Saturday, September 30, 2006
Shigellosis
Shigellosis
What is shigellosis?
Shigellosis is an infectious disease caused by a group of bacteria called Shigella. Most who are infected with Shigella develop diarrhea, fever, and stomach cramps starting a day or two after they are exposed to the bacterium. The diarrhea is often bloody. Shigellosis usually resolves in 5 to 7 days. In some persons, especially young children and the elderly, the diarrhea can be so severe that the patient needs to be hospitalized. A severe infection with high fever may also be associated with seizures in children less than 2 years old. Some persons who are infected may have no symptoms at all, but may still pass the Shigella bacteria to others.
What sort of germ is Shigella?
The Shigella germ is actually a family of bacteria that can cause diarrhea in humans. They are microscopic living creatures that pass from person to person. Shigella were discovered over 100 years ago by a Japanese scientist named Shiga, for whom they are named. There are several different kinds of Shigella bacteria: Shigella sonnei, also known as "Group D" Shigella, accounts for over two-thirds of the shigellosis in the United States. A second type, Shigella flexneri, or "group B" Shigella, accounts for almost all of the rest. Other types of Shigella are rare in this country, though they continue to be important causes of disease in the developing world. One type found in the developing world, Shigella dysenteriae type 1, causes deadly epidemics there.
How can Shigella infections be diagnosed?
Many different kinds of diseases can cause diarrhea and bloody diarrhea, and the treatment depends on which germ is causing the diarrhea. Determining that Shigella is the cause of the illness depends on laboratory tests that identify Shigella in the stools of an infected person. These tests are sometimes not performed unless the laboratory is instructed specifically to look for the organism. The laboratory can also do special tests to tell which type of Shigella the person has and which antibiotics, if any, would be best to treat it.
How can Shigella infections be treated?
Shigellosis can usually be treated with antibiotics. The antibiotics commonly used for treatment are ampicillin, trimethoprim/sulfamethoxazole (also known as Bactrim* or Septra*), nalidixic acid, or ciprofloxacin. Appropriate treatment kills the Shigella bacteria that might be present in the patient's stools, and shortens the illness. Unfortunately, some Shigella bacteria have become resistant to antibiotics and using antibiotics to treat shigellosis can actually make the germs more resistant in the future. Persons with mild infections will usually recover quickly without antibiotic treatment. Therefore, when many persons in a community are affected by shigellosis, antibiotics are sometimes used selectively to treat only the more severe cases. Antidiarrheal agents such as loperamide (Imodium*) or diphenoxylate with atropine (Lomotil*) are likely to make the illness worse and should be avoided.
Are there long term consequences to a Shigella infection?
Persons with diarrhea usually recover completely, although it may be several months before their bowel habits are entirely normal. About 3% of persons who are infected with one type of Shigella, Shigella flexneri, will later develop pains in their joints, irritation of the eyes, and painful urination. This is called Reiter's syndrome. It can last for months or years, and can lead to chronic arthritis which is difficult to treat. Reiter's syndrome is caused by a reaction to Shigella infection that happens only in people who are genetically predisposed to it.
Once someone has had shigellosis, they are not likely to get infected with that specific type again for at least several years. However, they can still get infected with other types of Shigella.
How do people catch Shigella?
The Shigella bacteria pass from one infected person to the next. Shigella are present in the diarrheal stools of infected persons while they are sick and for a week or two afterwards. Most Shigella infections are the result of the bacterium passing from stools or soiled fingers of one person to the mouth of another person. This happens when basic hygiene and handwashing habits are inadequate. It is particularly likely to occur among toddlers who are not fully toilet-trained. Family members and playmates of such children are at high risk of becoming infected.
Shigella infections may be acquired from eating contaminated food. Contaminated food may look and smell normal. Food may become contaminated by infected food handlers who forget to wash their hands with soap after using the bathroom. Vegetables can become contaminated if they are harvested from a field with sewage in it. Flies can breed in infected feces and then contaminate food. Shigella infections can also be acquired by drinking or swimming in contaminated water. Water may become contaminated if sewage runs into it, or if someone with shigellosis swims in it.
What can a person do to prevent this illness?
There is no vaccine to prevent shigellosis. However, the spread of Shigella from an infected person to other persons can be stopped by frequent and careful handwashing with soap. Frequent and careful handwashing is important among all age groups. Frequent, supervised handwashing of all children should be followed in day care centers and in homes with children who are not completely toilet-trained (including children in diapers). When possible, young children with a Shigella infection who are still in diapers should not be in contact with uninfected children.
People who have shigellosis should not prepare food or pour water for others until they have been shown to no longer be carrying the Shigella bacterium.
If a child in diapers has shigellosis, everyone who changes the child's diapers should be sure the diapers are disposed of properly in a closed-lid garbage can, and should wash his or her hands carefully with soap and warm water immediately after changing the diapers. After use, the diaper changing area should be wiped down with a disinfectant such as household bleach, Lysol* or bactericidal wipes.
Basic food safety precautions and regular drinking water treatment prevents shigellosis. At swimming beaches, having enough bathrooms near the swimming area helps keep the water from becoming contaminated.
Simple precautions taken while traveling to the developing world can prevent getting shigellosis. Drink only treated or boiled water, and eat only cooked hot foods or fruits you peel yourself. The same precautions prevent traveler's diarrhea in general.
How common is shigellosis?
Every year, about 18,000 cases of shigellosis are reported in the United States. Because many milder cases are not diagnosed or reported, the actual number of infections may be twenty times greater. Shigellosis is particularly common and causes recurrent problems in settings where hygiene is poor and can sometimes sweep through entire communities. Shigellosis is more common in summer than winter. Children, especially toddlers aged 2 to 4, are the most likely to get shigellosis. Many cases are related to the spread of illness in child-care settings, and many more are the result of the spread of the illness in families with small children.
In the developing world, shigellosis is far more common and is present in most communities most of the time.
What else can be done to prevent shigellosis?
It is important for the public health department to know about cases of shigellosis. It is important for clinical laboratories to send isolates of Shigella to the City, County or State Public Health Laboratory so the specific type can be determined and compared to other Shigella. If many cases occur at the same time, it may mean that a restaurant, food or water supply has a problem which needs correction by the public health department. If a number of cases occur in a day-care center, the public health department may need to coordinate efforts to improve handwashing among the staff, children, and their families. When a community-wide outbreak occurs, a community-wide approach to promote handwashing and basic hygiene among children can stop the outbreak. Improvements in hygiene for vegetables and fruit picking and packing may prevent shigellosis caused by contaminated produce.
Some prevention steps occur everyday, without you thinking about it. Making municipal water supplies safe and treating sewage are highly effective prevention measures that have been in place for many years.
What is the government doing about shigellosis?
The Centers for Disease Control and Prevention (CDC) monitors the frequency of Shigella infections in the country, and assists local and State health departments to investigate outbreaks, determine means of transmission and devise control measures. CDC also conducts research to better understand how to identify and treat shigellosis. The Food and Drug Administration inspects imported foods, and promotes better food preparation techniques in restaurants and food processing plants. The Environmental Protection Agency regulates and monitors the safety of our drinking water supplies. The government has also maintained active research into the development of a Shigella vaccine.
How can I learn more about this and other public health problems?
You can discuss any medical concerns you may have with your doctor or other heath care provider. Your local city or county health department can provide more information about this and other public health problems that are occurring in your area. General information about the public health of the nation is published every week in the "Morbidity and Mortality Weekly Report", by the CDC in Atlanta, GA. Epidemiologists in your local and State Health Departments are tracking a number of important public health problems, investigating special problems that arise, and helping to prevent them form occurring in the first place, or from spreading if they do occur.
Some tips for preventing the spread of shigellosis:
wash hands with soap carefully and frequently, especially after going to the bathroom, after changing diapers, and before preparing foods or beverages
dispose of soiled diapers properly
disinfect diaper changing areas after using them
keep children with diarrhea out of child care settings
supervise handwashing of toddlers and small children after they use the toilet
persons with diarrheal illness should not prepare food for others
if you are traveling to the developing world, "boil it, cook it, peel it, or forget it"
avoid drinking pool water (See more information about this.)
Centers for Disease Control
What is shigellosis?
Shigellosis is an infectious disease caused by a group of bacteria called Shigella. Most who are infected with Shigella develop diarrhea, fever, and stomach cramps starting a day or two after they are exposed to the bacterium. The diarrhea is often bloody. Shigellosis usually resolves in 5 to 7 days. In some persons, especially young children and the elderly, the diarrhea can be so severe that the patient needs to be hospitalized. A severe infection with high fever may also be associated with seizures in children less than 2 years old. Some persons who are infected may have no symptoms at all, but may still pass the Shigella bacteria to others.
What sort of germ is Shigella?
The Shigella germ is actually a family of bacteria that can cause diarrhea in humans. They are microscopic living creatures that pass from person to person. Shigella were discovered over 100 years ago by a Japanese scientist named Shiga, for whom they are named. There are several different kinds of Shigella bacteria: Shigella sonnei, also known as "Group D" Shigella, accounts for over two-thirds of the shigellosis in the United States. A second type, Shigella flexneri, or "group B" Shigella, accounts for almost all of the rest. Other types of Shigella are rare in this country, though they continue to be important causes of disease in the developing world. One type found in the developing world, Shigella dysenteriae type 1, causes deadly epidemics there.
How can Shigella infections be diagnosed?
Many different kinds of diseases can cause diarrhea and bloody diarrhea, and the treatment depends on which germ is causing the diarrhea. Determining that Shigella is the cause of the illness depends on laboratory tests that identify Shigella in the stools of an infected person. These tests are sometimes not performed unless the laboratory is instructed specifically to look for the organism. The laboratory can also do special tests to tell which type of Shigella the person has and which antibiotics, if any, would be best to treat it.
How can Shigella infections be treated?
Shigellosis can usually be treated with antibiotics. The antibiotics commonly used for treatment are ampicillin, trimethoprim/sulfamethoxazole (also known as Bactrim* or Septra*), nalidixic acid, or ciprofloxacin. Appropriate treatment kills the Shigella bacteria that might be present in the patient's stools, and shortens the illness. Unfortunately, some Shigella bacteria have become resistant to antibiotics and using antibiotics to treat shigellosis can actually make the germs more resistant in the future. Persons with mild infections will usually recover quickly without antibiotic treatment. Therefore, when many persons in a community are affected by shigellosis, antibiotics are sometimes used selectively to treat only the more severe cases. Antidiarrheal agents such as loperamide (Imodium*) or diphenoxylate with atropine (Lomotil*) are likely to make the illness worse and should be avoided.
Are there long term consequences to a Shigella infection?
Persons with diarrhea usually recover completely, although it may be several months before their bowel habits are entirely normal. About 3% of persons who are infected with one type of Shigella, Shigella flexneri, will later develop pains in their joints, irritation of the eyes, and painful urination. This is called Reiter's syndrome. It can last for months or years, and can lead to chronic arthritis which is difficult to treat. Reiter's syndrome is caused by a reaction to Shigella infection that happens only in people who are genetically predisposed to it.
Once someone has had shigellosis, they are not likely to get infected with that specific type again for at least several years. However, they can still get infected with other types of Shigella.
How do people catch Shigella?
The Shigella bacteria pass from one infected person to the next. Shigella are present in the diarrheal stools of infected persons while they are sick and for a week or two afterwards. Most Shigella infections are the result of the bacterium passing from stools or soiled fingers of one person to the mouth of another person. This happens when basic hygiene and handwashing habits are inadequate. It is particularly likely to occur among toddlers who are not fully toilet-trained. Family members and playmates of such children are at high risk of becoming infected.
Shigella infections may be acquired from eating contaminated food. Contaminated food may look and smell normal. Food may become contaminated by infected food handlers who forget to wash their hands with soap after using the bathroom. Vegetables can become contaminated if they are harvested from a field with sewage in it. Flies can breed in infected feces and then contaminate food. Shigella infections can also be acquired by drinking or swimming in contaminated water. Water may become contaminated if sewage runs into it, or if someone with shigellosis swims in it.
What can a person do to prevent this illness?
There is no vaccine to prevent shigellosis. However, the spread of Shigella from an infected person to other persons can be stopped by frequent and careful handwashing with soap. Frequent and careful handwashing is important among all age groups. Frequent, supervised handwashing of all children should be followed in day care centers and in homes with children who are not completely toilet-trained (including children in diapers). When possible, young children with a Shigella infection who are still in diapers should not be in contact with uninfected children.
People who have shigellosis should not prepare food or pour water for others until they have been shown to no longer be carrying the Shigella bacterium.
If a child in diapers has shigellosis, everyone who changes the child's diapers should be sure the diapers are disposed of properly in a closed-lid garbage can, and should wash his or her hands carefully with soap and warm water immediately after changing the diapers. After use, the diaper changing area should be wiped down with a disinfectant such as household bleach, Lysol* or bactericidal wipes.
Basic food safety precautions and regular drinking water treatment prevents shigellosis. At swimming beaches, having enough bathrooms near the swimming area helps keep the water from becoming contaminated.
Simple precautions taken while traveling to the developing world can prevent getting shigellosis. Drink only treated or boiled water, and eat only cooked hot foods or fruits you peel yourself. The same precautions prevent traveler's diarrhea in general.
How common is shigellosis?
Every year, about 18,000 cases of shigellosis are reported in the United States. Because many milder cases are not diagnosed or reported, the actual number of infections may be twenty times greater. Shigellosis is particularly common and causes recurrent problems in settings where hygiene is poor and can sometimes sweep through entire communities. Shigellosis is more common in summer than winter. Children, especially toddlers aged 2 to 4, are the most likely to get shigellosis. Many cases are related to the spread of illness in child-care settings, and many more are the result of the spread of the illness in families with small children.
In the developing world, shigellosis is far more common and is present in most communities most of the time.
What else can be done to prevent shigellosis?
It is important for the public health department to know about cases of shigellosis. It is important for clinical laboratories to send isolates of Shigella to the City, County or State Public Health Laboratory so the specific type can be determined and compared to other Shigella. If many cases occur at the same time, it may mean that a restaurant, food or water supply has a problem which needs correction by the public health department. If a number of cases occur in a day-care center, the public health department may need to coordinate efforts to improve handwashing among the staff, children, and their families. When a community-wide outbreak occurs, a community-wide approach to promote handwashing and basic hygiene among children can stop the outbreak. Improvements in hygiene for vegetables and fruit picking and packing may prevent shigellosis caused by contaminated produce.
Some prevention steps occur everyday, without you thinking about it. Making municipal water supplies safe and treating sewage are highly effective prevention measures that have been in place for many years.
What is the government doing about shigellosis?
The Centers for Disease Control and Prevention (CDC) monitors the frequency of Shigella infections in the country, and assists local and State health departments to investigate outbreaks, determine means of transmission and devise control measures. CDC also conducts research to better understand how to identify and treat shigellosis. The Food and Drug Administration inspects imported foods, and promotes better food preparation techniques in restaurants and food processing plants. The Environmental Protection Agency regulates and monitors the safety of our drinking water supplies. The government has also maintained active research into the development of a Shigella vaccine.
How can I learn more about this and other public health problems?
You can discuss any medical concerns you may have with your doctor or other heath care provider. Your local city or county health department can provide more information about this and other public health problems that are occurring in your area. General information about the public health of the nation is published every week in the "Morbidity and Mortality Weekly Report", by the CDC in Atlanta, GA. Epidemiologists in your local and State Health Departments are tracking a number of important public health problems, investigating special problems that arise, and helping to prevent them form occurring in the first place, or from spreading if they do occur.
Some tips for preventing the spread of shigellosis:
wash hands with soap carefully and frequently, especially after going to the bathroom, after changing diapers, and before preparing foods or beverages
dispose of soiled diapers properly
disinfect diaper changing areas after using them
keep children with diarrhea out of child care settings
supervise handwashing of toddlers and small children after they use the toilet
persons with diarrheal illness should not prepare food for others
if you are traveling to the developing world, "boil it, cook it, peel it, or forget it"
avoid drinking pool water (See more information about this.)
Centers for Disease Control
# posted by Pat O'Connor @ 1:57 PM
Friday, September 22, 2006
Escherichia coli O157:H7
Escherichia coli O157:H7
Centers for Disease Control
Escherichia coli O157:H7 is an emerging cause of foodborne illness. An estimated 73,000 cases of infection and 61 deaths occur in the United States each year. Infection often leads to bloody diarrhea, and occasionally to kidney failure. Most illness has been associated with eating undercooked, contaminated ground beef. Person-to-person contact in families and child care centers is also an important mode of transmission. Infection can also occur after drinking raw milk and after swimming in or drinking sewage-contaminated water.
Consumers can prevent E. coli O157:H7 infection by thoroughly cooking ground beef, avoiding unpasteurized milk, and washing hands carefully.Because the organism lives in the intestines of healthy cattle, preventive measures on cattle farms and during meat processing are beinginvestigated.
What is Escherichia coli O157:H7?
E. coli O157:H7 is one of hundreds of strains of the bacterium Escherichia coli. Although most strains are harmless and live in the intestines of healthy humans and animals, this strain produces a powerful toxin and can cause severe illness.
E. coli O157:H7 was first recognized as a cause of illness in 1982 during an outbreak of severe bloody diarrhea; the outbreak was traced to contaminated hamburgers. Since then, most infections have come from eating undercooked ground beef. The combination of letters and numbers in the name of the bacterium refers to the specific markers found on its surface and distinguishes it from other types of E. coli.
How is E. coli O157:H7 spread?
The organism can be found on a small number of cattle farms and can live in the intestines of healthy cattle. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground. Bacteria present on the cow's udders or on equipment may get into raw milk.
Eating meat, especially ground beef, that has not been cooked sufficiently to kill E. coli O157:H7 can cause infection. Contaminated meat looks and smells normal. Although the number of organisms required to cause disease is not known, it is suspected to be very small. Among other known sources of infection are consumption of sprouts, lettuce, salami, unpasteurized milk and juice, and swimming in or drinking sewage-contaminated water.
Bacteria in diarrheal stools of infected persons can be passed from one person to another if hygiene or handwashing habits are inadequate.This is particularly likely among toddlers who are not toilet trained. Family members and playmates of these children are at high risk of becoming infected. Young children typically shed the organism in their feces for a week or two after their illness resolves. Older children rarely carry the organism without symptoms.
What illness does E. coli O157:H7 cause?
E. coli O157:H7 infection often causes severe bloody diarrhea and abdominal cramps; sometimes the infection causes nonbloody diarrhea or no symptoms. Usually little or no fever is present, and the illness resolves in 5 to 10 days. In some persons, particularly children under 5 years of age and the elderly, the infection can also cause a complication called hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail. About 2%-7% of infections lead to this complication. In the United States, hemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of hemolytic uremic syndrome are caused by E. coli O157:H7.
How is E. coli O157:H7 infection diagnosed?
Infection with E. coli O157:H7 is diagnosed by detecting the bacterium in the stool. Most laboratories that culture stool do not test for E. coli O157:H7, so it is important to request that the stool specimen be tested on sorbitol-MacConkey (SMAC) agar for this organism. All persons who suddenly have diarrhea with blood should get their stool tested for E. coli O157:H7.
How is the illness treated?
Most persons recover without antibiotics or other specific treatment in 5-10 days. There is no evidence that antibiotics improve the course of disease, and it is thought that treatment with some antibiotics may precipitate kidney complications. Antidiarrheal agents, such as loperamide (Imodium), should also be avoided. Hemolytic uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is 3%-5%.
What are the long-term consequences of infection?
Persons who only have diarrhea usually recover completely. About one-third of persons with hemolytic uremic syndrome have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with hemolytic uremic syndrome have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their bowel removed.
What can be done to prevent the infection?
E. coli O157:H7 will continue to be an important public health concern as long as it contaminates meat. Preventive measures may reduce the number of cattle that carry it and the contamination of meat during slaughter and grinding. Research into such prevention measures is just beginning.
What can you do to prevent E. coli O157:H7 infection?
Cook all ground beef and hamburger thoroughly. Because ground beef can turn brown before disease-causing bacteria are killed, use a digital instant-read meat thermometer to ensure thorough cooking. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160º F. Persons who cook ground beef without using a thermometer can decrease their risk of illness by not eating ground beef patties that are still pink in the middle.
If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking. You may want to ask for a new bun and a clean plate, too.
Avoid spreading harmful bacteria in your kitchen. Keep raw meat separate from ready-to-eat foods.
Wash hands, counters, and utensils with hot soapy water after they touch raw meat.
Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties. Wash meat thermometers in between tests of patties that require further cooking.
Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life that is sold at room temperature (e.g. juice in cardboard boxes, vacuum sealed juice in glass containers) has been pasteurized, although this is generally not indicated on the label. Juice concentrates are also heated sufficiently to kill pathogens.
Wash fruits and vegetables thoroughly, especially those that will not be cooked. Children under 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured. Methods to decontaminate alfalfa seeds and sprouts are being investigated.
Drink municipal water that has been treated with chlorine or other effective disinfectants.
Avoid swallowing lake or pool water while swimming.
See more information about this.
Make sure that persons with diarrhea, especially children, wash their hands carefully with soap after bowel movements to reduce the risk of spreading infection, and that persons wash hands after changing soiled diapers. Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.
For more information about reducing your risk of foodborne illness, visit the US Department of Agriculture’s Food Safety and Inspection Service website or the Partnership for Food Safety Education at: For more advice on cooking ground beef, visit the U.S. Department of Agriculture web site.
Date: October 6, 2005 Content source: Coordinating Center for Infectious Diseases / Division of Bacterial Diseases
----------
Update on Multi-State Outbreak of E. coli O157:H7 Infections From Fresh Spinach, September 21, 2006
As of 1 PM (ET) September 21, 2006, Thursday, 157 persons infected with the outbreak strain of E. coli O157:H7 have been reported to CDC from 23 states.
Among the ill persons, 83 (52%) were hospitalized, 27 (17%) developed a type of kidney failure called hemolytic-uremic syndrome (HUS), and an adult in Wisconsin died. One hundred thirteen (71%) were female and 11 (7%) were children under 5 years old. Among ill persons who provided the date when their illnesses began, 92% became ill between August 19 and September 5. The case with the earliest illness onset known to be associated with consumption of fresh spinach began having symptoms on August 19.
Idaho is currently investigating a suspect case in a 2-year-old child with HUS who died on September 20 and reportedly had recently consumed spinach. E. coli O157 has not been detected in the child.
The states that have reported cases are Arizona (4 cases), California (1), Colorado (1), Connecticut (3), Idaho (4), Illinois (1), Indiana (8), Kentucky (7), Maine (2), Michigan (4), Minnesota (2), Nebraska (8), New Mexico (5), Nevada (1), New York (11), Ohio (20), Oregon (5), Pennsylvania (7), Utah (17), Virginia (1), Washington (3), Wisconsin (41), and Wyoming (1).
CDC Advice for Consumers
The following is advice for consumers about this outbreak:
Currently, we are advising consumers to not eat any fresh spinach or salad blends containing fresh spinach that are consumed raw.
E. coli O157:H7 in spinach can be killed by cooking at 160° Fahrenheit for 15 seconds. (Water boils at 212° Fahrenheit.) If spinach is cooked in a frying pan, and all parts do not reach 160° Fahrenheit, all bacteria may not be killed. If consumers choose to cook the spinach, they should not allow the raw spinach to contaminate other foods and food contact surfaces, and they should wash hands, utensils, and surfaces with hot, soapy water before and after handling the spinach.
Persons who develop diarrhea after consuming fresh spinach or salad blends containing fresh spinach are urged to visit their health care provider and ask that their stool specimen be tested for E. coli O157.
Persons who ate fresh spinach or salad blends and feel well do not need to see a health care provider.
More Information
For more information about the outbreak, about the investigation, and for prevention guidance, see E. coli O157:H7 Outbreak from Fresh Spinach.
Centers for Disease Control
Escherichia coli O157:H7 is an emerging cause of foodborne illness. An estimated 73,000 cases of infection and 61 deaths occur in the United States each year. Infection often leads to bloody diarrhea, and occasionally to kidney failure. Most illness has been associated with eating undercooked, contaminated ground beef. Person-to-person contact in families and child care centers is also an important mode of transmission. Infection can also occur after drinking raw milk and after swimming in or drinking sewage-contaminated water.
Consumers can prevent E. coli O157:H7 infection by thoroughly cooking ground beef, avoiding unpasteurized milk, and washing hands carefully.Because the organism lives in the intestines of healthy cattle, preventive measures on cattle farms and during meat processing are beinginvestigated.
What is Escherichia coli O157:H7?
E. coli O157:H7 is one of hundreds of strains of the bacterium Escherichia coli. Although most strains are harmless and live in the intestines of healthy humans and animals, this strain produces a powerful toxin and can cause severe illness.
E. coli O157:H7 was first recognized as a cause of illness in 1982 during an outbreak of severe bloody diarrhea; the outbreak was traced to contaminated hamburgers. Since then, most infections have come from eating undercooked ground beef. The combination of letters and numbers in the name of the bacterium refers to the specific markers found on its surface and distinguishes it from other types of E. coli.
How is E. coli O157:H7 spread?
The organism can be found on a small number of cattle farms and can live in the intestines of healthy cattle. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground. Bacteria present on the cow's udders or on equipment may get into raw milk.
Eating meat, especially ground beef, that has not been cooked sufficiently to kill E. coli O157:H7 can cause infection. Contaminated meat looks and smells normal. Although the number of organisms required to cause disease is not known, it is suspected to be very small. Among other known sources of infection are consumption of sprouts, lettuce, salami, unpasteurized milk and juice, and swimming in or drinking sewage-contaminated water.
Bacteria in diarrheal stools of infected persons can be passed from one person to another if hygiene or handwashing habits are inadequate.This is particularly likely among toddlers who are not toilet trained. Family members and playmates of these children are at high risk of becoming infected. Young children typically shed the organism in their feces for a week or two after their illness resolves. Older children rarely carry the organism without symptoms.
What illness does E. coli O157:H7 cause?
E. coli O157:H7 infection often causes severe bloody diarrhea and abdominal cramps; sometimes the infection causes nonbloody diarrhea or no symptoms. Usually little or no fever is present, and the illness resolves in 5 to 10 days. In some persons, particularly children under 5 years of age and the elderly, the infection can also cause a complication called hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail. About 2%-7% of infections lead to this complication. In the United States, hemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of hemolytic uremic syndrome are caused by E. coli O157:H7.
How is E. coli O157:H7 infection diagnosed?
Infection with E. coli O157:H7 is diagnosed by detecting the bacterium in the stool. Most laboratories that culture stool do not test for E. coli O157:H7, so it is important to request that the stool specimen be tested on sorbitol-MacConkey (SMAC) agar for this organism. All persons who suddenly have diarrhea with blood should get their stool tested for E. coli O157:H7.
How is the illness treated?
Most persons recover without antibiotics or other specific treatment in 5-10 days. There is no evidence that antibiotics improve the course of disease, and it is thought that treatment with some antibiotics may precipitate kidney complications. Antidiarrheal agents, such as loperamide (Imodium), should also be avoided. Hemolytic uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is 3%-5%.
What are the long-term consequences of infection?
Persons who only have diarrhea usually recover completely. About one-third of persons with hemolytic uremic syndrome have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with hemolytic uremic syndrome have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their bowel removed.
What can be done to prevent the infection?
E. coli O157:H7 will continue to be an important public health concern as long as it contaminates meat. Preventive measures may reduce the number of cattle that carry it and the contamination of meat during slaughter and grinding. Research into such prevention measures is just beginning.
What can you do to prevent E. coli O157:H7 infection?
Cook all ground beef and hamburger thoroughly. Because ground beef can turn brown before disease-causing bacteria are killed, use a digital instant-read meat thermometer to ensure thorough cooking. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160º F. Persons who cook ground beef without using a thermometer can decrease their risk of illness by not eating ground beef patties that are still pink in the middle.
If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking. You may want to ask for a new bun and a clean plate, too.
Avoid spreading harmful bacteria in your kitchen. Keep raw meat separate from ready-to-eat foods.
Wash hands, counters, and utensils with hot soapy water after they touch raw meat.
Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties. Wash meat thermometers in between tests of patties that require further cooking.
Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life that is sold at room temperature (e.g. juice in cardboard boxes, vacuum sealed juice in glass containers) has been pasteurized, although this is generally not indicated on the label. Juice concentrates are also heated sufficiently to kill pathogens.
Wash fruits and vegetables thoroughly, especially those that will not be cooked. Children under 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured. Methods to decontaminate alfalfa seeds and sprouts are being investigated.
Drink municipal water that has been treated with chlorine or other effective disinfectants.
Avoid swallowing lake or pool water while swimming.
See more information about this.
Make sure that persons with diarrhea, especially children, wash their hands carefully with soap after bowel movements to reduce the risk of spreading infection, and that persons wash hands after changing soiled diapers. Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.
For more information about reducing your risk of foodborne illness, visit the US Department of Agriculture’s Food Safety and Inspection Service website or the Partnership for Food Safety Education at: For more advice on cooking ground beef, visit the U.S. Department of Agriculture web site.
Date: October 6, 2005 Content source: Coordinating Center for Infectious Diseases / Division of Bacterial Diseases
----------
Update on Multi-State Outbreak of E. coli O157:H7 Infections From Fresh Spinach, September 21, 2006
As of 1 PM (ET) September 21, 2006, Thursday, 157 persons infected with the outbreak strain of E. coli O157:H7 have been reported to CDC from 23 states.
Among the ill persons, 83 (52%) were hospitalized, 27 (17%) developed a type of kidney failure called hemolytic-uremic syndrome (HUS), and an adult in Wisconsin died. One hundred thirteen (71%) were female and 11 (7%) were children under 5 years old. Among ill persons who provided the date when their illnesses began, 92% became ill between August 19 and September 5. The case with the earliest illness onset known to be associated with consumption of fresh spinach began having symptoms on August 19.
Idaho is currently investigating a suspect case in a 2-year-old child with HUS who died on September 20 and reportedly had recently consumed spinach. E. coli O157 has not been detected in the child.
The states that have reported cases are Arizona (4 cases), California (1), Colorado (1), Connecticut (3), Idaho (4), Illinois (1), Indiana (8), Kentucky (7), Maine (2), Michigan (4), Minnesota (2), Nebraska (8), New Mexico (5), Nevada (1), New York (11), Ohio (20), Oregon (5), Pennsylvania (7), Utah (17), Virginia (1), Washington (3), Wisconsin (41), and Wyoming (1).
CDC Advice for Consumers
The following is advice for consumers about this outbreak:
Currently, we are advising consumers to not eat any fresh spinach or salad blends containing fresh spinach that are consumed raw.
E. coli O157:H7 in spinach can be killed by cooking at 160° Fahrenheit for 15 seconds. (Water boils at 212° Fahrenheit.) If spinach is cooked in a frying pan, and all parts do not reach 160° Fahrenheit, all bacteria may not be killed. If consumers choose to cook the spinach, they should not allow the raw spinach to contaminate other foods and food contact surfaces, and they should wash hands, utensils, and surfaces with hot, soapy water before and after handling the spinach.
Persons who develop diarrhea after consuming fresh spinach or salad blends containing fresh spinach are urged to visit their health care provider and ask that their stool specimen be tested for E. coli O157.
Persons who ate fresh spinach or salad blends and feel well do not need to see a health care provider.
More Information
For more information about the outbreak, about the investigation, and for prevention guidance, see E. coli O157:H7 Outbreak from Fresh Spinach.
# posted by Pat O'Connor @ 5:29 AM
Wednesday, September 20, 2006
The threat of CA-MRSA is no longer emerging; it's here
The threat of CA-MRSA is no longer emerging; it's here
Doctors may need to consider adding MRSA coverage to patients with skin and soft tissue infection who are candidates for empiric antibiotic therapy.
by Theodore C. Eickhoff, MD IDN Chief Medical Editor
September 2006
Two months ago, I discussed a presentation that I had given at the May meeting of the Southeastern Society for Emerging Biological Threats. In that presentation, I reviewed the threat posed by hospital-acquired staphylococcal infection during the late 1950s and early 1960s.
These epidemic penicillin-resistant staphylococci were mostly of bacteriophage type 52/52A/80/81, and for the most part seemed to disappear during the late 1960s and early 1970s. The reasons for the virtual disappearance of this epidemic threat were never clarified, whether it was due to infection control practices, the introduction of methicillin and its congeners, or simply a long-term secular trend. I also alluded to some limited evidence that the current CA- MRSA of the USA 300 type was genetically related to the epidemic 52/52A/80/81 staphylococci of 50 years ago.
There were a number of other presentations at that meeting that were devoted to the challenges posed by CA-MRSA. I will discuss only two of these: a presentation by Scott Weese, MD, of the Ontario Veterinary College, on CA-MRSA in animals, and one by Elizabeth Bancroft, MD, from the Acute Communicable Disease Control section of the Los Angeles County Department of Health Services.
Transmission of MRSA
In his presentation about CA-MRSA in animals, Dr. Weese outlined several concerns: the transmission of MRSA from infected animals to humans (and vice versa); whether colonized animals acted as reservoirs of MRSA in the community and whether these reservoirs were of human or animal origin; and the nature and extent of disease that occurred in animals. Each major animal species presented different issues: Among horses, the major issues were nasal or facial contact, fecal contamination and international movements, particularly among race horses; among household pets the significant issues were the degree, duration and intensity of contact; among pet birds the issues were fecal contact and aerosolization of fecal matter. Finally, there are issues in processing animals raised for human consumption as food.
In horses, MRSA appears to be endemic in certain horse populations worldwide. The organism seems to transmit regularly between horses and humans. The USA 500 strain appears to dominate globally. Infection control measures, entirely similar to those we employ in a human health care setting, can eradicate MRSA from horse farms.
Among household pets, there have been rapid increases in reported cases of MRSA infection in recent years. However, colonization has been generally uncommon in household pet populations. Where studied, colonization rates have varied from zero to 2% in dogs, and there was no colonization at all in cats. However, there have been sporadic episodes in veterinary clinics in which colonization rates have been as high as 9%. In general, pet isolates have been indistinguishable from common human clones.
It is clear that there is both intra- and inter-species transmission of MRSA in veterinary clinics. Does this occur in households as well? Is there a household cycle that can be broken? How common are such household "outbreaks"? Answers to these questions await further study. It is clear, however, that colonization of veterinary personnel with MRSA from infected animals does occur and appears to be a risk factor for infection of veterinary personnel.
Finally, important questions arise in considering the threat, if any, posed by therapy animals. For example, should therapy animals and their contacts be screened in some way before visitation? Have infection control protocols been established to deal with MRSA colonization or infection of therapy dogs? There seems to be no end of legitimate questions that could be asked about the implications in this area.
Pediatric MRSA Through the Los Angeles County Department of Health Services, Dr. Bancroft carried out an MRSA surveillance study of pediatric MRSA hospital admissions during a six-month period in 2003. There were 140 such admissions to Los Angeles hospitals during this period, 92% of which were skin and soft tissue infections.
Frequency was highest in those younger than 2 years, but cases occurred at all ages. Twenty-three percent of the cases were initially misdiagnosed as spider bites. Most of the strains (96%) were of the USA 300 type. Significant risk factors that emerged were: exposure within the previous month to someone who had been incarcerated; the presence of traditional risk factors for nosocomial MRSA; and household contact with a skin/soft tissue infection within the previous month. Participation in contact sports also seemed to be a risk factor.
Specific recommendations for outbreak control in athletic teams, correctional institutions, and day care or developmentally disabled settings were developed and are available at the following Web site: Infectious Disease News
Doctors may need to consider adding MRSA coverage to patients with skin and soft tissue infection who are candidates for empiric antibiotic therapy.
by Theodore C. Eickhoff, MD IDN Chief Medical Editor
September 2006
Two months ago, I discussed a presentation that I had given at the May meeting of the Southeastern Society for Emerging Biological Threats. In that presentation, I reviewed the threat posed by hospital-acquired staphylococcal infection during the late 1950s and early 1960s.
These epidemic penicillin-resistant staphylococci were mostly of bacteriophage type 52/52A/80/81, and for the most part seemed to disappear during the late 1960s and early 1970s. The reasons for the virtual disappearance of this epidemic threat were never clarified, whether it was due to infection control practices, the introduction of methicillin and its congeners, or simply a long-term secular trend. I also alluded to some limited evidence that the current CA- MRSA of the USA 300 type was genetically related to the epidemic 52/52A/80/81 staphylococci of 50 years ago.
There were a number of other presentations at that meeting that were devoted to the challenges posed by CA-MRSA. I will discuss only two of these: a presentation by Scott Weese, MD, of the Ontario Veterinary College, on CA-MRSA in animals, and one by Elizabeth Bancroft, MD, from the Acute Communicable Disease Control section of the Los Angeles County Department of Health Services.
Transmission of MRSA
In his presentation about CA-MRSA in animals, Dr. Weese outlined several concerns: the transmission of MRSA from infected animals to humans (and vice versa); whether colonized animals acted as reservoirs of MRSA in the community and whether these reservoirs were of human or animal origin; and the nature and extent of disease that occurred in animals. Each major animal species presented different issues: Among horses, the major issues were nasal or facial contact, fecal contamination and international movements, particularly among race horses; among household pets the significant issues were the degree, duration and intensity of contact; among pet birds the issues were fecal contact and aerosolization of fecal matter. Finally, there are issues in processing animals raised for human consumption as food.
In horses, MRSA appears to be endemic in certain horse populations worldwide. The organism seems to transmit regularly between horses and humans. The USA 500 strain appears to dominate globally. Infection control measures, entirely similar to those we employ in a human health care setting, can eradicate MRSA from horse farms.
Among household pets, there have been rapid increases in reported cases of MRSA infection in recent years. However, colonization has been generally uncommon in household pet populations. Where studied, colonization rates have varied from zero to 2% in dogs, and there was no colonization at all in cats. However, there have been sporadic episodes in veterinary clinics in which colonization rates have been as high as 9%. In general, pet isolates have been indistinguishable from common human clones.
It is clear that there is both intra- and inter-species transmission of MRSA in veterinary clinics. Does this occur in households as well? Is there a household cycle that can be broken? How common are such household "outbreaks"? Answers to these questions await further study. It is clear, however, that colonization of veterinary personnel with MRSA from infected animals does occur and appears to be a risk factor for infection of veterinary personnel.
Finally, important questions arise in considering the threat, if any, posed by therapy animals. For example, should therapy animals and their contacts be screened in some way before visitation? Have infection control protocols been established to deal with MRSA colonization or infection of therapy dogs? There seems to be no end of legitimate questions that could be asked about the implications in this area.
Pediatric MRSA Through the Los Angeles County Department of Health Services, Dr. Bancroft carried out an MRSA surveillance study of pediatric MRSA hospital admissions during a six-month period in 2003. There were 140 such admissions to Los Angeles hospitals during this period, 92% of which were skin and soft tissue infections.
Frequency was highest in those younger than 2 years, but cases occurred at all ages. Twenty-three percent of the cases were initially misdiagnosed as spider bites. Most of the strains (96%) were of the USA 300 type. Significant risk factors that emerged were: exposure within the previous month to someone who had been incarcerated; the presence of traditional risk factors for nosocomial MRSA; and household contact with a skin/soft tissue infection within the previous month. Participation in contact sports also seemed to be a risk factor.
Specific recommendations for outbreak control in athletic teams, correctional institutions, and day care or developmentally disabled settings were developed and are available at the following Web site: Infectious Disease News
# posted by Pat O'Connor @ 1:32 AM
Sunday, September 17, 2006
Human Plague --- Four States, 2006
Human Plague --- Four States, 2006
September 1, 2006 / 55(34);940-943
Plague is a zoonotic disease caused by the bacterium Yersinia pestis. In 2006, a total of 13 human plague cases have been reported among residents of four states: New Mexico (seven cases), Colorado (three cases), California (two cases), and Texas (one case). This is the largest number of cases reported in a single year in the United States since 1994. Dates of illness onset ranged from February 16 to August 14; two (15%) cases were fatal. The median age of patients was 43 years (range: 13--79 years); eight (62%) patients were female. Five (38%) patients had primary septicemic plague, and the remaining eight (62%) had bubonic plague. Two (15%) patients developed secondary plague pneumonia, leading to administration of antibiotic prophylaxis to their health-care providers. This report summarizes six of the 13 cases, highlighting the severity and diverse clinical presentations of plague and underscoring the need for prompt diagnosis and treatment when plague is suspected.
Case 1. On February 17, a man aged 39 years from Travis County, Texas, was hospitalized with a 1-day history of high fever, delirium, nausea, and vomiting. Although lymphadenopathy was not detected on the initial examination, a prominent axillary bubo was noted later. Blood cultures yielded Y. pestis. The patient recovered after treatment with multiple antibiotics, including gentamicin, doxycycline, ciprofloxacin, and levofloxacin. Before his illness, the patient had hunted rabbits in Lea County, New Mexico, and skinned the rabbit carcasses. Cultures from one of the carcasses yielded Y. pestis that was indistinguishable from the clinical isolates when subtyped by pulsed-field gel electrophoresis (PFGE).
Case 2. On April 17, a woman aged 28 years received the first diagnosis of plague in Los Angeles County, California, since 1984. The woman was hospitalized with fever, septic shock, and a painful right axillary swelling; blood cultures grew Y. pestis. She responded to treatment with gentamicin and levofloxacin. Although symptoms were compatible with bubonic plague, the diagnosis had not been suspected because the patient did not report traveling outside her urban Los Angeles neighborhood. Later, health-care providers learned that the patient had handled raw meat from a rabbit that had been killed in Kern County, California, and transported to her home. An environmental investigation in Kern County revealed evidence of die-off among jackrabbits and cottontails; rabbit carcasses collected in the area yielded Y. pestis. PFGE patterns of isolates from the patient and rabbits were indistinguishable. A total of 16 medical contacts and family members and friends who had visited the patient's residence received antibiotic prophylaxis.
Case 3. On May 17, a woman aged 54 years from Bernalillo County, New Mexico, went to a local urgent care center with a 4-day history of fever, severe abdominal pain, and bloody stools. No lymphadenopathy was noted. While being evaluated, the patient began vomiting blood and experienced acute respiratory distress. She was transferred to a regional hospital but died within a few hours of arrival. Blood and lung cultures obtained at autopsy yielded Y. pestis; however, no histologic evidence of plague pneumonia was discovered. One of the patient's dogs and a rock squirrel (Spermophilus variegatus) that had been trapped by investigators on her property had serologic evidence of past infection with Y. pestis.
Case 4. On May 25, a man aged 45 years from Santa Fe County, New Mexico, went to a hospital emergency department with a 3-day history of nausea, vomiting, and fever to 104ºF (40ºC). Initial chest radiographs revealed right lower lobe infiltrates; he was admitted with a diagnosis of pneumonia. The patient was treated with gentamicin but was not placed in respiratory isolation. On hospital day 1, the patient required intubation for respiratory distress. On hospital day 2, blood cultures drawn at admission yielded Y. pestis. The patient remained on mechanical ventilation for 4 weeks and eventually recovered. At least 37 hospital workers who had contact with the patient before he was intubated received postexposure prophylaxis with doxycycline. Both of the patient's dogs had serologic evidence of past Y. pestis infection. Y. pestis was isolated from fleas (Anomiopsyllus nudatus) combed from a woodrat (Neotoma micropus) that was trapped by investigators on the patient's property.
Case 5. On July 9, a man aged 30 years from La Plata County, Colorado, went to a hospital emergency department with a 3-day history of fever, nausea, vomiting, and right inguinal lymphadenopathy. He was discharged home without treatment. Three days later, the man returned and was hospitalized with sepsis and bilateral pulmonary infiltrates. Plague was considered immediately, and the patient was placed in respiratory isolation. He was treated with gentamicin and recovered. Five hospital workers were administered doxycycline prophylaxis because of exposures before respiratory isolation had been initiated. Cultures of blood and a lymph node aspirate grew Y. pestis. One of the patient's dogs had serologic evidence of past Y. pestis infection. Y. pestis was recovered from fleas of two species (Aetheca wagneri and Pulex simulans) collected near the patient's home. A plague epizootic had been noted in the area, and four other human plague cases have been reported from La Plata County since July 2005.
Case 6. On July 18, a woman aged 43 years from Torrance County, New Mexico, went to a local clinic with a 1-day history of vomiting, diarrhea, abdominal pain, and fever. The patient reported a recent dog bite and was treated for presumed cellulitis. The next day, the woman returned to the clinic because of worsening symptoms and pain in the left side of her groin. She was transported by ambulance to the emergency department, where inguinal lymphadenopathy was noted and plague was suspected. She was admitted to the hospital, placed in the intensive care unit, and administered gentamicin and doxycycline. Y. pestis was isolated from blood cultures. Despite treatment, she died on July 22. Animals trapped on the patient's property, including four mice (Peromyscus spp.) and five rock squirrels, did not have laboratory evidence of infection with Y. pestis.
Reported by: L Bertram-Sosa, C Jaso, A Valadez, MD, Austin/Travis County Health and Human Svcs Dept; B Nix, DVM, R Jones, MPH, T Sidwa, DVM, J Walker, MD, Texas Dept of State Health Svcs. A Anglim, MD, Univ of Southern California; R Reporter, MD, L Mascola, MD, G Van Gordon, MS, J Ramirez, Los Angeles County Dept of Health Svcs; C Fritz, DVM, R Davis, ScD, California Dept of Health Svcs. J Ross, MD, K Chongsiriwatana, MD, Infectious Diseases and Internal Medicine Associates of New Mexico; M DiMenna, PhD, J Sheyka, MS, City of Albuquerque Environmental Health Dept; P Ettestad, DVM, C Smelser, MD, N Powers, PhD, P Reynolds, New Mexico Dept of Health. J Fowler, San Juan Basin Health Dept, Durango; J Pape, D Tanda, Colorado Dept of Public Health and Environment. P Mead, MD, K Griffith, MD, KL Gage, PhD, J Montenieri, G Dietrich, MS, K Kubota, MPH, J Young, Div of Vector-Borne Infectious Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed); LH Gould, PhD, EIS Officer, CDC.
Editorial Note:
The natural reservoir of plague is wild rodents. Human infection usually is acquired through the bites of infected rodent fleas and has an incubation period of 1--6 days (1). Plague also can be contracted from handling infected animals, especially rodents, lagomorphs (e.g., rabbits or hares), and domestic cats, or through close contact with patients with pneumonic plague. However, person-to-person transmission is extremely rare; the last such transmission in the United States was reported in 1925. During 1990--2005, a total of 107 cases of plague were reported in the United States (CDC, unpublished data, 2006), a median of seven cases per year. The increased plague activity in 2006 is consistent with the predicted relationship between climate and the frequency of human plague in the southwestern United States. Two consecutive February-March periods with high precipitation and an intervening cool summer predicts increased cases of plague the next summer; this effect is thought to lead to increased reproduction and survival rates among rodents and fleas (2).
The principal forms of plague are bubonic, septicemic, and pneumonic (3). All of these forms can be accompanied by fever and systemic manifestations of gram-negative sepsis. Bubonic plague is distinguished by the presence of a bubo (i.e., one or more enlarged, tender, regional lymph nodes). Patients with septicemic plague often have prominent gastrointestinal symptoms, including nausea, vomiting, diarrhea, and abdominal pain (4), and patients with pneumonic plague have dyspnea, chest pain, and a cough that can produce bloody sputum. During 1990--2005, a total of 81 (76%) of 107 plague cases in the United States were classified as primary bubonic plague, 19 (18%) as primary septicemic plague, and five (5%) as primary pneumonic plague; two (2%) were not classified (CDC, unpublished data, 2006). Eleven (10%) cases were fatal. In 2006, five (38%) of the 13 patients had primary septicemic plague, underscoring the need for clinicians to consider this diagnosis in patients who do not have an obvious bubo. Septicemic and pneumonic plague progress rapidly and are usually fatal without prompt treatment; bubonic plague has a mortality rate of 50%--60% if untreated.
In the United States, nearly all fatal plague cases are associated with delays in diagnosis and treatment. In its early stages, plague is treatable with appropriate antibiotics. Health-care providers should consider a diagnosis of plague in persons who 1) have unexplained fever, suspected sepsis, or pneumonia with or without lymphadenopathy or a classic bubo, and 2) live in or have traveled to a plague-endemic region (e.g., the western United States) (3). When plague is suspected, appropriate antibiotic treatment should be initiated immediately and not delayed for laboratory confirmation. Drugs effective against plague include streptomycin and the tetracyclines. Although not approved by the Food and Drug Administration (FDA) for treatment of plague, gentamicin is more readily available than streptomycin and has been used successfully (5). Fluoroquinolones are used empirically to treat critically ill patients and have demonstrated activity against Y. pestis but are not FDA approved for this indication (6).
The majority of exposures to plague occur in the peridomestic environment (3); free-roaming pets that bring infected rodent fleas into the home have been suspected as a potential source of human infections. Persons residing in areas where plague is endemic should keep their dogs and cats free of fleas through regular use of flea treatments and by keeping them indoors. Year-round rodent control should be conducted, including rodent proofing of structures and eliminating food sources (e.g., pet food or garbage) and harborage (e.g., piles of wood or debris) in the peridomestic environment. Persons who participate in outdoor recreational activities, particularly rabbit hunting (7), in areas of epizootic plague activity also are at risk for plague. Personal protective measures include using insect repellents, wearing protective clothing, and avoiding sick or dead animals. In areas of epizootic plague activity, public health officials should treat rodent habitats with insecticides and should educate the public regarding plague prevention and control. Health- care providers and veterinarians should be educated regarding the manifestations and diagnosis of plague. Antibiotic prophylaxis might be indicated for close contacts (who come within 2 m) of patients with plague pneumonia (5). Appropriate respiratory droplet precautions should be taken when treating patients with suspected plague who have evidence of respiratory involvement (8).
Acknowledgments
This report is based, in part, on contributions by D Gardner, MD, R Irvine, MD, S Lathrop, DVM, Univ of New Mexico Health Sciences Center, Office of the Medical Investigator. R Eisen, PhD, R Vera-Tudela, X Liang, A Janusz, Div of Vector-Borne Infectious Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed), CDC.
References
CDC. Prevention of plague: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(No. RR-14).
Enscore RE, Biggerstaff BJ, Brown TL, et al. Modeling relationships between climate and the frequency of human plague cases in the southwestern United States, 1960--1997. Am J Trop Med Hyg 2002;66:186--96.
Dennis DT, Campbell GL. Plague and other Yersinia infections. In: Kasper DL, Braunwald E, Fauci AS, et al, eds. Harrison's principles of internal medicine. 16th edition. New York, NY: McGraw-Hill; 2004.
Hull HF, Montes JM, Mann JM. Plague masquerading as gastrointestinal illness. West J Med 1986;145:485--7.
Dennis DT. Plague, method of. In: Rakel RE, ed. Conn's current therapy. Philadelphia, PA: WB Saunders Co.; 2001:115--7.
Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and public health management. Working Group on Civilian Biodefense. JAMA 2000;283:2281--90.
von Reyn CF, Barnes AM, Weber NS, Hodgin UG. Bubonic plague from exposure to a rabbit: a documented case, and a review of rabbit-associated plague cases in the United States. Am J Epidemiol 1976; 104:81--7.
CDC, Association for Professionals in Infection Control and Epidemiology. Bioterrorism readiness plan: a template for healthcare facilities. Atlanta, GA: CDC, Association for Professionals in Infection Control and Epidemiology; 1999:19--20.
CDC
September 1, 2006 / 55(34);940-943
Plague is a zoonotic disease caused by the bacterium Yersinia pestis. In 2006, a total of 13 human plague cases have been reported among residents of four states: New Mexico (seven cases), Colorado (three cases), California (two cases), and Texas (one case). This is the largest number of cases reported in a single year in the United States since 1994. Dates of illness onset ranged from February 16 to August 14; two (15%) cases were fatal. The median age of patients was 43 years (range: 13--79 years); eight (62%) patients were female. Five (38%) patients had primary septicemic plague, and the remaining eight (62%) had bubonic plague. Two (15%) patients developed secondary plague pneumonia, leading to administration of antibiotic prophylaxis to their health-care providers. This report summarizes six of the 13 cases, highlighting the severity and diverse clinical presentations of plague and underscoring the need for prompt diagnosis and treatment when plague is suspected.
Case 1. On February 17, a man aged 39 years from Travis County, Texas, was hospitalized with a 1-day history of high fever, delirium, nausea, and vomiting. Although lymphadenopathy was not detected on the initial examination, a prominent axillary bubo was noted later. Blood cultures yielded Y. pestis. The patient recovered after treatment with multiple antibiotics, including gentamicin, doxycycline, ciprofloxacin, and levofloxacin. Before his illness, the patient had hunted rabbits in Lea County, New Mexico, and skinned the rabbit carcasses. Cultures from one of the carcasses yielded Y. pestis that was indistinguishable from the clinical isolates when subtyped by pulsed-field gel electrophoresis (PFGE).
Case 2. On April 17, a woman aged 28 years received the first diagnosis of plague in Los Angeles County, California, since 1984. The woman was hospitalized with fever, septic shock, and a painful right axillary swelling; blood cultures grew Y. pestis. She responded to treatment with gentamicin and levofloxacin. Although symptoms were compatible with bubonic plague, the diagnosis had not been suspected because the patient did not report traveling outside her urban Los Angeles neighborhood. Later, health-care providers learned that the patient had handled raw meat from a rabbit that had been killed in Kern County, California, and transported to her home. An environmental investigation in Kern County revealed evidence of die-off among jackrabbits and cottontails; rabbit carcasses collected in the area yielded Y. pestis. PFGE patterns of isolates from the patient and rabbits were indistinguishable. A total of 16 medical contacts and family members and friends who had visited the patient's residence received antibiotic prophylaxis.
Case 3. On May 17, a woman aged 54 years from Bernalillo County, New Mexico, went to a local urgent care center with a 4-day history of fever, severe abdominal pain, and bloody stools. No lymphadenopathy was noted. While being evaluated, the patient began vomiting blood and experienced acute respiratory distress. She was transferred to a regional hospital but died within a few hours of arrival. Blood and lung cultures obtained at autopsy yielded Y. pestis; however, no histologic evidence of plague pneumonia was discovered. One of the patient's dogs and a rock squirrel (Spermophilus variegatus) that had been trapped by investigators on her property had serologic evidence of past infection with Y. pestis.
Case 4. On May 25, a man aged 45 years from Santa Fe County, New Mexico, went to a hospital emergency department with a 3-day history of nausea, vomiting, and fever to 104ºF (40ºC). Initial chest radiographs revealed right lower lobe infiltrates; he was admitted with a diagnosis of pneumonia. The patient was treated with gentamicin but was not placed in respiratory isolation. On hospital day 1, the patient required intubation for respiratory distress. On hospital day 2, blood cultures drawn at admission yielded Y. pestis. The patient remained on mechanical ventilation for 4 weeks and eventually recovered. At least 37 hospital workers who had contact with the patient before he was intubated received postexposure prophylaxis with doxycycline. Both of the patient's dogs had serologic evidence of past Y. pestis infection. Y. pestis was isolated from fleas (Anomiopsyllus nudatus) combed from a woodrat (Neotoma micropus) that was trapped by investigators on the patient's property.
Case 5. On July 9, a man aged 30 years from La Plata County, Colorado, went to a hospital emergency department with a 3-day history of fever, nausea, vomiting, and right inguinal lymphadenopathy. He was discharged home without treatment. Three days later, the man returned and was hospitalized with sepsis and bilateral pulmonary infiltrates. Plague was considered immediately, and the patient was placed in respiratory isolation. He was treated with gentamicin and recovered. Five hospital workers were administered doxycycline prophylaxis because of exposures before respiratory isolation had been initiated. Cultures of blood and a lymph node aspirate grew Y. pestis. One of the patient's dogs had serologic evidence of past Y. pestis infection. Y. pestis was recovered from fleas of two species (Aetheca wagneri and Pulex simulans) collected near the patient's home. A plague epizootic had been noted in the area, and four other human plague cases have been reported from La Plata County since July 2005.
Case 6. On July 18, a woman aged 43 years from Torrance County, New Mexico, went to a local clinic with a 1-day history of vomiting, diarrhea, abdominal pain, and fever. The patient reported a recent dog bite and was treated for presumed cellulitis. The next day, the woman returned to the clinic because of worsening symptoms and pain in the left side of her groin. She was transported by ambulance to the emergency department, where inguinal lymphadenopathy was noted and plague was suspected. She was admitted to the hospital, placed in the intensive care unit, and administered gentamicin and doxycycline. Y. pestis was isolated from blood cultures. Despite treatment, she died on July 22. Animals trapped on the patient's property, including four mice (Peromyscus spp.) and five rock squirrels, did not have laboratory evidence of infection with Y. pestis.
Reported by: L Bertram-Sosa, C Jaso, A Valadez, MD, Austin/Travis County Health and Human Svcs Dept; B Nix, DVM, R Jones, MPH, T Sidwa, DVM, J Walker, MD, Texas Dept of State Health Svcs. A Anglim, MD, Univ of Southern California; R Reporter, MD, L Mascola, MD, G Van Gordon, MS, J Ramirez, Los Angeles County Dept of Health Svcs; C Fritz, DVM, R Davis, ScD, California Dept of Health Svcs. J Ross, MD, K Chongsiriwatana, MD, Infectious Diseases and Internal Medicine Associates of New Mexico; M DiMenna, PhD, J Sheyka, MS, City of Albuquerque Environmental Health Dept; P Ettestad, DVM, C Smelser, MD, N Powers, PhD, P Reynolds, New Mexico Dept of Health. J Fowler, San Juan Basin Health Dept, Durango; J Pape, D Tanda, Colorado Dept of Public Health and Environment. P Mead, MD, K Griffith, MD, KL Gage, PhD, J Montenieri, G Dietrich, MS, K Kubota, MPH, J Young, Div of Vector-Borne Infectious Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed); LH Gould, PhD, EIS Officer, CDC.
Editorial Note:
The natural reservoir of plague is wild rodents. Human infection usually is acquired through the bites of infected rodent fleas and has an incubation period of 1--6 days (1). Plague also can be contracted from handling infected animals, especially rodents, lagomorphs (e.g., rabbits or hares), and domestic cats, or through close contact with patients with pneumonic plague. However, person-to-person transmission is extremely rare; the last such transmission in the United States was reported in 1925. During 1990--2005, a total of 107 cases of plague were reported in the United States (CDC, unpublished data, 2006), a median of seven cases per year. The increased plague activity in 2006 is consistent with the predicted relationship between climate and the frequency of human plague in the southwestern United States. Two consecutive February-March periods with high precipitation and an intervening cool summer predicts increased cases of plague the next summer; this effect is thought to lead to increased reproduction and survival rates among rodents and fleas (2).
The principal forms of plague are bubonic, septicemic, and pneumonic (3). All of these forms can be accompanied by fever and systemic manifestations of gram-negative sepsis. Bubonic plague is distinguished by the presence of a bubo (i.e., one or more enlarged, tender, regional lymph nodes). Patients with septicemic plague often have prominent gastrointestinal symptoms, including nausea, vomiting, diarrhea, and abdominal pain (4), and patients with pneumonic plague have dyspnea, chest pain, and a cough that can produce bloody sputum. During 1990--2005, a total of 81 (76%) of 107 plague cases in the United States were classified as primary bubonic plague, 19 (18%) as primary septicemic plague, and five (5%) as primary pneumonic plague; two (2%) were not classified (CDC, unpublished data, 2006). Eleven (10%) cases were fatal. In 2006, five (38%) of the 13 patients had primary septicemic plague, underscoring the need for clinicians to consider this diagnosis in patients who do not have an obvious bubo. Septicemic and pneumonic plague progress rapidly and are usually fatal without prompt treatment; bubonic plague has a mortality rate of 50%--60% if untreated.
In the United States, nearly all fatal plague cases are associated with delays in diagnosis and treatment. In its early stages, plague is treatable with appropriate antibiotics. Health-care providers should consider a diagnosis of plague in persons who 1) have unexplained fever, suspected sepsis, or pneumonia with or without lymphadenopathy or a classic bubo, and 2) live in or have traveled to a plague-endemic region (e.g., the western United States) (3). When plague is suspected, appropriate antibiotic treatment should be initiated immediately and not delayed for laboratory confirmation. Drugs effective against plague include streptomycin and the tetracyclines. Although not approved by the Food and Drug Administration (FDA) for treatment of plague, gentamicin is more readily available than streptomycin and has been used successfully (5). Fluoroquinolones are used empirically to treat critically ill patients and have demonstrated activity against Y. pestis but are not FDA approved for this indication (6).
The majority of exposures to plague occur in the peridomestic environment (3); free-roaming pets that bring infected rodent fleas into the home have been suspected as a potential source of human infections. Persons residing in areas where plague is endemic should keep their dogs and cats free of fleas through regular use of flea treatments and by keeping them indoors. Year-round rodent control should be conducted, including rodent proofing of structures and eliminating food sources (e.g., pet food or garbage) and harborage (e.g., piles of wood or debris) in the peridomestic environment. Persons who participate in outdoor recreational activities, particularly rabbit hunting (7), in areas of epizootic plague activity also are at risk for plague. Personal protective measures include using insect repellents, wearing protective clothing, and avoiding sick or dead animals. In areas of epizootic plague activity, public health officials should treat rodent habitats with insecticides and should educate the public regarding plague prevention and control. Health- care providers and veterinarians should be educated regarding the manifestations and diagnosis of plague. Antibiotic prophylaxis might be indicated for close contacts (who come within 2 m) of patients with plague pneumonia (5). Appropriate respiratory droplet precautions should be taken when treating patients with suspected plague who have evidence of respiratory involvement (8).
Acknowledgments
This report is based, in part, on contributions by D Gardner, MD, R Irvine, MD, S Lathrop, DVM, Univ of New Mexico Health Sciences Center, Office of the Medical Investigator. R Eisen, PhD, R Vera-Tudela, X Liang, A Janusz, Div of Vector-Borne Infectious Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed), CDC.
References
CDC. Prevention of plague: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(No. RR-14).
Enscore RE, Biggerstaff BJ, Brown TL, et al. Modeling relationships between climate and the frequency of human plague cases in the southwestern United States, 1960--1997. Am J Trop Med Hyg 2002;66:186--96.
Dennis DT, Campbell GL. Plague and other Yersinia infections. In: Kasper DL, Braunwald E, Fauci AS, et al, eds. Harrison's principles of internal medicine. 16th edition. New York, NY: McGraw-Hill; 2004.
Hull HF, Montes JM, Mann JM. Plague masquerading as gastrointestinal illness. West J Med 1986;145:485--7.
Dennis DT. Plague, method of. In: Rakel RE, ed. Conn's current therapy. Philadelphia, PA: WB Saunders Co.; 2001:115--7.
Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and public health management. Working Group on Civilian Biodefense. JAMA 2000;283:2281--90.
von Reyn CF, Barnes AM, Weber NS, Hodgin UG. Bubonic plague from exposure to a rabbit: a documented case, and a review of rabbit-associated plague cases in the United States. Am J Epidemiol 1976; 104:81--7.
CDC, Association for Professionals in Infection Control and Epidemiology. Bioterrorism readiness plan: a template for healthcare facilities. Atlanta, GA: CDC, Association for Professionals in Infection Control and Epidemiology; 1999:19--20.
CDC
# posted by Pat O'Connor @ 5:27 AM
Friday, September 08, 2006
Severe pseudomonal infections.
Severe pseudomonal infections.
Oct. 2006
Mutlu GM,
Wunderink RG.
Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
PURPOSE OF REVIEW: To review the most recent data on severe Pseudomonas aeruginosa infections. The focus will be on clinical studies with an emphasis on the critically ill.
RECENT FINDINGS: The frequency of P. aeruginosa as the etiologic agent of infections associated with high morbidity and mortality in hospitalized patients continues to increase. Unfortunately, pan-resistant isolates are now emerging as a significant clinical problem. Highly or pan-resistant isolates are associated with more frequent inappropriate initial therapy and increased mortality. Prevention relies on limitation of antibiotic pressure. Unfortunately, antibiotic class rotation has not resulted in persistent decreases in resistant isolates and the increased use of treatment protocols may actually increase selection.
SUMMARY: Because of the frequency of antibiotic resistance in clinical isolates of P. aeruginosa and the high associated mortality, combination, broad-spectrum antibiotic therapy should be used for empiric coverage of suspected P. aeruginosa infections. Accurate diagnostic testing can help to discontinue unnecessary antibiotics and decrease the overall selective pressure. Increasing resistance without new antibiotic classes on the horizon suggests the need for better use of available antibiotics and an emphasis on innovative treatment strategies in the future.
PMID: 16943726 [PubMed - in process]
------------
Update on Pseudomonas aeruginosa and Acinetobacter baumannii infections in the healthcare setting.
Navon-Venezia S,
Ben-Ami R,
Carmeli Y.
Divisions of Epidemiology and Infectious Diseases, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
PURPOSE OF REVIEW: Infections with Pseudomonas aeruginosa and Acinetobacter baumannii are of great concern for hospitalized patients, especially with multidrug-resistant strains. This review focuses on recent data that may help us to understand the emergence, spread, and persistence of antibiotic resistance, and summarizes the optional treatment feasible for these resistant bacteria.
RECENT FINDINGS: Multidrug-resistant P. aeruginosa and A. baumannii are increasingly causing nosocomial infections; multidrug-resistant clones are spreading into new geographic areas, and susceptible strains are acquiring resistance genes. New extended-spectrum beta-lactamases and carbapenemases are emerging, leading to pan-resistant strains. Current studies focus on the effect of antibiotics on gene expression in P. aeruginosa biofilms and their contribution to resistance to therapy. Treatment options for multidrug-resistant P. aeruginosa and A. baumannii infections are limited in most cases to carbapenems. Sulbactam is a treatment option for pan-resistant A. baumannii, and or renewed use of an old drug, colistin, is being entertained for pan-resistant A. baumannii and P. aeruginosa. Immunotherapy is a promising new modality being explored. Prevention of emergence of resistance through combination therapy and pharmacokinetic strategies are studied.
SUMMARY: The emergence and spread of multidrug-resistant P. aeruginosa and A. baumannii and their genetic potential to carry and transfer diverse antibiotic resistance determinants pose a major threat in hospitals. The complex interplay of clonal spread, persistence, transfer of resistance elements, and cell-cell interaction contribute to the difficulty in treating infections caused by these multidrug-resistant strains. In the absence of new antibiotic agents, new modalities of treatment should be developed.
PMID: 15985826 [PubMed - indexed for MEDLINE]
-----------
Related Abstracts:
-----------
The emergence of multidrug resistant Acinetobacter species: a major concern in the hospital setting.
Bloodstream infections caused by antibiotic-resistant gram-negative bacilli: risk factors for mortality and impact of inappropriate initial antimicrobial therapy on outcome.
Treatment and control of severe infections caused by multiresistant Pseudomonas aeruginosa.
Pseudomonas aeruginosa pneumonia.
Oct. 2006
Mutlu GM,
Wunderink RG.
Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
PURPOSE OF REVIEW: To review the most recent data on severe Pseudomonas aeruginosa infections. The focus will be on clinical studies with an emphasis on the critically ill.
RECENT FINDINGS: The frequency of P. aeruginosa as the etiologic agent of infections associated with high morbidity and mortality in hospitalized patients continues to increase. Unfortunately, pan-resistant isolates are now emerging as a significant clinical problem. Highly or pan-resistant isolates are associated with more frequent inappropriate initial therapy and increased mortality. Prevention relies on limitation of antibiotic pressure. Unfortunately, antibiotic class rotation has not resulted in persistent decreases in resistant isolates and the increased use of treatment protocols may actually increase selection.
SUMMARY: Because of the frequency of antibiotic resistance in clinical isolates of P. aeruginosa and the high associated mortality, combination, broad-spectrum antibiotic therapy should be used for empiric coverage of suspected P. aeruginosa infections. Accurate diagnostic testing can help to discontinue unnecessary antibiotics and decrease the overall selective pressure. Increasing resistance without new antibiotic classes on the horizon suggests the need for better use of available antibiotics and an emphasis on innovative treatment strategies in the future.
PMID: 16943726 [PubMed - in process]
------------
Update on Pseudomonas aeruginosa and Acinetobacter baumannii infections in the healthcare setting.
Navon-Venezia S,
Ben-Ami R,
Carmeli Y.
Divisions of Epidemiology and Infectious Diseases, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
PURPOSE OF REVIEW: Infections with Pseudomonas aeruginosa and Acinetobacter baumannii are of great concern for hospitalized patients, especially with multidrug-resistant strains. This review focuses on recent data that may help us to understand the emergence, spread, and persistence of antibiotic resistance, and summarizes the optional treatment feasible for these resistant bacteria.
RECENT FINDINGS: Multidrug-resistant P. aeruginosa and A. baumannii are increasingly causing nosocomial infections; multidrug-resistant clones are spreading into new geographic areas, and susceptible strains are acquiring resistance genes. New extended-spectrum beta-lactamases and carbapenemases are emerging, leading to pan-resistant strains. Current studies focus on the effect of antibiotics on gene expression in P. aeruginosa biofilms and their contribution to resistance to therapy. Treatment options for multidrug-resistant P. aeruginosa and A. baumannii infections are limited in most cases to carbapenems. Sulbactam is a treatment option for pan-resistant A. baumannii, and or renewed use of an old drug, colistin, is being entertained for pan-resistant A. baumannii and P. aeruginosa. Immunotherapy is a promising new modality being explored. Prevention of emergence of resistance through combination therapy and pharmacokinetic strategies are studied.
SUMMARY: The emergence and spread of multidrug-resistant P. aeruginosa and A. baumannii and their genetic potential to carry and transfer diverse antibiotic resistance determinants pose a major threat in hospitals. The complex interplay of clonal spread, persistence, transfer of resistance elements, and cell-cell interaction contribute to the difficulty in treating infections caused by these multidrug-resistant strains. In the absence of new antibiotic agents, new modalities of treatment should be developed.
PMID: 15985826 [PubMed - indexed for MEDLINE]
-----------
Related Abstracts:
-----------
The emergence of multidrug resistant Acinetobacter species: a major concern in the hospital setting.
Bloodstream infections caused by antibiotic-resistant gram-negative bacilli: risk factors for mortality and impact of inappropriate initial antimicrobial therapy on outcome.
Treatment and control of severe infections caused by multiresistant Pseudomonas aeruginosa.
Pseudomonas aeruginosa pneumonia.
# posted by Pat O'Connor @ 5:19 AM
Friday, September 01, 2006
Bacterial Infection of the Foot
Infection of the Foot - Diabetic Foot Disease Article
People with diabetes, especially those with very high blood glucose levels, have poorer defence against infection. Minor cuts and abrasions to the foot that we all get from time to time can turn into infection. So protect the feet with appropriate footwear. If there is a foot ulcer, the break in skin would also make infection much more likely to occur.It is essential to distinguish between localized versus generalized foot infection because they require different intensity of treatment.
Localized foot infection is recognized by redness, heat and swelling confined to an area. Note the foot as a whole is not swollen. Oral antibiotics for a few days can usually eliminate the infection.
Generalized foot infection. Note the whole foot is red and swollen. Oral antibiotics in higher dosage can be tried but if there is no rapid response (eg. within 24 hours), intravenous antibiotics and sometimes surgical intervention are urgently required because there is likely to be infected tissue deep inside the foot.
Infection of the Foot
People with diabetes, especially those with very high blood glucose levels, have poorer defence against infection. Minor cuts and abrasions to the foot that we all get from time to time can turn into infection. So protect the feet with appropriate footwear. If there is a foot ulcer, the break in skin would also make infection much more likely to occur.It is essential to distinguish between localized versus generalized foot infection because they require different intensity of treatment.
Localized foot infection is recognized by redness, heat and swelling confined to an area. Note the foot as a whole is not swollen. Oral antibiotics for a few days can usually eliminate the infection.
Localized foot infection associated with a neuropathic ulcer. Due to the neuropathy, the patient may not feel any pain or discomfort. Oral antibiotics are usually satisfactory but may need to be continued until the ulcer has healed.
Generalized foot infection. Note the whole foot is red and swollen. Oral antibiotics in higher dosage can be tried but if there is no rapid response (eg. within 24 hours), intravenous antibiotics and sometimes surgical intervention are urgently required because there is likely to be infected tissue deep inside the foot.
Foot infection complicated by osteomyelitis. In the presence of a foot ulcer there is a risk of the underlying bones being involved. X-ray may show bone destruction. Once there is osteomyelitis, a much higher dose of antibiotics and for a longer period (eg. several months) is often required to eradicate the infection. Quite often, intravenous antibiotic therapy is required. Sometimes the infected bones need to be surgically removed to help the foot heal.
Osteomyelitis in the early phase does not show up on X-ray but can be detected as a hot spot on a technetium bone scan, confirmed by a similar uptake in a white cell bone scan. MRI scan has emerged as the most sensitive and specific test for osteomyelitis and should be performed if the diagnosis is in doubt. If an ulcer is big (> 2cm) or so deep that bone can be probed at the bottom of the ulcer, one should suspect that osteomyelitis is present.
Infection of the Foot - Appendix
Infection of the foot
Is antibiotic therapy really necessary ?
If a foot, with or without an ulcer, is showing signs of infection (red, hot, swollen), there is really no question that antibiotic therapy is required. What is controversial is whether an uninfected foot ulcer should be treated with antibiotics. Recently, Edmonds et al had conducted a clinical trial which showed clinically uninfected foot ulcers may nevertheless benefit from antibiotic therapy. In any case, very few ulcers are truly uninfected. Therefore we tend to err on the cautious side and use antibiotics if we are in any doubt at all.
How long should antibiotic therapy be continued ?
This depends on the severity of the infection. If it is superficial and localized, treat until infection has resolved and then a few more days to give a safety margin. If the infection involves an ulcer, treatment may need to continue until the ulcer has healed. If the infection involves underlying bone, treatment needs to continue for several months, even after superficial signs of infection and ulcer have resolved.
What oral antibiotic therapy should be used ?
Staphylococci aureus is the usual bacteria involved. Choice of therapy is based on this assumption and modified according to response. If the wound is dirty and smelly, it is worthwhile also treating for anaerobic organisms. Swabs are usually not of great use but should be performed if a wound is not responding to treatment. Particular emphasis is on looking for multi-resistant staphylococci.
The choice of antibiotics is often restricted by cost, availability and government regulations. The following are commonly used regimens:
Dicloxacillin or flucloxacillin 250mg to 1gm 6 hrly. Use the higher dose if infection is severe or involves bones. Absorption can be erratic, so if there is any doubt use a higher dose. Dicloxacillin is less likely to cause hepato-toxicity.
Augmentin. Dosage depends on whether it is Augmentin or Augmentin Forte or Augmentin Duo. The clauvulinic acid makes this agent active against staphylococci. It is also active against anaerobic organisms.
Clindamycin. 150mg 6 hrly. A very good and probably under-used antibiotic. It is well tolerated. The main drawback is that it can cause pseudo-membranous colitis, especially in elderly people. Ask the patient to stop treatment if there is diarrhoea more than 5-6 times a day. In severe infection, especially if osteomyelitis is suspected, can be used in combination with ciprofloxacin.
Ciprofloxacin. 250-750mg bd. Just about the only oral agent effective against the occasional pseudomona infection. For this purpose the 750mg bd dosage is required. Can be used in combination with clindamycin. In Australia, an Authority Script is required.
Keflex. 500mg 6 hrly. A good antibiotic for superficial and minor infection. Not all that effective for severe infection and when used, a high dosage should be prescribed.
Rifampicin 450mg mane and Fucidin 500mg bd. This is a good combination for patients with multi-resistant staphylococci infection. A combination is required to prevent development of resistance. Warn the patient that Rifampicin may turn the tears and urine pinkish in colour. Rifampicin can also increase the metabolism of many other drugs.
When should a patient be admitted to hospital ?
This will depend on bed availability and social and geographical situation of the patient. Generally, if the foot is very swollen or the patient is systemically unwell, then hospital admission is advisable. When this is not possible, we sometimes use 'Hospital in the Home' type of arrangement and give antibiotics such as Rociphen or Vancomycin which can be administered intravenously once daily.
How is osteomyelitis diagnosed ?
Osteomyelitis should be suspected whenever there is a big or deep foot ulcer, especially when healing is slow. It is also likely to be present if bones can be probed at the bottom of the ulcer. X-ray should be the first test requested. It is quite specific but not very sensitive. In other words, if osteomyelitis is seen, the diagnosis is reasonably well established. However, if it is not seen, it may still be present. The next test we usually then rely on is a white cell scan. White cells are obtained from the patient's blood, labelled with radioactive isotope and reinjected. They localize at the site of infection and an area of discrete uptake in the bone is good evidence of osteomyelitis. Sometimes it is useful to do an ordinary bone scan at the same time. It helps to tell whether the uptake of white cells is specific.
How would the presence of osteomyelitis affect the treatment ?
If osteomyelitis is present, antibiotic therapy needs to be given for a much longer time and usually in a higher dosage. Intravenous administration is sometimes required. Decision must also be made whether it is necessary to surgically remove the infected bone.Last-Modified: Thursday, 15 October 2003 10:19:26 GMT
Diabetic Foot Problems
People with diabetes, especially those with very high blood glucose levels, have poorer defence against infection. Minor cuts and abrasions to the foot that we all get from time to time can turn into infection. So protect the feet with appropriate footwear. If there is a foot ulcer, the break in skin would also make infection much more likely to occur.It is essential to distinguish between localized versus generalized foot infection because they require different intensity of treatment.
Localized foot infection is recognized by redness, heat and swelling confined to an area. Note the foot as a whole is not swollen. Oral antibiotics for a few days can usually eliminate the infection.
Generalized foot infection. Note the whole foot is red and swollen. Oral antibiotics in higher dosage can be tried but if there is no rapid response (eg. within 24 hours), intravenous antibiotics and sometimes surgical intervention are urgently required because there is likely to be infected tissue deep inside the foot.
Infection of the Foot
People with diabetes, especially those with very high blood glucose levels, have poorer defence against infection. Minor cuts and abrasions to the foot that we all get from time to time can turn into infection. So protect the feet with appropriate footwear. If there is a foot ulcer, the break in skin would also make infection much more likely to occur.It is essential to distinguish between localized versus generalized foot infection because they require different intensity of treatment.
Localized foot infection is recognized by redness, heat and swelling confined to an area. Note the foot as a whole is not swollen. Oral antibiotics for a few days can usually eliminate the infection.
Localized foot infection associated with a neuropathic ulcer. Due to the neuropathy, the patient may not feel any pain or discomfort. Oral antibiotics are usually satisfactory but may need to be continued until the ulcer has healed.
Generalized foot infection. Note the whole foot is red and swollen. Oral antibiotics in higher dosage can be tried but if there is no rapid response (eg. within 24 hours), intravenous antibiotics and sometimes surgical intervention are urgently required because there is likely to be infected tissue deep inside the foot.
Foot infection complicated by osteomyelitis. In the presence of a foot ulcer there is a risk of the underlying bones being involved. X-ray may show bone destruction. Once there is osteomyelitis, a much higher dose of antibiotics and for a longer period (eg. several months) is often required to eradicate the infection. Quite often, intravenous antibiotic therapy is required. Sometimes the infected bones need to be surgically removed to help the foot heal.
Osteomyelitis in the early phase does not show up on X-ray but can be detected as a hot spot on a technetium bone scan, confirmed by a similar uptake in a white cell bone scan. MRI scan has emerged as the most sensitive and specific test for osteomyelitis and should be performed if the diagnosis is in doubt. If an ulcer is big (> 2cm) or so deep that bone can be probed at the bottom of the ulcer, one should suspect that osteomyelitis is present.
Infection of the Foot - Appendix
Infection of the foot
Is antibiotic therapy really necessary ?
If a foot, with or without an ulcer, is showing signs of infection (red, hot, swollen), there is really no question that antibiotic therapy is required. What is controversial is whether an uninfected foot ulcer should be treated with antibiotics. Recently, Edmonds et al had conducted a clinical trial which showed clinically uninfected foot ulcers may nevertheless benefit from antibiotic therapy. In any case, very few ulcers are truly uninfected. Therefore we tend to err on the cautious side and use antibiotics if we are in any doubt at all.
How long should antibiotic therapy be continued ?
This depends on the severity of the infection. If it is superficial and localized, treat until infection has resolved and then a few more days to give a safety margin. If the infection involves an ulcer, treatment may need to continue until the ulcer has healed. If the infection involves underlying bone, treatment needs to continue for several months, even after superficial signs of infection and ulcer have resolved.
What oral antibiotic therapy should be used ?
Staphylococci aureus is the usual bacteria involved. Choice of therapy is based on this assumption and modified according to response. If the wound is dirty and smelly, it is worthwhile also treating for anaerobic organisms. Swabs are usually not of great use but should be performed if a wound is not responding to treatment. Particular emphasis is on looking for multi-resistant staphylococci.
The choice of antibiotics is often restricted by cost, availability and government regulations. The following are commonly used regimens:
Dicloxacillin or flucloxacillin 250mg to 1gm 6 hrly. Use the higher dose if infection is severe or involves bones. Absorption can be erratic, so if there is any doubt use a higher dose. Dicloxacillin is less likely to cause hepato-toxicity.
Augmentin. Dosage depends on whether it is Augmentin or Augmentin Forte or Augmentin Duo. The clauvulinic acid makes this agent active against staphylococci. It is also active against anaerobic organisms.
Clindamycin. 150mg 6 hrly. A very good and probably under-used antibiotic. It is well tolerated. The main drawback is that it can cause pseudo-membranous colitis, especially in elderly people. Ask the patient to stop treatment if there is diarrhoea more than 5-6 times a day. In severe infection, especially if osteomyelitis is suspected, can be used in combination with ciprofloxacin.
Ciprofloxacin. 250-750mg bd. Just about the only oral agent effective against the occasional pseudomona infection. For this purpose the 750mg bd dosage is required. Can be used in combination with clindamycin. In Australia, an Authority Script is required.
Keflex. 500mg 6 hrly. A good antibiotic for superficial and minor infection. Not all that effective for severe infection and when used, a high dosage should be prescribed.
Rifampicin 450mg mane and Fucidin 500mg bd. This is a good combination for patients with multi-resistant staphylococci infection. A combination is required to prevent development of resistance. Warn the patient that Rifampicin may turn the tears and urine pinkish in colour. Rifampicin can also increase the metabolism of many other drugs.
When should a patient be admitted to hospital ?
This will depend on bed availability and social and geographical situation of the patient. Generally, if the foot is very swollen or the patient is systemically unwell, then hospital admission is advisable. When this is not possible, we sometimes use 'Hospital in the Home' type of arrangement and give antibiotics such as Rociphen or Vancomycin which can be administered intravenously once daily.
How is osteomyelitis diagnosed ?
Osteomyelitis should be suspected whenever there is a big or deep foot ulcer, especially when healing is slow. It is also likely to be present if bones can be probed at the bottom of the ulcer. X-ray should be the first test requested. It is quite specific but not very sensitive. In other words, if osteomyelitis is seen, the diagnosis is reasonably well established. However, if it is not seen, it may still be present. The next test we usually then rely on is a white cell scan. White cells are obtained from the patient's blood, labelled with radioactive isotope and reinjected. They localize at the site of infection and an area of discrete uptake in the bone is good evidence of osteomyelitis. Sometimes it is useful to do an ordinary bone scan at the same time. It helps to tell whether the uptake of white cells is specific.
How would the presence of osteomyelitis affect the treatment ?
If osteomyelitis is present, antibiotic therapy needs to be given for a much longer time and usually in a higher dosage. Intravenous administration is sometimes required. Decision must also be made whether it is necessary to surgically remove the infected bone.Last-Modified: Thursday, 15 October 2003 10:19:26 GMT
Diabetic Foot Problems
# posted by Pat O'Connor @ 5:13 AM
