defined, Brucella spp. are facultative, intracellular parasites able to invade, and replicate in, phagocytes of the host and to multiply in bacteriologic media. CO2dependent B. abortus strains exist, and B. ovis grows only in atmospheres containing 5-10% CO2. While evidence suggests that Brucella spp. can survive in the environment, it is less clear whether or not the bacteria can proliferate extensively outside the host. Unlike other pathogenic bacteria, Brucella spp. do not possess plasmids or lysogenic bacteriophages, which accounts for the organism’s relatively (but not entirely) static genome. Were Brucella to possess these factors, they would likely result in changes to the organism’s pathogenicity, by enabling the organism to undergo more rapid exchange of genetic material or by introduction of the attacking bacteriophage’s DNA into Brucella’s DNA, respectively.
Brucella species is their strong preference for a particular animal host (sheep/goat, cattle, pigs, desert wood rats, dogs, sheep human)
B. melitensis (sheep, goat), B. abortus (cattle), B. suis (pigs, hares, reindeer, wild rodents), B. neotomae (desert wood rats), B. canis (dogs), and B. ovis (sheep). All except B. ovis and B. neotomae are known to be infectious to humans
Brucella smooth strains and ‘rough’ strains based on slide agglutination
slide agglutination is very useful for distinguishing “smooth” strains (i.e., those with an O-polysaccharide-containing outer-membrane lipopolysaccharide: B. melitensis, B. abortus, B. suis, and B. neotomae) from “rough” strains (i.e., those without an O-polysaccharide-containing outer-membrane lipopolysaccharide: B. ovis and B. canis).
Brucellosis Mortality:
Mortality: Less than 2%.
Brucellosis Infective dose:
Infective dose: Undefined for humans; however, it is estimated that fewer than 500 cells are enough to establish infection. Humans appear to be more susceptible to B. melitensis than to the other species that infect humans.
Brucellosis Onset
Onset: Following exposure, signs of illness usually appear within 3 weeks, but longer incubation periods are not unusual.
Brucellosis Disease / complications:
Disease / complications: In the beginning stage of illness, septicemia results after multiplication of the organism in regional lymph nodes. Patients have the intermittent fevers and sweating that are the hallmarks of brucellosis, along with other potential symptoms (described in Symptoms section, below). If the diagnosis of brucellosis is delayed or the disease is left untreated, the disease may become chronic, and focalizations of brucellosis in bones (i.e., brucellar spondylitis) and joints may occur. Other potential complications include bacterial endocarditis, meningioencephalitis, and myocarditis. Allergic hypersensitivity (dermal) is not uncommon and should be a consideration for laboratory workers or others with repeated exposures to the organism or antigens.
Brucellosis antibiotics most commonly used to treat human brucellosis
The antibiotics most commonly used to treat human brucellosis include tetracycline, rifampicin, and the aminoglycosides. However, due to a high likelihood of relapse, health officials recommend the administration of more than one antibiotic for up to 6 weeks. Common combinations include doxycycline plus rifampicin or doxycycline plus streptomycin. For approximately 90% of patients, such aggressive therapy is enough to treat the infection and prevent relapse.
Brucellosis Symptoms
Symptoms: Potential initial signs of illness include intermittent (i.e., “undulant”) fever, chills, sweating, weakness, malaise, headache, and joint and muscle pain. Patients who develop complications may show symptoms of endocarditis or myocarditis, such as shortness of breath, arrhythmia, edema, or chest pain; meningoencephalitis, such as severe headache, stiff neck, confusion, or seizures; or spondylitis, such as back pain.
Brucellosis Duration
Duration: With appropriate antibacterial therapy, it is possible to see resolution of disease in only a few weeks; however, even with treatment, symptoms may reappear and last for months or even years.
Brucellosis Route of entry:
Route of entry: Oral; e.g., through ingestion of contaminated raw milk or milk products. Inhalation; e.g., by laboratory personnel in the clinical setting. Via skin wounds; e.g., in slaughterhouse workers and veterinarians. In rare instances, human-to-human transmission may occur through, e.g., reproduction or breast-feeding.
Brucellosis Pathway
Pathway: Humans most commonly come into contact with Brucella through cutaneous, respiratory, or gastrointestinal routes of exposure, allowing the bacteria access to both the blood and reticuloendothelial system. How Brucella, an intracellular parasite, survives intracellularly and its pathogenesis pathway in humans are not well understood. It is clear that the organism’s ability to live and replicate within the phagocytic cells of the reticuloendothelial system (e.g., macrophages) is a critical component of its ability to evade host defenses and establish disease chronicity. Once inside the macrophage, some bacteria are killed; however, a subpopulation can be transported into the intracellular spaces (i.e., the replicative phagosome) of the macrophage and multiply unnoticed and without inducing cell death. When moved to the lymph nodes, macrophages die and can release large amounts of bacteria. In humans, the infection is primarily focused within the reticuloendothelial system, but, in other animal hosts, the organism targets the placental trophoblast cells of pregnant animals, causing fetuses to be aborted. Human cases of spontaneous abortion have been noted following infections with Brucella, similar to occurrences associated with another intracellular pathogen, Listeria monocytogenes, that likewise affects dairy products.
one reason B. melitensis might be more pathogenic to humans than are other species
Study of human neutrophils found in the bloodstream demonstrated different responses for different species of Brucella. For example, the bacteria were killed more readily in neutrophils infected with B. abortus than in those infected with B. melitensis. However, strains of B. abortus andB. melitensis in which the virulence was attenuated showed no difference.
Brucellosis Effects of Brucella on animal hosts:
Effects of Brucella on animal hosts: Brucella species generally do not cause illness in their primary (animal) hosts. In many cases, the only evidence of infection appears when a pregnant host suffers an abortion. Male animals can asymptomatically harbor the organism in their reproductive organs. Although Brucella strains have a strong preference for their host animals, interspecies transmission does occur through close physical contact with the bacterium. B. ovis and B. canis appear to have a substantially reduced virulence for animals other than their hosts.
Brucellosis Frequency
According to a recent estimate by the Centers for Disease Control and Prevention (CDC), 839 cases of foodborne brucellosis occur each year in the United States, if under-reporting and under-diagnosis are taken into account. Vaccination of domestic livestock has largely controlled the disease in the U.S. and Canada.
Brucellosis Sources
Brucellosis in humans is usually associated with consumption of unpasteurized milk and soft cheeses made from the milk of infected animals.
Brucellosis Diagnosis
Most often, the diagnosis of brucellosis relies on the isolation of the organism from blood or bone marrow. In addition, a number of immunologic techniques exist for detection of anti-Brucella antibodies. The organism may also be isolated from the liver, spleen, bone marrow, or cerebrospinal fluid. The growth of Brucella from blood culture is notoriously slow, contributing to difficulties in diagnosis. In the case of disease progression to focalizations or chronic infections, histologic changes and radiologic evidence of erosion of lumbar vertebrae are useful for diagnosis. Localization of infection in the spinal column, brucellar spondylitis, is not uncommon with chronic infection. Appearance of Pedro Pons’ sign (erosion at the anterior superior angle of lumbar vertebra) and bone spurs (osteophytosis) are classic indications of brucellar spondylitis
Brucellosis Target Populations
Veterinarians and farm workers are at particular risk of infection, due to occupational exposure to tissues of aborted animal fetuses, which may contain millions of organisms. Brucellosis in humans tracks the distribution of animal illness. Human cases of brucellosis are found primarily in developing countries with animal cases and a high level of consumption of unpasteurized milk products. In the U.S., human cases linked to domestically produced milk or milk products are largely nonexistent; cases are almost exclusively linked to unpasteurized milk products imported from certain areas of Latin America. This is in contrast to countries such as Mexico, where both human and animal infection of B. melitensis have been reported in every state. Other focal points for both animal and human infection caused by B. melitensis include countries with large goat populations, including Mediterranean Europe, Africa, the Middle East, India, and parts of Asia.
Reason Brucellosis is the most commonly reported laboratory-acquired infection among clinical laboratory personnel
Risk of transmission arises during laboratory procedures that cause the organism to become airborne (e.g., pouring of broths, sample centrifugation). For this reason, all manipulations generating bioaerosols should be done in a class II biological safety cabinet, using Biosafety 3 containment practices and facilities.
Brucellosis Food Analysis
Currently no method is available for routine analysis of foods for Brucella spp.
Bacteria responsible for epidemics and pandemic cholera outbreaks
Vibrio cholerae serogroups O1 and O139
Virulence of V. cholerae serogroups O1 and O139 is predicted by what toxins
Virulence of V. cholerae serogroups O1 and O139 is predicted by the production of an enterotoxin called cholerae toxin (CT) and the toxin co-regulated pilus (TCP).
Characteristics of Vibrio cholerae Serogroups O1 and O139
These organisms are Gram-negative, slightly curved, rod-shaped bacteria that occur naturally in aquatic environments. V. cholerae O1 and O139 are the most hardy of the pathogenic Vibrio spp. and have the ability to survive in freshwater and in water composed of up to ~3% salt. However, these organisms are very susceptible to disinfectants, cold temperatures (especially freezing), and acidic environments. They are readily inactivated at temperatures >45 C, and cooking food is lethal to V. cholerae O1 and O139. V. cholerae O139 is unique among V. cholerae strains, in that it is encapsulated. However, this does not appear to provide greater pathogenicity or resistance to common disinfectants, such as ethanol and bleach
Cholera Mortality
Mortality: Without rehydration therapy, this disease has a 30% to 50% mortality rate; however, with timely treatment, the fatality rate is less than 1%.
Cholera Infective dose
Infective dose: It is estimated that ingestion of 1 million organisms is required to cause illness.
Cholera Onset
Onset: Symptoms usually appear within a few hours to 3 days of ingestion.
Cholera Illness / complications
Illness / complications: Infection with V. cholerae serogroups O1 or O139 causes mild to severe diarrhea. Approximately 20% of those infected have watery diarrhea, and 10% to 20% of those develop severe watery diarrhea (characteristic rice-water stools) and vomiting. Cholera gravis, the most severe form of cholera infection, is characterized by severe fluid and electrolyte loss from vomiting and profuse, watery diarrhea. Complications include tachycardia, hypotension, and dehydration.
Cholera treatment
V. cholerae O1 and O139 infections can be treated with antibiotics, though rehydration therapy is generally sufficient. Doxycycline and/or tetracycline are the antibiotics of choice; however, some resistance to tetracycline has been reported
Cholera Symptoms
Symptoms: The illness generally presents with abdominal discomfort and diarrhea that may vary from mild and watery to acute, with rice-water stools. Vomiting also occurs in some cases.
Cholera Duration
Duration: Mild gastroenteritis cases usually resolve within a few days of symptom onset. Cases requiring medical intervention via rehydration therapy or antibiotic treatment can persist longer, depending on severity of illness when treatment is initiated.
Cholera Route of entry:
Route of entry: Oral.
Cholera Pathway
Pathway: CT is an enterotoxin that enters epithelial cells of the intestine and causes secretion of electrolytes and water into the lumen of the intestine. This water loss results in severe diarrhea and dehydration. It is known that CT is a multi-subunit toxin encoded by the ctxAB operon. Additionally, genes responsible for formation of the TCP (toxin coregulated pilus) are essential for infection.
Cholera Frequency
No major outbreaks of cholera have occurred in the United States since 1911. However, sporadic cases and small outbreaks have been reported since 1973, suggesting an environmental reservoir in the U.S. The Centers for Disease Control and Prevention (CDC) estimates that 84 cases of foodborne cholera occur in the U.S. annually. This organism causes an estimated 11 million cases per year worldwide, excluding outbreaks. Nearly 90% of cases and 70% of outbreaks from 1995 to 2005 occurred in Africa.
Cholera Sources
Sources In the U.S., infections with these organisms have been associated with a variety of seafoods, including molluscan shellfish (oysters, mussels, and clams), crab, lobster, shrimp, squid, and finfish. Illness generally results from consumption of these seafoods raw, improperly cooked, or cross contaminated by a raw product. Although cooking kills these bacteria, serogroups O1 and O139 can grow in shellfish that have been contaminated after cooking, and prompt refrigeration of food remnants is important for prevention of this illness. In areas where V. cholerae serogroup O1 and/or O139 is endemic, infections can occur from ingestion of water; ice; unwashed, contaminated food; and seafood.
Cholera Diagnosis
Diagnosis Cholera can be confirmed only by isolation of the causative organism from the diarrheic stools of infected people.
Cholera Target Populations
Target Populations All people are believed to be susceptible to infection. However, infection is more likely to occur among people in impoverished areas, poorly developed areas, and areas with a high population density. Cholera is most severe in children suffering from malnutrition. People who have not previously been exposed to the organism are more likely to become infected, as immunity is usually conferred by infection. Improved sanitation and hygiene can help prevent the disease
Cholera Food Analysis
Food Analysis FDA’s Bacteriological Analytical Manual (BAM) describes the methods most commonly used to isolate this organism from foods. Pathogenic and non-pathogenic forms of the organisms do exist; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a PCR method for detection of the gene responsible for cholera toxin (CT) production.
Cholera Examples of Outbreaks
Examples of Outbreaks In the U.S., two cases of cholera were reported following Hurricanes Katrina and Rita, in 2005. Internationally, the reported outbreak of cholera that occurred in Haiti, in October 2010, included an estimated 530,000 illnesses and at least 7,000 deaths. As is the case with the other Vibrio spp., there is a seasonal trend associated with outbreaks; illnesses are more likely to occur in the warmer months.
Vibrio cholerae non-O1 non-O139 characteristics
V. cholerae non-O1 non-O139 are more hardy than most of the other pathogenic Vibrio spp. and have the ability to survive in freshwater and in water composed of up to ~3% salt. However, these organisms are very susceptible to cold temperatures, including freezing, and acid environments. Additionally, cooking food thoroughly kills V. cholerae non-O1 non-O139. V. cholerae nonO1 non-O139 are not encapsulated, and are susceptible to common disinfectants, such as ethanol and bleach.
Vibrio cholerae non-O1 non-O139 Mortality:
Mortality: The fatality rate is about 5%, generally among people with the predisposing conditions listed above.
Vibrio cholerae non-O1 non-O139 Infective dose
Infective dose: It is suspected that large numbers (more than 1 million) of the organism must be ingested to cause illness.
Vibrio cholerae non-O1 non-O139 Onset
Onset: Symptoms usually appear within 1 to 3 days of ingestion
Vibrio cholerae non-O1 non-O139 Illness / complications:
Illness / complications: Diarrhea resulting from ingestion of this organism is generally self-limiting. However, septicemia infections can result, and there is approximately a 5% fatality rate associated with non-O1 non-O139 V. cholerae, generally in people having predisposing conditions similar to those for V. vulnificus infection.
Vibrio cholerae non-O1 non-O139 Symptoms
Symptoms: Diarrhea, abdominal cramps, and fever are the predominant symptoms associated with this illness, with vomiting and nausea occurring in approximately 25% of infected people. Approximately 25% of infected people have blood and mucus in their stool.
Vibrio cholerae non-O1 non-O139 Duration
Duration: Symptoms usually resolve within 7 days.
Vibrio cholerae non-O1 non-O139 Route of entry
Route of entry: Oral. (Occasionally, infections with this organism that are not foodborne occur in wounds and ears.)
Vibrio cholerae non-O1 non-O139 Pathway
Pathway: Very little is known about how non-CT producing strains of V. cholerae cause disease. These strains generally produce other types of enterotoxins, such as RTX (repeats in toxin); however, none have been shown to be absolutely necessary for infection.
Vibrio cholerae non-O1 non-O139 Frequency
The Centers for Disease Control and Prevention (CDC) estimates that 17,564 cases of foodborne illness from these Vibrio species occur annually in the U.S. In the spring of 2011, the first oyster-associated V. cholerae O75 outbreak in the U.S. occurred. There were 10 illnesses associated with consumption of raw oysters from Florida.
Vibrio cholerae non-O1 non-O139 Sources
Sporadic cases generally occur along the coasts of the U.S. and are associated with consumption of raw, improperly cooked, or cross-contaminated seafood during the warmer months.
Vibrio cholerae non-O1 non-O139 Diagnosis
Diagnosis Diagnosis of a V. cholerae infection is made by culturing the organism from patients’ diarrheic stool or from the blood of patients with septicemia.
Vibrio cholerae non-O1 non-O139 Target Populations
Target Populations Anyone who eats raw shellfish is susceptible to diarrhea caused by this organism. As noted above, cirrhotic or immunocompromised people may develop severe complications, such as septicemia.
Vibrio cholerae non-O1 non-O139 Food Analysis
Food Analysis FDA’s Bacteriological Analytical Manual (BAM) describes the methods most commonly used to isolate this organism from foods. Pathogenic and non-pathogenic forms of the organisms do exist; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a PCR method for the detection of the gene responsible for CT production
Vibrio cholerae non-O1 non-O139 Examples of Outbreaks
This organism generally is associated with sporadic illnesses and rarely causes outbreaks. In the spring of 2011, the first oyster-associated V. cholerae O75 outbreak in the U.S. occurred. There were 10 illnesses associated with consumption of raw oysters from Florida
Vibrio vulnificus 1. Organism
s Gram-negative, curve-shaped bacterium is found in estuarine environments and is associated with various marine species, such as plankton, shellfish, crustaceans, and finfish. It is found throughout coastal waters of the continental United States. Optimal temperatures for V. vulnificus are between 20°C to 35°C; it can grow at temperatures up to 41°C. It is slowly inactivated at temperatures <10°C (minimum growth temperature), and cultures should never be stored in refrigerators. V. vulnificus is halophilic; the highest abundance in oysters is at 23ppt. It is lysed almost immediately in freshwater; thus, it is not usually transmitted via the fecal-oral route. At least 0.5% NaCl is required in all media, and 2% NaCl is optimal. Like other vibrios, V. vulnificus is highly susceptible to low pH, freezing, and cooking. Most strains of V. vulnificus produce a capsule, but all strains can be killed by common disinfectants, such as bleach and alcohol
Vibrio vulnificus Mortality
Mortality: Death occurs in an average of 35% of septicemia cases (and 20% of woundinfection cases).
Vibrio vulnificus Infective dose:
Infective dose: The infective dose from ingestion of V. vulnificus is largely unknown, since human feeding studies involving this organism would be unethical. The FAO/WHO V. vulnificus Risk Assessment (VVRA) provides a dose response based on U.S. epidemiologic data and estimates that (1) a dose of 1,000 organisms can cause illness and (2) at a total dose of 1 million organisms, the risk of disease for susceptible people is 1:50,000
Vibrio vulnificus Onset
Onset: The range of time to onset of gastroenteritis symptoms may be approximately 12 hours to 21 days. (Onset of symptoms in cases of wound infection may be in as few as 4 hours.) The mean time to septicemia is 4 days.
Vibrio vulnificus Illness / complications:
Illness / complications: In healthy people, ingestion of this organism can cause gastroenteritis that generally remains localized and is self-limiting. Among susceptible people, the organism may cause primary septicemia (septic shock). Susceptible people include those with a predisposing condition; for example, those who are immunocompromised or have high serum iron levels (usually due to liver disease). More than 60% of those with septicemia develop secondary lesions on the extremities, similar to those found in wound infections. V. vulnificus also can cause wound infections directly, either through wounds incurred while handling fish, crustaceans, or shellfish, or when a pre-existing wound is exposed to marine or estuarine waters harboring the organism. Wound infections caused by V. vulnificus are characterized by inflammation at the wound site, which can progress to cellulitis, bullous lesions, and necrosis. The infection can become systemic, with affected people developing fever, chills, altered mental status, and hypotension. Secondary lesions from septicemia, as well as primary wound infections caused by direct contact, frequently require surgical debridement or amputation
Vibrio vulnificus Symptoms
Symptoms: Gastroenteritis caused by V. vulnificus is characterized by fever, diarrhea, abdominal cramps, nausea, and vomiting. Onset of septicemia is characterized by fever and chills, occasionally accompanied by vomiting, diarrhea, abdominal pain, and/or pain in the extremities.
Vibrio vulnificus Duration
Duration: In uncomplicated cases, gastroenteritis is self-limiting. The mean duration of septic illness is 1.6 days (i.e., the brief duration is reflective, in part, of the high mortality associated with septicemia).
Vibrio vulnificus Route of entry:
Route of entry: The gastroenteritis form of illness caused by V. vulnificus results from ingestion of the organism.
Vibrio vulnificus Pathway
Pathway: V. vulnificus harbors many putative virulence factors, including capsule, pili, hemolysins, metalloproteases, and enterotoxins. However, none of these factors has been shown unequivocally to be essential in causing disease; much remains unknown
Vibrio vulnificus Frequency
Sporadic illnesses have been attributed to this organism, but no foodborne outbreaks have been reported. The Centers for Disease Control and Prevention (CDC) estimates that 96 cases of foodborne illness from V. vulnificus occur annually in the U.S. Sporadic cases are more prevalent during the warmer months, when water temperatures are higher than 20°C (68°F).
