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This revascularization can be from bone, such as from the fibula to the lateral circumflex artery and from the iliac crest to deep circumflex iliac vessels; or from muscle, such as from the quadratus femoris, sartorius, tensor fascia lata, and gluteus medius
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Ran- domized controlled trials examining core decompression and MSCs compared with core decompression alone have shown favorable outcomes regarding Harris Hip Score, le- sion size, and time to collapse in 100 patients followed up for 60 months
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Previously, concerns existed that osteonecrosis could hinder ingrowth in noncemented implants
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However, a 2013 study reported significantly lower rates of aseptic loosening in noncemented implants compared with ce- mented implants
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higher failure rates were reported in patients who had osteonecrosis secondary to sickle cell disease, Gaucher disease, and following renal transplantation. Lower rates of osteonecrosis were seen in patients with idiopathic disease, with SLE, and fol- lowing heart transplantatio
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There are three types of knee osteo- necrosis: primary (or spontaneous osteonecrosis of the knee [SONK]), secondary (also called atraumatic, idio- pathic, or ischemic osteonecrosis), and postarthroscopic. SONK
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commonly occurs at the medial femoral condyle
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radiographs may show increased bone density from new bone formation next to the necrotic bone, accentuated by surrounding osteopenia.
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Koshino classification 48 was later modified so that stage 1 is nor- mal, stage 2 is a mild flattening of weight-bearing surface, stage 3 is a subchondral lucency, stage 4 is a collapse of the subchondral bone, and stage 5 is characterized by secondary degenerative change
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t is theorized that minor trauma in the setting of osteopenic bone, which affects 75% of patients with SONK, causes subchondral insufficiency fractures. Fluid accumulates in these potential spaces, causing
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With SONK, tender- ness is found on the medial femoral condyle
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promising nonsurgical treatment is pulsed electromagnetic field therapy, which has been shown to reduce pain and the size of the necrotic lesion in SONK at 6 months.
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urgery is indicated when no clinical or radiographic im- provement is seen after 3 months of nonsurgical treatment or in patients with large osteonecrotic lesions (larger than 3.5 cm 2 or greater than 50% of the condyle
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Flashcard 7080872905996

Question
1. Patient has high aldosterone. What are the arrows (i.e., ! or ¯) for serum Na + , K + , pH, bicarb, and CO2?
Answer
[default - edit me]

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Flashcard 7080873954572

Question
[default - edit me]
Answer
- ! Na + , ¯ K + , ! pH, ! bicarb, ! CO2. - Remember that all arrows go the same direction as aldosterone, except for potassium, which is the opposite. - Aldosterone upregulates the sodium-potassium ATPase pump on the basolateral membrane of the cortical collecting duct in the kidney. This causes Na + reabsorption and K + secretion. Water follows sodium; this will function to increase volume status and blood pressure. - Aldosterone also upregulates an apical H + -ATPase pump. If protons are kicked out into the urine, the patient develops metabolic alkalosis (i.e., bicarb goes up). - CO2 is acidic. If we have a metabolic alkalosis, we want to retain acidic CO2, so we slow respiratory rate – i.e., metabolic alkalosis with respiratory compensation.

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Flashcard 7080877886732

Tags
#causality #statistics
Question
An estimate (noun) is [...] of some estimand, which we get using data
Answer
an approximation

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An estimate (noun) is an approximation of some estimand, which we get using data

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Flashcard 7080879721740

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#causality #has-images #statistics


Question
This is known as [...] due to the M shape that this non-causal association flows along when the graph is drawn with children below their parents.
Answer
M-bias

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This is known as M-bias due to the M shape that this non-causal association flows along when the graph is drawn with children below their parents.

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Flashcard 7080881556748

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Question
Well, what assumption(s) would make it so that the ATE is simply the [...] difference? This is equivalent to saying “what makes it valid to calculate the ATE by taking the average of the 𝑌(0) column, ignoring the question marks, and subtracting that from the average of the 𝑌(1) column, ignoring the question marks?” 6 This ignoring of the question marks (missing data) is known as ignorability
Answer
associational

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Well, what assumption(s) would make it so that the ATE is simply the associational difference? This is equivalent to saying “what makes it valid to calculate the ATE by taking the average of the 𝑌(0) column, ignoring the question marks, and subtracting that from the a

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Flashcard 7080883916044

Tags
#causality #statistics
Question
If there is a directed path that starts at node 𝑋 and ends at node 𝑌 , then 𝑋 is [...] of 𝑌
Answer
an ancestor

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If there is a directed path that starts at node 𝑋 and ends at node 𝑌 , then 𝑋 is an ancestor of 𝑌

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#causality #statistics
It might seem like consistency is obviously true, but that is not always the case. For example, if the treatment specification is simply “get a dog” or “don’t get a dog,” this can be too coarse to yield it (it means this assumption)
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It might seem like consistency is obviously true, but that is not always the case. For example, if the treatment specification is simply “get a dog” or “don’t get a dog,” this can be too coarse to yield consistency. It might be that if I were to get a puppy, I would observe 𝑌 = 1 (happiness) because I needed an energetic friend, but if I were to get an old, low-energy dog, I would obse

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Flashcard 7080888372492

Tags
#causality #statistics
Question
The idea is that although the treatment and potential outcomes may be unconditionally associated (due to confounding), within levels of 𝑋 , they are not associated. In other words, there is no confounding within levels of 𝑋 because [...] for 𝑋 has made the treatment groups comparable.
Answer
controlling

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t and potential outcomes may be unconditionally associated (due to confounding), within levels of 𝑋 , they are not associated. In other words, there is no confounding within levels of 𝑋 because <span>controlling for 𝑋 has made the treatment groups comparable. <span>

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Flashcard 7080890207500

Tags
#causality #statistics
Question
More generally, the potential outcome 𝑌(𝑡) denotes what your outcome [...], if you were to take treatment 𝑡
Answer
would be

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More generally, the potential outcome 𝑌(𝑡) denotes what your outcome would be, if you were to take treatment 𝑡

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Flashcard 7080892042508

Tags
#causality #statistics
Question
Association flows along [...] unblocked paths. In causal graphs, causation flows along directed paths.
Answer
all

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Association flows along all unblocked paths. In causal graphs, causation flows along directed paths.

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#causality #statistics
In causal graphs, causation flows along directed paths.
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Association flows along all unblocked paths. In causal graphs, causation flows along directed paths.

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Flashcard 7080895450380

Tags
#causality #has-images #statistics


Question
if the DAG were simply two connected nodes 𝑋 and 𝑌 as in Figure 3.8, the local Markov assumption would tell us that we can factorize 𝑃(𝑥, 𝑦) as 𝑃(𝑥)𝑃(𝑦|𝑥) , but it would also allow us to factorize 𝑃(𝑥, 𝑦) as 𝑃(𝑥)𝑃(𝑦) , meaning it allows distributions where 𝑋 and 𝑌 are independent. In contrast, the [...] assumption does not allow this additional independence
Answer
minimality

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ll us that we can factorize 𝑃(𝑥, 𝑦) as 𝑃(𝑥)𝑃(𝑦|𝑥) , but it would also allow us to factorize 𝑃(𝑥, 𝑦) as 𝑃(𝑥)𝑃(𝑦) , meaning it allows distributions where 𝑋 and 𝑌 are independent. In contrast, the <span>minimality assumption does not allow this additional independence <span>

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Flashcard 7080897285388

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#causality #has-images #statistics


Question
We do not have [...] in the data because 𝑋 is a common cause of 𝑇 and 𝑌
Answer
exchangeability

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We do not have exchangeability in the data because 𝑋 is a common cause of 𝑇 and 𝑌

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#causality #statistics
if we take the graph from Figure 4.5 and intervene on 𝑇 , then we get the manipulated graph in Figure 4.6. In this manipulated graph, there cannot be any backdoor paths because no edges are going into the backdoor of 𝑇 . Therefore, all of the association that flows from 𝑇 to 𝑌 in the manipulated graph is purely causal
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Flashcard 7080900693260

Tags
#causality #statistics
Question
The flow of association is [...], whereas the flow of causation is not.
Answer
symmetric

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The flow of association is symmetric, whereas the flow of causation is not.

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Flashcard 7080902528268

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#causality #has-images #statistics


Question
If we condition on a descendant of 𝑇 that [...] a mediator, it could unblock a path from 𝑇 to 𝑌 that was blocked by a collider. For example, this is the case with conditioning on 𝑍 in Figure 4.13. This induces non-causal association between 𝑇 and 𝑌 , which biases the estimate of the causal effect
Answer
isn’t

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If we condition on a descendant of 𝑇 that isn’t a mediator, it could unblock a path from 𝑇 to 𝑌 that was blocked by a collider. For example, this is the case with conditioning on 𝑍 in Figure 4.13. This induces non-causal association

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Flashcard 7080904363276

Tags
#causality #statistics
Question
If there is a directed path that starts at node 𝑋 and ends at node 𝑌 , 𝑌 is [...] of 𝑋
Answer
a descendant

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If there is a directed path that starts at node 𝑋 and ends at node 𝑌 , 𝑌 is a descendant of 𝑋

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#Campylobacter #Epidemiologie #Epidemiology
Campylobacters are small gram-negative bacteria first recognized as causes of abortion in cattle and sheep in the early twentieth century [1].
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2022. | This topic last updated: May 10, 2021. INTRODUCTION — <span>Campylobacters are small gram-negative bacteria first recognized as causes of abortion in cattle and sheep in the early twentieth century [1]. A few decades later, the organism (originally called Vibrio) was reported as an occasional cause of illness in humans [2]. In 1973, a new genus, Campylobacter, was designated [3]. It wa




#Campylobacter #Epidemiologie #Epidemiology
It was not until the 1980s that the full impact of Campylobacter infections on human health began to be appreciated; they are now known to be a leading cause of acute diarrhea and systemic illness worldwide.
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century [1]. A few decades later, the organism (originally called Vibrio) was reported as an occasional cause of illness in humans [2]. In 1973, a new genus, Campylobacter, was designated [3]. <span>It was not until the 1980s that the full impact of Campylobacter infections on human health began to be appreciated; they are now known to be a leading cause of acute diarrhea and systemic illness worldwide. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-rich settings".) Campylobacter spp are common commensals in the gastrointestinal tract of animals, es




#Campylobacter #Epidemiologie #Epidemiology
Campylobacter spp are common commensals in the gastrointestinal tract of animals, especially poultry; thus, animal-to-human transmission of infections occurs frequently.
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; they are now known to be a leading cause of acute diarrhea and systemic illness worldwide. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-rich settings".) <span>Campylobacter spp are common commensals in the gastrointestinal tract of animals, especially poultry; thus, animal-to-human transmission of infections occurs frequently. The microbiology, pathogenesis, and epidemiology of Campylobacter infection will be reviewed here. The clinical features and treatment of Campylobacter infection are discussed separatel




#Campylobacter #Epidemiologie #Epidemiology
Campylobacters are found worldwide, including arctic, temperate, and tropical climates
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r polysaccharides suggest the presence of homologous protective immunity between strains [49]. EPIDEMIOLOGY — Campylobacter enteritis is a leading cause of acute diarrhea worldwide. Incidence — <span>Campylobacters are found worldwide, including arctic, temperate, and tropical climates. In the United States, the incidence of Campylobacter is assessed through the Foodborne Diseases Active Surveillance Network (FoodNet), which has collected data on nine major foodborne




#Campylobacter #Epidemiologie #Epidemiology
In Europe and Israel, the incidence of Campylobacter infections has increased over the last decade [53,54]
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the incidence of Campylobacter infections between states, with infections being more common in western states; for example, the infection rate in California is triple that in Tennessee [51,52]. <span>In Europe and Israel, the incidence of Campylobacter infections has increased over the last decade [53,54]. Burden of disease — Mortality due to Campylobacter infection is low, even in patients who develop bacteremia [55]. In the United States, estimates are that 50 to 150 deaths annually ar




#Campylobacter #Epidemiologie #Epidemiology
Mortality due to Campylobacter infection is low, even in patients who develop bacteremia [55]
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infection rate in California is triple that in Tennessee [51,52]. In Europe and Israel, the incidence of Campylobacter infections has increased over the last decade [53,54]. Burden of disease — <span>Mortality due to Campylobacter infection is low, even in patients who develop bacteremia [55]. In the United States, estimates are that 50 to 150 deaths annually are at least in part attributable to Campylobacter infection [10]. The total cost of health care and lost productivit




#Campylobacter #Epidemiologie #Epidemiology
The age distribution of Campylobacter enteritis in industrialized countries is different from that of other enteric infections. Like most other infections, there is a high incidence in early childhood but, unlike others, there is a pronounced secondary peak in young adults (figure 1) with a mild male predominance [10,52,57]. The reasons for this peak are unknown
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mpylobacter infection [10]. The total cost of health care and lost productivity for Campylobacter enteritis in the United States is estimated at $1.5 to $8.0 billion annually [56]. Demography — <span>The age distribution of Campylobacter enteritis in industrialized countries is different from that of other enteric infections. Like most other infections, there is a high incidence in early childhood but, unlike others, there is a pronounced secondary peak in young adults (figure 1) with a mild male predominance [10,52,57]. The reasons for this peak are unknown. Adults tend to be more severely affected than children, while infants usually tolerate the infection well. Older adults are more likely to have severe illness and be hospitalized. Howe




#Campylobacter #Epidemiologie #Epidemiology
Adults tend to be more severely affected than children, while infants usually tolerate the infection well. Older adults are more likely to have severe illness and be hospitalized. However, older adults are also less likely to report typical symptoms (eg, bloody diarrhea, abdominal pain) associated with Campylobacter infection [58]
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incidence in early childhood but, unlike others, there is a pronounced secondary peak in young adults (figure 1) with a mild male predominance [10,52,57]. The reasons for this peak are unknown. <span>Adults tend to be more severely affected than children, while infants usually tolerate the infection well. Older adults are more likely to have severe illness and be hospitalized. However, older adults are also less likely to report typical symptoms (eg, bloody diarrhea, abdominal pain) associated with Campylobacter infection [58]. A different pattern is seen in resource-limited settings where infection is hyperendemic. High transmission rates mean that children become repeatedly infected early in life. Initial i




#Campylobacter #Epidemiologie #Epidemiology
A different pattern is seen in resource-limited settings where infection is hyperendemic. High transmission rates mean that children become repeatedly infected early in life. Initial infections are often associated with diarrhea, but as immunity is gained, subsequent infections are increasingly likely to be asymptomatic [59,60]
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ave severe illness and be hospitalized. However, older adults are also less likely to report typical symptoms (eg, bloody diarrhea, abdominal pain) associated with Campylobacter infection [58]. <span>A different pattern is seen in resource-limited settings where infection is hyperendemic. High transmission rates mean that children become repeatedly infected early in life. Initial infections are often associated with diarrhea, but as immunity is gained, subsequent infections are increasingly likely to be asymptomatic [59,60]. Thus, the disease is virtually unknown in older children and adults. In one series of children from Bangladesh and Thailand, IgG antibodies to surface protein antigens of C. jejuni ros




#Campylobacter #Epidemiologie #Epidemiology
In temperate zones, Campylobacter enteritis has a remarkably constant seasonal pattern characterized by a sharp rise of incidence in early summer, a peak in midsummer, and then a steady decline to base levels in winter (figure 2). A slight secondary peak is sometimes evident in late fall. The reasons for this seasonal pattern are unknown. The seasonal variations in the incidence of Campylobacter infection are not observed in tropical climates
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Thailand, IgG antibodies to surface protein antigens of C. jejuni rose early in childhood and then gradually fell; in comparison, IgA antibodies increased progressively through childhood [59]. <span>In temperate zones, Campylobacter enteritis has a remarkably constant seasonal pattern characterized by a sharp rise of incidence in early summer, a peak in midsummer, and then a steady decline to base levels in winter (figure 2). A slight secondary peak is sometimes evident in late fall. The reasons for this seasonal pattern are unknown. The seasonal variations in the incidence of Campylobacter infection are not observed in tropical climates. Sources and transmission — C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds [61]; C. coli is particularly associated with pigs. The bacte




#Campylobacter #Epidemiologie #Epidemiology
C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds [61]; C. coli is particularly associated with pigs.
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te fall. The reasons for this seasonal pattern are unknown. The seasonal variations in the incidence of Campylobacter infection are not observed in tropical climates. Sources and transmission — <span>C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds [61]; C. coli is particularly associated with pigs. The bacteria are shed widely and can be found in almost any natural water, fresh or saline, in which they can survive for many weeks at temperatures below 15ºC. Water can be a direct so




#Campylobacter #Epidemiologie #Epidemiology
The bacteria are shed widely and can be found in almost any natural water, fresh or saline, in which they can survive for many weeks at temperatures below 15ºC.
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tropical climates. Sources and transmission — C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds [61]; C. coli is particularly associated with pigs. <span>The bacteria are shed widely and can be found in almost any natural water, fresh or saline, in which they can survive for many weeks at temperatures below 15ºC. Water can be a direct source of human infection, though food contamination from food-producing animals is a more significant problem [62]. Any raw meat can be contaminated with campylob




#Campylobacter #Epidemiologie #Epidemiology
Water can be a direct source of human infection, though food contamination from food-producing animals is a more significant problem [ 62]
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rticularly associated with pigs. The bacteria are shed widely and can be found in almost any natural water, fresh or saline, in which they can survive for many weeks at temperatures below 15ºC. <span>Water can be a direct source of human infection, though food contamination from food-producing animals is a more significant problem [62]. Any raw meat can be contaminated with campylobacters. It is almost impossible to prevent contamination of carcasses from gut contents at slaughter. With large animals (eg, cattle, shee




#Campylobacter #Epidemiologie #Epidemiology
Any raw meat can be contaminated with campylobacters. It is almost impossible to prevent contamination of carcasses from gut contents at slaughter.
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can survive for many weeks at temperatures below 15ºC. Water can be a direct source of human infection, though food contamination from food-producing animals is a more significant problem [62]. <span>Any raw meat can be contaminated with campylobacters. It is almost impossible to prevent contamination of carcasses from gut contents at slaughter. With large animals (eg, cattle, sheep, pigs), the use of air-blast chilling causes surface drying and substantially reduces the number of organisms. Thus, red meats, except offal, are s




#Campylobacter #Epidemiologie #Epidemiology
Thus, red meats, except offal, are seldom heavily contaminated [ 63,64]
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of carcasses from gut contents at slaughter. With large animals (eg, cattle, sheep, pigs), the use of air-blast chilling causes surface drying and substantially reduces the number of organisms. <span>Thus, red meats, except offal, are seldom heavily contaminated [63,64]. Contamination of poultry occurs more frequently. Broiler chicken flocks can become heavily colonized, and the bacteria are spread liberally when the carcasses undergo mass processing [




#Campylobacter #Epidemiologie #Epidemiology
Contamination of poultry occurs more frequently. Broiler chicken flocks can become heavily colonized, and the bacteria are spread liberally when the carcasses undergo mass processing [65]. As a result, approximately 60 percent of retail broiler carcasses and their juices are contaminated with campylobacters, often with counts as high as 106 to 107 per chicken [66].
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tle, sheep, pigs), the use of air-blast chilling causes surface drying and substantially reduces the number of organisms. Thus, red meats, except offal, are seldom heavily contaminated [63,64]. <span>Contamination of poultry occurs more frequently. Broiler chicken flocks can become heavily colonized, and the bacteria are spread liberally when the carcasses undergo mass processing [65]. As a result, approximately 60 percent of retail broiler carcasses and their juices are contaminated with campylobacters, often with counts as high as 106 to 107 per chicken [66]. According to one study approximately 48 percent of Campylobacter infections are attributable to transmission via poultry [67-71]. Chickens are also a major source of quinolone-resistant




#Campylobacter #Epidemiologie #Epidemiology
According to one study approximately 48 percent of Campylobacter infections are attributable to transmission via poultry [67-71]. Chickens are also a major source of quinolone-resistant Campylobacter infections, an effect that is related to quinolone use in poultry feeds in both the United States and Europe [72].
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ocessing [65]. As a result, approximately 60 percent of retail broiler carcasses and their juices are contaminated with campylobacters, often with counts as high as 106 to 107 per chicken [66]. <span>According to one study approximately 48 percent of Campylobacter infections are attributable to transmission via poultry [67-71]. Chickens are also a major source of quinolone-resistant Campylobacter infections, an effect that is related to quinolone use in poultry feeds in both the United States and Europe [72]. (See "Clinical manifestations, diagnosis, and treatment of Campylobacter infection", section on 'Antimicrobial therapy'.) In general, infection is acquired from meat in one of two ways:




#Campylobacter #Epidemiologie #Epidemiology
In general, infection is acquired from meat in one of two ways: consumption of raw or undercooked meat, or eating food that has become cross contaminated from raw meat [73]. A typical example of cross contamination would be the cutting up of bread or salad on an unwashed board that had just been used to handle raw chicken.
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inolone use in poultry feeds in both the United States and Europe [72]. (See "Clinical manifestations, diagnosis, and treatment of Campylobacter infection", section on 'Antimicrobial therapy'.) <span>In general, infection is acquired from meat in one of two ways: consumption of raw or undercooked meat, or eating food that has become cross contaminated from raw meat [73]. A typical example of cross contamination would be the cutting up of bread or salad on an unwashed board that had just been used to handle raw chicken. In a substantial proportion of Campylobacter cases the source of infection is unknown [67,74]. One survey of 218 human cases identified the following sources [74]: ●Chicken consumption




#Campylobacter #Epidemiologie #Epidemiology

In a substantial proportion of Campylobacter cases the source of infection is unknown [67,74]. One survey of 218 human cases identified the following sources [74]:

● Chicken consumption – 48 percent

● Travel to underdeveloped countries – 9 percent

● Drinking non-home well or surface water – 8 percent

● Exposure to an animal with diarrhea – 6 percent

● Drinking raw milk – 5 percent

● Unknown – 24 percent

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ome cross contaminated from raw meat [73]. A typical example of cross contamination would be the cutting up of bread or salad on an unwashed board that had just been used to handle raw chicken. <span>In a substantial proportion of Campylobacter cases the source of infection is unknown [67,74]. One survey of 218 human cases identified the following sources [74]: ●Chicken consumption – 48 percent ●Travel to underdeveloped countries – 9 percent ●Drinking non-home well or surface water – 8 percent ●Exposure to an animal with diarrhea – 6 percent ●Drinking raw milk – 5 percent ●Unknown – 24 percent In resource-rich countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. Community outbreaks are uncommon, probably because campylobacters are u




#Campylobacter #Epidemiologie #Epidemiology
In resource-rich countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. Community outbreaks are uncommon, probably because campylobacters are unable to multiply in food like Salmonellae. Important exceptions are outbreaks caused by the distribution of contaminated water or milk, which have infected as many as 3000 people at a time [75-79].
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o underdeveloped countries – 9 percent ●Drinking non-home well or surface water – 8 percent ●Exposure to an animal with diarrhea – 6 percent ●Drinking raw milk – 5 percent ●Unknown – 24 percent <span>In resource-rich countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. Community outbreaks are uncommon, probably because campylobacters are unable to multiply in food like Salmonellae. Important exceptions are outbreaks caused by the distribution of contaminated water or milk, which have infected as many as 3000 people at a time [75-79]. Updated information on outbreaks may be found on websites maintained by the United States Centers for Disease Control and Prevention and the US Food and Drug Administration. The followi




#Campylobacter #Epidemiologie #Epidemiology
In waterborne outbreaks, the water has been unchlorinated or there has been a fault in the chlorination or distribution system [75-77,80]
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e found on websites maintained by the United States Centers for Disease Control and Prevention and the US Food and Drug Administration. The following observations have been noted in outbreaks: ●<span>In waterborne outbreaks, the water has been unchlorinated or there has been a fault in the chlorination or distribution system [75-77,80]. ●In milk-borne outbreaks, the consumed milk has been raw or there has been a failure in the pasteurization process [78,79,81-84]. As an example, in England, increased sales of unpasteu




#Campylobacter #Epidemiologie #Epidemiology
In milk-borne outbreaks, the consumed milk has been raw or there has been a failure in the pasteurization process [78,79,81-84].
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following observations have been noted in outbreaks: ●In waterborne outbreaks, the water has been unchlorinated or there has been a fault in the chlorination or distribution system [75-77,80]. ●<span>In milk-borne outbreaks, the consumed milk has been raw or there has been a failure in the pasteurization process [78,79,81-84]. As an example, in England, increased sales of unpasteurized milk in vending machines have been associated new outbreaks of Campylobacter infection [85]. It is almost impossible to preve




#Campylobacter #Epidemiologie #Epidemiology
Occasionally, the source of an outbreak is unknown. As an example, the first reported Campylobacter outbreak in China in more than 20 years occurred in 2018 among a group of Beijing high school students on a school trip [86].
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almost impossible to prevent milk becoming fecally contaminated even in the best run milking parlors. As a result, compulsory pasteurization of all milk sold to the public is the only remedy. ●<span>Occasionally, the source of an outbreak is unknown. As an example, the first reported Campylobacter outbreak in China in more than 20 years occurred in 2018 among a group of Beijing high school students on a school trip [86]. The source was never identified, although a common poultry source was suspected. Infection can also be acquired directly from animals or their carcasses. Direct transmission of this sor




#Campylobacter #Epidemiologie #Epidemiology
Infection can also be acquired directly from animals or their carcasses. Direct transmission of this sort is usually occupational (eg, farmers, slaughterhouse workers, poultry processors), but domestic infection can also arise from contact with a pet, usually a puppy or kitten with Campylobacter diarrhea [74,87,88].
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hina in more than 20 years occurred in 2018 among a group of Beijing high school students on a school trip [86]. The source was never identified, although a common poultry source was suspected. <span>Infection can also be acquired directly from animals or their carcasses. Direct transmission of this sort is usually occupational (eg, farmers, slaughterhouse workers, poultry processors), but domestic infection can also arise from contact with a pet, usually a puppy or kitten with Campylobacter diarrhea [74,87,88]. Person-to-person infectivity is generally low, although caretakers for children in diapers or incontinent individuals are at risk for transmission. Sexual transmission, presumably throu




#Campylobacter #Epidemiologie #Epidemiology
Person-to-person infectivity is generally low, although caretakers for children in diapers or incontinent individuals are at risk for transmission. Sexual transmission, presumably through fecal-oral contact, has also been reported.
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ional (eg, farmers, slaughterhouse workers, poultry processors), but domestic infection can also arise from contact with a pet, usually a puppy or kitten with Campylobacter diarrhea [74,87,88]. <span>Person-to-person infectivity is generally low, although caretakers for children in diapers or incontinent individuals are at risk for transmission. Sexual transmission, presumably through fecal-oral contact, has also been reported. As an example, in one study of a prolonged outbreak of a particular drug-resistant C. jejuni isolate, the vast majority of the 31 affected individuals were men who have sex with men, am




#Campylobacter #Epidemiologie #Epidemiology
The near universal contamination of poultry and the heavy bacterial burden makes such elimination impractical, if not impossible. Therefore, careful food handling practices in the kitchen should be directed towards reducing the risk of transmission to humans. Because C. jejuni is killed by heat, all meat, especially chicken, should be cooked to proper temperature (breasts to 170ºF, thighs to 180ºF).
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tion with Campylobacter. Food handling — Even with the employment of the best agricultural practices, it is unlikely that elimination of Campylobacter contamination of poultry will be achieved. <span>The near universal contamination of poultry and the heavy bacterial burden makes such elimination impractical, if not impossible. Therefore, careful food handling practices in the kitchen should be directed towards reducing the risk of transmission to humans. Because C. jejuni is killed by heat, all meat, especially chicken, should be cooked to proper temperature (breasts to 170ºF, thighs to 180ºF). In addition to thorough cooking, care should be taken to avoid cross-contamination: cutting boards, knives, and other utensils used to prepare chicken should be thoroughly washed with h




#Campylobacter #Epidemiologie #Epidemiology
In addition to thorough cooking, care should be taken to avoid cross-contamination: cutting boards, knives, and other utensils used to prepare chicken should be thoroughly washed with hot, soapy water before being used to prepare salads or other foods eaten raw. Irradiation of food will kill Campylobacter as well as other pathogens, but is not yet acceptable to the public
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wards reducing the risk of transmission to humans. Because C. jejuni is killed by heat, all meat, especially chicken, should be cooked to proper temperature (breasts to 170ºF, thighs to 180ºF). <span>In addition to thorough cooking, care should be taken to avoid cross-contamination: cutting boards, knives, and other utensils used to prepare chicken should be thoroughly washed with hot, soapy water before being used to prepare salads or other foods eaten raw. Irradiation of food will kill Campylobacter as well as other pathogens, but is not yet acceptable to the public. Animal transmission — The direct transmission from animals may also be prevented by simple hygienic measures of which hand washing is by far the most important; this is particularly re




#Campylobacter #Epidemiologie #Epidemiology
C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds. The bacteria are shed widely and can be found in almost any natural water, in which they can survive for many weeks at temperatures below 15ºC. Although water can be a direct source of human infection, it is the contamination by campylobacters of the food chain from food-producing animals that is the greater problem.
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of incidence in early summer, a peak in midsummer, and then a steady decline to base levels in winter. The seasonal variations are not observed in tropical climates. (See 'Demography' above.) ●<span>C. jejuni and C. coli are carried by a wide variety of wild and domestic animals, notably birds. The bacteria are shed widely and can be found in almost any natural water, in which they can survive for many weeks at temperatures below 15ºC. Although water can be a direct source of human infection, it is the contamination by campylobacters of the food chain from food-producing animals that is the greater problem. (See 'Sources and transmission' above.) ●Any raw meat is likely to be contaminated with campylobacters as it is almost impossible to prevent contamination of carcasses from gut contents




#Campylobacter #Epidemiologie #Epidemiology
There are two ways infection is acquired from meats: eating raw or undercooked meat and eating uncooked or previously cooked food that has become cross contaminated from raw meat.
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of carcasses from gut contents at slaughter. Approximately 60 percent of retail broiler carcasses and their juices are contaminated with campylobacters. (See 'Sources and transmission' above.) ●<span>There are two ways infection is acquired from meats: eating raw or undercooked meat and eating uncooked or previously cooked food that has become cross contaminated from raw meat. (See 'Sources and transmission' above.) ●In industrialized countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. An important exception is com




#Campylobacter #Epidemiologie #Epidemiology
In industrialized countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. An important exception is community outbreaks caused by the distribution of contaminated water or milk.
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n is acquired from meats: eating raw or undercooked meat and eating uncooked or previously cooked food that has become cross contaminated from raw meat. (See 'Sources and transmission' above.) ●<span>In industrialized countries, most cases of Campylobacter enteritis are sporadic or part of small family outbreaks. An important exception is community outbreaks caused by the distribution of contaminated water or milk. (See 'Sources and transmission' above.) ●Because most Campylobacter infections are transmitted by preparing and consuming chicken, control of Campylobacter infections in broiler flocks




#Campylobacter #Epidemiologie #Epidemiology
Because most Campylobacter infections are transmitted by preparing and consuming chicken, control of Campylobacter infections in broiler flocks and care to prevent cross contamination during food handling are the most effective means to prevent transmission.
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are sporadic or part of small family outbreaks. An important exception is community outbreaks caused by the distribution of contaminated water or milk. (See 'Sources and transmission' above.) ●<span>Because most Campylobacter infections are transmitted by preparing and consuming chicken, control of Campylobacter infections in broiler flocks and care to prevent cross contamination during food handling are the most effective means to prevent transmission. (See 'Prevention' above and 'Food handling' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES MacFadyean F, Stockman S. Report of the department committee appointed by




#Campylobacter #Clinical #Clinique #Infection
Campylobacter enteritis is typically caused by Campylobacter jejuni or Campylobacter coli.
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ugh: Apr 2022. | This topic last updated: Aug 20, 2021. INTRODUCTION — Campylobacter infection is an important cause of acute diarrhea worldwide; the organism also may produce systemic illness. <span>Campylobacter enteritis is typically caused by Campylobacter jejuni or Campylobacter coli. The organism inhabits the intestinal tracts of a wide range of animal hosts, notably poultry; contamination from these sources can lead to foodborne disease. Campylobacter infection can




#Campylobacter #Clinical #Clinique #Infection
The clinical features of Campylobacter enteritis due to C. jejuni and C. coli are clinically indistinguishable from one another and from illness due to other bacterial pathogens, such as Salmonellae or Shigellae
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r species. (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection" and "Infection with less common Campylobacter species and related bacteria".) CLINICAL MANIFESTATIONS — <span>The clinical features of Campylobacter enteritis due to C. jejuni and C. coli are clinically indistinguishable from one another and from illness due to other bacterial pathogens, such as Salmonellae or Shigellae. Incubation period — The mean incubation period is three days (range one to seven days) (figure 1) [1-3]. Asymptomatic infection — Asymptomatic infection in both adults and children is




#Campylobacter #Clinical #Clinique #Infection
The mean incubation period is three days (range one to seven days) (figure 1) [1-3]
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enteritis due to C. jejuni and C. coli are clinically indistinguishable from one another and from illness due to other bacterial pathogens, such as Salmonellae or Shigellae. Incubation period — <span>The mean incubation period is three days (range one to seven days) (figure 1) [1-3]. Asymptomatic infection — Asymptomatic infection in both adults and children is rare in resource-rich settings but is more common in resource-limited countries. Asymptomatic infections




#Campylobacter #Clinical #Clinique #Infection
Asymptomatic infection in both adults and children is rare in resource-rich settings but is more common in resource-limited countries. Asymptomatic infections in children may impact growth in early life [4].
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to other bacterial pathogens, such as Salmonellae or Shigellae. Incubation period — The mean incubation period is three days (range one to seven days) (figure 1) [1-3]. Asymptomatic infection — <span>Asymptomatic infection in both adults and children is rare in resource-rich settings but is more common in resource-limited countries. Asymptomatic infections in children may impact growth in early life [4]. Common presenting features Adults — Early symptoms include abrupt onset of abdominal pain and diarrhea. In about one-third of cases, a prodromal period characterized by high fever accom




#Campylobacter #Clinical #Clinique #Infection
Early symptoms include abrupt onset of abdominal pain and diarrhea. In about one-third of cases, a prodromal period characterized by high fever accompanied by rigors, generalized aches, dizziness, and delirium is observed. It may last for one day (rarely two or three days) prior to onset of gastrointestinal symptoms. Patients presenting with prodromal symptoms tend to have more severe disease than those presenting with diarrhea
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is rare in resource-rich settings but is more common in resource-limited countries. Asymptomatic infections in children may impact growth in early life [4]. Common presenting features Adults — <span>Early symptoms include abrupt onset of abdominal pain and diarrhea. In about one-third of cases, a prodromal period characterized by high fever accompanied by rigors, generalized aches, dizziness, and delirium is observed. It may last for one day (rarely two or three days) prior to onset of gastrointestinal symptoms. Patients presenting with prodromal symptoms tend to have more severe disease than those presenting with diarrhea. The acute illness is characterized by cramping, periumbilical abdominal pain, and diarrhea. Patients frequently report ten or more bowel movements per day [5]. Bloody stools are observ




#Campylobacter #Clinical #Clinique #Infection
The acute illness is characterized by cramping, periumbilical abdominal pain, and diarrhea. Patients frequently report ten or more bowel movements per day [5]. Bloody stools are observed on the second or third day of diarrhea in about 15 percent of patients; infection with an organism containing plasmid pVir may be correlated with more severe invasive disease and higher likelihood of bloody diarrhea [6,7]
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one day (rarely two or three days) prior to onset of gastrointestinal symptoms. Patients presenting with prodromal symptoms tend to have more severe disease than those presenting with diarrhea. <span>The acute illness is characterized by cramping, periumbilical abdominal pain, and diarrhea. Patients frequently report ten or more bowel movements per day [5]. Bloody stools are observed on the second or third day of diarrhea in about 15 percent of patients; infection with an organism containing plasmid pVir may be correlated with more severe invasive disease and higher likelihood of bloody diarrhea [6,7]. Abdominal pain also may occur without diarrhea [8]. The pain may become continuous and radiate to the right iliac fossa, mimicking acute appendicitis. Nausea is common; approximately 1




#Campylobacter #Clinical #Clinique #Infection
Abdominal pain also may occur without diarrhea [8]. The pain may become continuous and radiate to the right iliac fossa, mimicking acute appendicitis. Nausea is common; approximately 15 to 25 percent of patients report vomiting
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diarrhea in about 15 percent of patients; infection with an organism containing plasmid pVir may be correlated with more severe invasive disease and higher likelihood of bloody diarrhea [6,7]. <span>Abdominal pain also may occur without diarrhea [8]. The pain may become continuous and radiate to the right iliac fossa, mimicking acute appendicitis. Nausea is common; approximately 15 to 25 percent of patients report vomiting. Diarrhea is self-limited and lasts for a mean of seven days [9,10]. Abdominal pain may persist after resolution of diarrhea, and weight loss of 5 kg or more may be observed. Organisms




#Campylobacter #Clinical #Clinique #Infection
Diarrhea is self-limited and lasts for a mean of seven days [9,10]. Abdominal pain may persist after resolution of diarrhea, and weight loss of 5 kg or more may be observed.
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ut diarrhea [8]. The pain may become continuous and radiate to the right iliac fossa, mimicking acute appendicitis. Nausea is common; approximately 15 to 25 percent of patients report vomiting. <span>Diarrhea is self-limited and lasts for a mean of seven days [9,10]. Abdominal pain may persist after resolution of diarrhea, and weight loss of 5 kg or more may be observed. Organisms may be excreted in the feces for several weeks after clinical recovery. One study reported a mean excretion period of 38 days [1]. Chronic carriage can occur in patients with




#Campylobacter #Clinical #Clinique #Infection
Organisms may be excreted in the feces for several weeks after clinical recovery. One study reported a mean excretion period of 38 days [ 1].
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ts report vomiting. Diarrhea is self-limited and lasts for a mean of seven days [9,10]. Abdominal pain may persist after resolution of diarrhea, and weight loss of 5 kg or more may be observed. <span>Organisms may be excreted in the feces for several weeks after clinical recovery. One study reported a mean excretion period of 38 days [1]. Chronic carriage can occur in patients with immune deficiency, although follow-up cultures are not necessary in the absence of clinical symptoms. Relapse may occur in 5 to 10 percent of




#Campylobacter #Clinical #Clinique #Infection
Chronic carriage can occur in patients with immune deficiency, although follow-up cultures are not necessary in the absence of clinical symptoms. Relapse may occur in 5 to 10 percent of patients
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ea, and weight loss of 5 kg or more may be observed. Organisms may be excreted in the feces for several weeks after clinical recovery. One study reported a mean excretion period of 38 days [1]. <span>Chronic carriage can occur in patients with immune deficiency, although follow-up cultures are not necessary in the absence of clinical symptoms. Relapse may occur in 5 to 10 percent of patients. The case fatality rate is low and most deaths occur in older adults or others with comorbid conditions [11-13]. Children — Clinical manifestations in children include diarrhea, fever,




#Campylobacter #Clinical #Clinique #Infection
The case fatality rate is low and most deaths occur in older adults or others with comorbid conditions [11-13]
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ronic carriage can occur in patients with immune deficiency, although follow-up cultures are not necessary in the absence of clinical symptoms. Relapse may occur in 5 to 10 percent of patients. <span>The case fatality rate is low and most deaths occur in older adults or others with comorbid conditions [11-13]. Children — Clinical manifestations in children include diarrhea, fever, abdominal pain, and vomiting. Bloody stools may be present in more than half of children. Fever tends to be pron




#Campylobacter #Clinical #Clinique #Infection
Clinical manifestations in children include diarrhea, fever, abdominal pain, and vomiting. Bloody stools may be present in more than half of children. Fever tends to be pronounced in children over one year of age and convulsions may occur.
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f clinical symptoms. Relapse may occur in 5 to 10 percent of patients. The case fatality rate is low and most deaths occur in older adults or others with comorbid conditions [11-13]. Children — <span>Clinical manifestations in children include diarrhea, fever, abdominal pain, and vomiting. Bloody stools may be present in more than half of children. Fever tends to be pronounced in children over one year of age and convulsions may occur. In a large milk-borne outbreak of Campylobacter enteritis affecting 2500 children, 9 were hospitalized with grand mal seizures [14]. The seizures arose prior to onset of diarrhea and th




#Campylobacter #Clinical #Clinique #Infection
In infants, vomiting and bloody stools are frequently observed; abdominal pain and fever are less common than in older children [16]. The presentation of bloody stools in the absence of diarrhea or fever can mimic intussusception.
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hospitalized with grand mal seizures [14]. The seizures arose prior to onset of diarrhea and their illnesses were unusually severe. Meningismus and encephalopathy have also been reported [15]. <span>In infants, vomiting and bloody stools are frequently observed; abdominal pain and fever are less common than in older children [16]. The presentation of bloody stools in the absence of diarrhea or fever can mimic intussusception. (See "Intussusception in children".) Among neonates with C. jejuni infection, grossly bloody stools or fever may be the only manifestations of infection. Neonatal infection is usually a




#Campylobacter #Clinical #Clinique #Infection
People with HIV — There is an increased incidence of Campylobacter infection in patients with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) [18,19]. Long-term carriage can occur, which can be associated with recurrent episodes of enteritis and bacteremia. Campylobacter infection in patients with HIV infection has been associated with severe, debilitating illness [19]. Antiretroviral therapy may reduce the risk of Campylobacter infection [20]
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e of birth from a mother who is excreting Campylobacter organism in her stools (with or without a history of recent diarrhea). Nosocomial infection in neonatal nurseries has been reported [17]. <span>People with HIV — There is an increased incidence of Campylobacter infection in patients with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) [18,19]. Long-term carriage can occur, which can be associated with recurrent episodes of enteritis and bacteremia. Campylobacter infection in patients with HIV infection has been associated with severe, debilitating illness [19]. Antiretroviral therapy may reduce the risk of Campylobacter infection [20]. Laboratory features — Transient bacteremia may be present in the early stages of infection. In the United States and Europe, bacteremia has been reported to occur in 0.1 to 1 percent o




#Campylobacter #Clinical #Clinique #Infection
Transient bacteremia may be present in the early stages of infection. In the United States and Europe, bacteremia has been reported to occur in 0.1 to 1 percent of Campylobacter cases [11,21-23]. Bacteremia appears to occur more frequently among immunosuppressed patients or those with other comorbidities [12,21,24], although a surveillance study in Finland noted that 53 of 76 cases of bacteremia (70 percent) occurred in patients without any underlying disease [22]
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tion in patients with HIV infection has been associated with severe, debilitating illness [19]. Antiretroviral therapy may reduce the risk of Campylobacter infection [20]. Laboratory features — <span>Transient bacteremia may be present in the early stages of infection. In the United States and Europe, bacteremia has been reported to occur in 0.1 to 1 percent of Campylobacter cases [11,21-23]. Bacteremia appears to occur more frequently among immunosuppressed patients or those with other comorbidities [12,21,24], although a surveillance study in Finland noted that 53 of 76 cases of bacteremia (70 percent) occurred in patients without any underlying disease [22]. A mild neutrophilic leukocytosis with bandemia is common [25]; although mild, transient leukopenia has also been reported [26]. Unique manifestations — Patients with Campylobacter infe




#Campylobacter #Clinical #Clinique #Infection
A mild neutrophilic leukocytosis with bandemia is common [25]; although mild, transient leukopenia has also been reported [26].
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hose with other comorbidities [12,21,24], although a surveillance study in Finland noted that 53 of 76 cases of bacteremia (70 percent) occurred in patients without any underlying disease [22]. <span>A mild neutrophilic leukocytosis with bandemia is common [25]; although mild, transient leukopenia has also been reported [26]. Unique manifestations — Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis). Pseudoappendiciti




#Campylobacter #Clinical #Clinique #Infection
Unique manifestations — Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis)
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ercent) occurred in patients without any underlying disease [22]. A mild neutrophilic leukocytosis with bandemia is common [25]; although mild, transient leukopenia has also been reported [26]. <span>Unique manifestations — Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis). Pseudoappendicitis — Severe abdominal pain prior to onset of diarrhea can mimic acute appendicitis. In some cases, diarrhea is absent (this is most frequently observed among children a




#Campylobacter #Clinical #Clinique #Infection
Severe abdominal pain prior to onset of diarrhea can mimic acute appendicitis. In some cases, diarrhea is absent (this is most frequently observed among children aged 6 to 15 years). The pain is caused by acute ileocecitis. On clinical examination, tenderness may be observed; rebound tenderness and guarding are usually absent.
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26]. Unique manifestations — Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis). Pseudoappendicitis — <span>Severe abdominal pain prior to onset of diarrhea can mimic acute appendicitis. In some cases, diarrhea is absent (this is most frequently observed among children aged 6 to 15 years). The pain is caused by acute ileocecitis. On clinical examination, tenderness may be observed; rebound tenderness and guarding are usually absent. Ultrasound or computed tomography examination may be useful for differentiating bacterial ileocecitis from acute appendicitis. In one series of 533 patients with suspected acute appendi




#Campylobacter #Clinical #Clinique #Infection
Campylobacter infection usually starts in the jejunum and ileum and progresses distally to affect the cecum and colon. However, some patients present with acute colitis and bloody diarrhea, which can mimic the acute colitis of inflammatory bowel disease (IBD) [29].
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acter infection has been found in up to 3 percent of inflamed appendices removed surgically [28]. Thus, Campylobacter-induced appendicitis is probably a real, though uncommon, entity. Colitis — <span>Campylobacter infection usually starts in the jejunum and ileum and progresses distally to affect the cecum and colon. However, some patients present with acute colitis and bloody diarrhea, which can mimic the acute colitis of inflammatory bowel disease (IBD) [29]. Histologic examination of the rectal or colonic mucosa in patients with Campylobacter colitis demonstrates acute inflammation without the chronic changes and crypt distortion usually se




#Campylobacter #Clinical #Clinique #Infection

Acute onset — Acute complications of Campylobacter enteritis include [5]:

● Cholecystitis, with or without preceding diarrhea [34].

● Peritonitis in patients on continuous ambulatory peritoneal dialysis, usually with preceding diarrhea [35,36].

● Rash (such as urticaria, erythema nodosum, vasculitis, cellulitis) [37].

● Osteomyelitis [24,38].

● Meningitis [39].

● Septic pseudoaneurysm [40].

● Pericarditis and myocarditis [41-44]. The typical clinical presentation involves acute chest pain, with electrocardiogram changes, and elevated levels of cardiac enzymes, in association with antecedent or coincident enteriti

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ng the possibility of an association between C. jejuni infection and lymphoma [33]. Additional investigation may lead to new insights into the pathogenesis of C. jejuni infection. Complications <span>Acute onset — Acute complications of Campylobacter enteritis include [5]: ●Cholecystitis, with or without preceding diarrhea [34]. ●Peritonitis in patients on continuous ambulatory peritoneal dialysis, usually with preceding diarrhea [35,36]. ●Rash (such as urticaria, erythema nodosum, vasculitis, cellulitis) [37]. ●Osteomyelitis [24,38]. ●Meningitis [39]. ●Septic pseudoaneurysm [40]. ●Pericarditis and myocarditis [41-44]. The typical clinical presentation involves acute chest pain, with electrocardiogram changes, and elevated levels of cardiac enzymes, in association with antecedent or coincident enteritis. Focal extraintestinal infections with C. jejuni and C. coli occur uncommonly, with or without preceding diarrhea. Examples include septic arthritis, bursitis, osteitis, soft tissue in




#Campylobacter #Clinical #Clinique #Infection
Focal extraintestinal infections with C. jejuni and C. coli occur uncommonly, with or without preceding diarrhea. Examples include septic arthritis, bursitis, osteitis, soft tissue infections, nodular skin eruptions [45], and fetal/placental infection [5]. Campylobacter abortion is also caused by Campylobacter fetus but is rarely associated with C. jejuni infection [46].
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44]. The typical clinical presentation involves acute chest pain, with electrocardiogram changes, and elevated levels of cardiac enzymes, in association with antecedent or coincident enteritis. <span>Focal extraintestinal infections with C. jejuni and C. coli occur uncommonly, with or without preceding diarrhea. Examples include septic arthritis, bursitis, osteitis, soft tissue infections, nodular skin eruptions [45], and fetal/placental infection [5]. Campylobacter abortion is also caused by Campylobacter fetus but is rarely associated with C. jejuni infection [46]. (See "Infection with less common Campylobacter species and related bacteria".) Late onset — There are two major late onset complications of Campylobacter infection: reactive arthritis a




#Campylobacter #Clinical #Clinique #Infection
Late onset — There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS).
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mpylobacter abortion is also caused by Campylobacter fetus but is rarely associated with C. jejuni infection [46]. (See "Infection with less common Campylobacter species and related bacteria".) <span>Late onset — There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS). Reactive arthritis — The reactive arthritis associated with Campylobacter enteritis is similar to arthritis that can occur following Salmonella, Shigella, and other bacterial diarrheal




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The reactive arthritis associated with Campylobacter enteritis is similar to arthritis that can occur following Salmonella, Shigella, and other bacterial diarrheal infections.
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species and related bacteria".) Late onset — There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS). Reactive arthritis — <span>The reactive arthritis associated with Campylobacter enteritis is similar to arthritis that can occur following Salmonella, Shigella, and other bacterial diarrheal infections. The rate of reactive arthritis is fairly low (up to 2.6 percent) [5,47-49], although the prevalence of joint symptoms may be as high as 9 to 13 percent [50,51]. The likelihood of develo




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The rate of reactive arthritis is fairly low (up to 2.6 percent) [ 5,47-49], although the prevalence of joint symptoms may be as high as 9 to 13 percent [50,51].
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ctive arthritis — The reactive arthritis associated with Campylobacter enteritis is similar to arthritis that can occur following Salmonella, Shigella, and other bacterial diarrheal infections. <span>The rate of reactive arthritis is fairly low (up to 2.6 percent) [5,47-49], although the prevalence of joint symptoms may be as high as 9 to 13 percent [50,51]. The likelihood of developing reactive arthritis following C. jejuni infection appears to be unrelated to the severity of diarrheal illness [52]. Reactive arthritis occurs more commonly




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The likelihood of developing reactive arthritis following C. jejuni infection appears to be unrelated to the severity of diarrheal illness [52]. Reactive arthritis occurs more commonly among patients with the HLA-B27 phenotype
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bacterial diarrheal infections. The rate of reactive arthritis is fairly low (up to 2.6 percent) [5,47-49], although the prevalence of joint symptoms may be as high as 9 to 13 percent [50,51]. <span>The likelihood of developing reactive arthritis following C. jejuni infection appears to be unrelated to the severity of diarrheal illness [52]. Reactive arthritis occurs more commonly among patients with the HLA-B27 phenotype. Joint pain and swelling typically appear one to two weeks (or occasionally several weeks) after the onset of diarrhea. Symptoms may mimic septic arthritis [53]. The ankles, knees, wris




#Campylobacter #Clinical #Clinique #Infection
Joint pain and swelling typically appear one to two weeks (or occasionally several weeks) after the onset of diarrhea. Symptoms may mimic septic arthritis [53]. The ankles, knees, wrists, and small joints of the hands are most frequently affected, often with considerable incapacity [54]. The duration of arthritis ranges from one week to several months. The prognosis is usually good; most patients remit spontaneously or with NSAID therapy within six months of onset. (See "Reactive arthritis".)
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ive arthritis following C. jejuni infection appears to be unrelated to the severity of diarrheal illness [52]. Reactive arthritis occurs more commonly among patients with the HLA-B27 phenotype. <span>Joint pain and swelling typically appear one to two weeks (or occasionally several weeks) after the onset of diarrhea. Symptoms may mimic septic arthritis [53]. The ankles, knees, wrists, and small joints of the hands are most frequently affected, often with considerable incapacity [54]. The duration of arthritis ranges from one week to several months. The prognosis is usually good; most patients remit spontaneously or with NSAID therapy within six months of onset. (See "Reactive arthritis".) Guillain-Barré syndrome — C. jejuni infection has been established as a trigger of GBS, an acute immune-mediated polyneuropathy [55,56]. It has been estimated that 30 to 40 percent of G




#Campylobacter #Clinical #Clinique #Infection
C. jejuni infection has been established as a trigger of GBS, an acute immune-mediated polyneuropathy [55,56]. It has been estimated that 30 to 40 percent of GBS illness is attributable to Campylobacter infection, which typically occurs between one and two weeks before the onset of neurologic symptoms [56]. In resource-limited settings, the proportion of GBS cases preceded by Campylobacter infection may be even higher [57]
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week to several months. The prognosis is usually good; most patients remit spontaneously or with NSAID therapy within six months of onset. (See "Reactive arthritis".) Guillain-Barré syndrome — <span>C. jejuni infection has been established as a trigger of GBS, an acute immune-mediated polyneuropathy [55,56]. It has been estimated that 30 to 40 percent of GBS illness is attributable to Campylobacter infection, which typically occurs between one and two weeks before the onset of neurologic symptoms [56]. In resource-limited settings, the proportion of GBS cases preceded by Campylobacter infection may be even higher [57]. Campylobacter-associated GBS is more likely to be associated with the axonal form of GBS (as opposed to the demyelinating form). GBS occurring after infection with C. jejuni has a wors




#Campylobacter #Clinical #Clinique #Infection
Campylobacter-associated GBS is more likely to be associated with the axonal form of GBS (as opposed to the demyelinating form). GBS occurring after infection with C. jejuni has a worse prognosis than other forms of GBS; recovery is slower, and the likelihood of residual neurologic disability is greater than with other forms of GBS [58].
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rs between one and two weeks before the onset of neurologic symptoms [56]. In resource-limited settings, the proportion of GBS cases preceded by Campylobacter infection may be even higher [57]. <span>Campylobacter-associated GBS is more likely to be associated with the axonal form of GBS (as opposed to the demyelinating form). GBS occurring after infection with C. jejuni has a worse prognosis than other forms of GBS; recovery is slower, and the likelihood of residual neurologic disability is greater than with other forms of GBS [58]. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis" and "Guillain-Barré syndrome in adults: Treatment and prognosis".) The risk for developing GBS d




#Campylobacter #Clinical #Clinique #Infection
The risk for developing GBS during the two months following a symptomatic episode of C. jejuni infection is approximately 100-fold higher than the risk of developing GBS in the general population [59,60]. In the United States, about 1 in 1000 patients with Campylobacter enteritis develops GBS [56]. Subclinical cases of Campylobacter infection can also trigger GBS [61].
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er than with other forms of GBS [58]. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis" and "Guillain-Barré syndrome in adults: Treatment and prognosis".) <span>The risk for developing GBS during the two months following a symptomatic episode of C. jejuni infection is approximately 100-fold higher than the risk of developing GBS in the general population [59,60]. In the United States, about 1 in 1000 patients with Campylobacter enteritis develops GBS [56]. Subclinical cases of Campylobacter infection can also trigger GBS [61]. GBS associated with C. jejuni infection is likely caused by antibodies formed in response to epitopes expressed by the infecting Campylobacter strain that are cross-reactive to GM1 gang




#Campylobacter #Clinical #Clinique #Infection
GBS associated with C. jejuni infection is likely caused by antibodies formed in response to epitopes expressed by the infecting Campylobacter strain that are cross-reactive to GM1 ganglioside (present in high concentrations in peripheral nerve myelin) [62-64]. Many Campylobacter strains isolated from patients with GBS belong to specific serotypes, notably Penner O19 and 041 strains [65-67].
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eneral population [59,60]. In the United States, about 1 in 1000 patients with Campylobacter enteritis develops GBS [56]. Subclinical cases of Campylobacter infection can also trigger GBS [61]. <span>GBS associated with C. jejuni infection is likely caused by antibodies formed in response to epitopes expressed by the infecting Campylobacter strain that are cross-reactive to GM1 ganglioside (present in high concentrations in peripheral nerve myelin) [62-64]. Many Campylobacter strains isolated from patients with GBS belong to specific serotypes, notably Penner O19 and 041 strains [65-67]. The production of antibodies to GM1 ganglioside may also occur due to mechanisms other than molecular mimicry [55], and many patients with Campylobacter infection form these antibodies




#Campylobacter #Clinical #Clinique #Infection
The production of antibodies to GM1 ganglioside may also occur due to mechanisms other than molecular mimicry [55], and many patients with Campylobacter infection form these antibodies in the absence of neurologic symptoms [62].
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in high concentrations in peripheral nerve myelin) [62-64]. Many Campylobacter strains isolated from patients with GBS belong to specific serotypes, notably Penner O19 and 041 strains [65-67]. <span>The production of antibodies to GM1 ganglioside may also occur due to mechanisms other than molecular mimicry [55], and many patients with Campylobacter infection form these antibodies in the absence of neurologic symptoms [62]. Some studies have suggested there may be an association between certain HLA types and the likelihood of developing GBS following C. jejuni infection [37,68,69]. Others have been unable




#Campylobacter #Clinical #Clinique #Infection
Some studies have suggested there may be an association between certain HLA types and the likelihood of developing GBS following C. jejuni infection [37,68,69]. Others have been unable to confirm this association [70]
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ganglioside may also occur due to mechanisms other than molecular mimicry [55], and many patients with Campylobacter infection form these antibodies in the absence of neurologic symptoms [62]. <span>Some studies have suggested there may be an association between certain HLA types and the likelihood of developing GBS following C. jejuni infection [37,68,69]. Others have been unable to confirm this association [70]. The Miller-Fisher variant of GBS, in which the cranial nerves are more prominently affected, has also been associated with Campylobacter infection. Cross-reacting antibodies to GQ1b ga




#Campylobacter #Clinical #Clinique #Infection
The Miller-Fisher variant of GBS, in which the cranial nerves are more prominently affected, has also been associated with Campylobacter infection. Cross-reacting antibodies to GQ1b ganglioside (which is present in cranial nerve myelin) have been observed in these cases [55]. The most common serotype observed in C. jejuni-associated Miller-Fisher syndrome is Penner O2 [71]
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ed there may be an association between certain HLA types and the likelihood of developing GBS following C. jejuni infection [37,68,69]. Others have been unable to confirm this association [70]. <span>The Miller-Fisher variant of GBS, in which the cranial nerves are more prominently affected, has also been associated with Campylobacter infection. Cross-reacting antibodies to GQ1b ganglioside (which is present in cranial nerve myelin) have been observed in these cases [55]. The most common serotype observed in C. jejuni-associated Miller-Fisher syndrome is Penner O2 [71]. DIAGNOSIS Clinical suspicion — Campylobacter enteritis should be suspected in the setting of severe abdominal pain with diarrhea. In particular, the following exposures or circumstance




#Campylobacter #Clinical #Clinique #Infection

Campylobacter enteritis should be suspected in the setting of severe abdominal pain with diarrhea. In particular, the following exposures or circumstances should prompt consideration of Campylobacter infection [72]:

● Diarrheal illness in the setting of a foodborne outbreak

● Consumption of raw or undercooked poultry

● Consumption of unpasteurized dairy products

● Travel to resource-limited settings

● Swimming in untreated freshwater

● House pet with diarrhea

● Other animal contact (eg, farm or petting zoo)

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cranial nerve myelin) have been observed in these cases [55]. The most common serotype observed in C. jejuni-associated Miller-Fisher syndrome is Penner O2 [71]. DIAGNOSIS Clinical suspicion — <span>Campylobacter enteritis should be suspected in the setting of severe abdominal pain with diarrhea. In particular, the following exposures or circumstances should prompt consideration of Campylobacter infection [72]: ●Diarrheal illness in the setting of a foodborne outbreak ●Consumption of raw or undercooked poultry ●Consumption of unpasteurized dairy products ●Travel to resource-limited settings ●Swimming in untreated freshwater ●House pet with diarrhea ●Other animal contact (eg, farm or petting zoo) Microbiologic diagnosis of acute disease — The diagnosis is established by stool culture (or, in cases complicated by bacteremia, by blood culture) or by culture-independent assays, suc




#Campylobacter #Clinical #Clinique #Infection
The diagnosis is established by stool culture (or, in cases complicated by bacteremia, by blood culture) or by culture-independent assays, such as molecular testing, on stool
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oducts ●Travel to resource-limited settings ●Swimming in untreated freshwater ●House pet with diarrhea ●Other animal contact (eg, farm or petting zoo) Microbiologic diagnosis of acute disease — <span>The diagnosis is established by stool culture (or, in cases complicated by bacteremia, by blood culture) or by culture-independent assays, such as molecular testing, on stool. ●Culture – Stool culture technique consists of plating on Campylobacter-selective media and incubation in a gas mixture of 5 to 10 percent oxygen, 1 to 10 percent carbon dioxide, and i




#Campylobacter #Diagnosis #Diagnostic #Infection
Culture – Stool culture technique consists of plating on Campylobacter-selective media and incubation in a gas mixture of 5 to 10 percent oxygen, 1 to 10 percent carbon dioxide, and ideally some hydrogen (picture 1). Campylobacter have a characteristic appearance under the microscope, as curved rods that sometimes have a gull-wing formation when located end to end. Campylobacters can also take on a spiral shape. Its characteristic morphology, together with detection of oxidase and catalase positivity, is sufficient for diagnosis
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acute disease — The diagnosis is established by stool culture (or, in cases complicated by bacteremia, by blood culture) or by culture-independent assays, such as molecular testing, on stool. ●<span>Culture – Stool culture technique consists of plating on Campylobacter-selective media and incubation in a gas mixture of 5 to 10 percent oxygen, 1 to 10 percent carbon dioxide, and ideally some hydrogen (picture 1). Campylobacter have a characteristic appearance under the microscope, as curved rods that sometimes have a gull-wing formation when located end to end. Campylobacters can also take on a spiral shape. Its characteristic morphology, together with detection of oxidase and catalase positivity, is sufficient for diagnosis. ●Culture-independent assays – Use of culture-independent techniques, such as nucleic acid amplification tests (NAAT), including reverse transcription-polymerase chain reaction (RT-PCR)




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NAATs are far more sensitive than culture, yielding rates of Campylobacter recovery in stool that are 20 to 40 percent higher [73] but have significant drawbacks.
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ys – Use of culture-independent techniques, such as nucleic acid amplification tests (NAAT), including reverse transcription-polymerase chain reaction (RT-PCR), has been rapidly expanding [72]. <span>NAATs are far more sensitive than culture, yielding rates of Campylobacter recovery in stool that are 20 to 40 percent higher [73] but have significant drawbacks. These techniques detect bacterial deoxynucleic acid (DNA), not viable organisms, and positive tests must therefore be interpreted with a high degree of clinical correlation. A further d




#Campylobacter #Diagnosis #Diagnostic #Infection
These techniques detect bacterial deoxynucleic acid (DNA), not viable organisms, and positive tests must therefore be interpreted with a high degree of clinical correlation. A further drawback of culture-independent techniques is that they impede outbreak detection and investigation; enhanced surveillance by using traditional cultures supplemented by molecular subtyping has resulted in the prevention of thousands of illnesses in the past
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s been rapidly expanding [72]. NAATs are far more sensitive than culture, yielding rates of Campylobacter recovery in stool that are 20 to 40 percent higher [73] but have significant drawbacks. <span>These techniques detect bacterial deoxynucleic acid (DNA), not viable organisms, and positive tests must therefore be interpreted with a high degree of clinical correlation. A further drawback of culture-independent techniques is that they impede outbreak detection and investigation; enhanced surveillance by using traditional cultures supplemented by molecular subtyping has resulted in the prevention of thousands of illnesses in the past. Furthermore, for the individual patient, use of culture-independent diagnostic technologies fails to provide information about antimicrobial susceptibility to guide management. Many cl




#Campylobacter #Diagnosis #Diagnostic #Infection
Furthermore, for the individual patient, use of culture-independent diagnostic technologies fails to provide information about antimicrobial susceptibility to guide management. Many clinical laboratories have adopted DNA-based syndromic panels, which often do not routinely reflex to stool cultures [ 74].
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tbreak detection and investigation; enhanced surveillance by using traditional cultures supplemented by molecular subtyping has resulted in the prevention of thousands of illnesses in the past. <span>Furthermore, for the individual patient, use of culture-independent diagnostic technologies fails to provide information about antimicrobial susceptibility to guide management. Many clinical laboratories have adopted DNA-based syndromic panels, which often do not routinely reflex to stool cultures [74]. (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection", section on 'Detection in the laboratory'.) It is customary for laboratories to report the presence of "Ca




#Campylobacter #Diagnosis #Diagnostic #Infection
It is customary for laboratories to report the presence of "Campylobacter" or "C. jejuni" without differentiating C. jejuni from C. coli. This is acceptable for routine diagnostic purposes since the distinction is of no clinical consequence, but speciation and strain identification is sometimes needed for epidemiological purposes.
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ic panels, which often do not routinely reflex to stool cultures [74]. (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection", section on 'Detection in the laboratory'.) <span>It is customary for laboratories to report the presence of "Campylobacter" or "C. jejuni" without differentiating C. jejuni from C. coli. This is acceptable for routine diagnostic purposes since the distinction is of no clinical consequence, but speciation and strain identification is sometimes needed for epidemiological purposes. (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection".) In rare cases of acute colitis or suspected appendicitis in which a rapid diagnosis is needed for clinic




#Campylobacter #Diagnosis #Diagnostic #Infection
C. jejuni appear as faint, gram-negative curved rods (picture 2).
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ion using dark-field, phase-contrast, and stained smears. This technique is less sensitive than culture (50 versus 94 percent) and is not practiced routinely. Gram stain is even less sensitive. <span>C. jejuni appear as faint, gram-negative curved rods (picture 2). (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection", section on 'Detection in the laboratory'.) Late-onset complications — Patients with late onset reactive a




#Campylobacter #Diagnosis #Diagnostic #Infection
In rare cases of acute colitis or suspected appendicitis in which a rapid diagnosis is needed for clinical management, presumptive identification is possible by stool microscopic examination using dark-field, phase-contrast, and stained smears. This technique is less sensitive than culture (50 versus 94 percent) and is not practiced routinely.
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clinical consequence, but speciation and strain identification is sometimes needed for epidemiological purposes. (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection".) <span>In rare cases of acute colitis or suspected appendicitis in which a rapid diagnosis is needed for clinical management, presumptive identification is possible by stool microscopic examination using dark-field, phase-contrast, and stained smears. This technique is less sensitive than culture (50 versus 94 percent) and is not practiced routinely. Gram stain is even less sensitive. C. jejuni appear as faint, gram-negative curved rods (picture 2). (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection", sect




#Campylobacter #Diagnosis #Diagnostic #Infection
Patients with late onset reactive arthritis or Guillain-Barré syndrome (GBS) may have negative stool studies. Serologic tests can be used to detect recent Campylobacter infection in these patients. In one study, a complement fixation test (using whole-cell antigens) had greatest sensitivity compared with enzyme-linked immunosorbent assay (ELISA) and other tests [75].
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int, gram-negative curved rods (picture 2). (See "Microbiology, pathogenesis, and epidemiology of Campylobacter infection", section on 'Detection in the laboratory'.) Late-onset complications — <span>Patients with late onset reactive arthritis or Guillain-Barré syndrome (GBS) may have negative stool studies. Serologic tests can be used to detect recent Campylobacter infection in these patients. In one study, a complement fixation test (using whole-cell antigens) had greatest sensitivity compared with enzyme-linked immunosorbent assay (ELISA) and other tests [75]. In general, these tests are available only in reference laboratories. Whole genome sequencing of Campylobacter isolates may be available in the future for use in outbreak investigations




#Campylobacter #Infection #Traitement #Treatment
Campylobacter infection is usually a mild, self-limited infection. The estimated mortality from symptomatic infection in the United States is 2.4 per 1000 culture-confirmed cases [77,78].
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enome sequencing of Campylobacter isolates may be available in the future for use in outbreak investigations and in further characterizing the epidemiology of these infections [76]. TREATMENT — <span>Campylobacter infection is usually a mild, self-limited infection. The estimated mortality from symptomatic infection in the United States is 2.4 per 1000 culture-confirmed cases [77,78]. Maintenance of proper hydration and correction of electrolyte abnormalities should be the focus of therapy. Antibiotics are not needed for most cases of C. jejuni gastroenteritis. In ge




#Campylobacter #Infection #Traitement #Treatment
Maintenance of proper hydration and correction of electrolyte abnormalities should be the focus of therapy. Antibiotics are not needed for most cases of C. jejuni gastroenteritis
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ENT — Campylobacter infection is usually a mild, self-limited infection. The estimated mortality from symptomatic infection in the United States is 2.4 per 1000 culture-confirmed cases [77,78]. <span>Maintenance of proper hydration and correction of electrolyte abnormalities should be the focus of therapy. Antibiotics are not needed for most cases of C. jejuni gastroenteritis. In general, antimotility agents such as loperamide should be avoided, especially if the patient is febrile. (See "Approach to the adult with acute diarrhea in resource-rich settings",




#Campylobacter #Infection #Traitement #Treatment
In general, antimotility agents such as loperamide should be avoided, especially if the patient is febrile.
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ases [77,78]. Maintenance of proper hydration and correction of electrolyte abnormalities should be the focus of therapy. Antibiotics are not needed for most cases of C. jejuni gastroenteritis. <span>In general, antimotility agents such as loperamide should be avoided, especially if the patient is febrile. (See "Approach to the adult with acute diarrhea in resource-rich settings", section on 'Symptomatic therapy'.) Antimicrobial therapy Indications — The efficacy of antimicrobial therapy




#Campylobacter #Infection #Traitement #Treatment
The efficacy of antimicrobial therapy for Campylobacter infection has been addressed in a small number of randomized trials. A meta-analysis of 11 small randomized trials noted that antimicrobial therapy reduced the duration of intestinal symptoms by only 1.3 days (95% CI 0.6-2.0 days) [79]. There was a nonsignificant trend toward greater benefit for patients treated within the first three days of illness.
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avoided, especially if the patient is febrile. (See "Approach to the adult with acute diarrhea in resource-rich settings", section on 'Symptomatic therapy'.) Antimicrobial therapy Indications — <span>The efficacy of antimicrobial therapy for Campylobacter infection has been addressed in a small number of randomized trials. A meta-analysis of 11 small randomized trials noted that antimicrobial therapy reduced the duration of intestinal symptoms by only 1.3 days (95% CI 0.6-2.0 days) [79]. There was a nonsignificant trend toward greater benefit for patients treated within the first three days of illness. Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with severe disease or




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Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with severe disease or risk for severe disease. Patients with severe disease include individuals with bloody stools, high fever, extraintestinal infection, worsening or relapsing symptoms, or symptoms lasting longer than one week [77]. Those at risk for severe disease include patients who are older, pregnant, or immunocompromised [80]
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duration of intestinal symptoms by only 1.3 days (95% CI 0.6-2.0 days) [79]. There was a nonsignificant trend toward greater benefit for patients treated within the first three days of illness. <span>Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with severe disease or risk for severe disease. Patients with severe disease include individuals with bloody stools, high fever, extraintestinal infection, worsening or relapsing symptoms, or symptoms lasting longer than one week [77]. Those at risk for severe disease include patients who are older, pregnant, or immunocompromised [80]. Choice of drug — We suggest azithromycin for treatment of Campylobacter gastroenteritis, when indicated. Fluoroquinolones are an alternative option. Although both azithromycin and fluo




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We suggest azithromycin for treatment of Campylobacter gastroenteritis, when indicated. Fluoroquinolones are an alternative option. Although both azithromycin and fluoroquinolones are highly effective against susceptible isolates, rates of resistance to fluoroquinolones are increasing worldwide and generally exceed those for azithromycin [81-84]. (See 'Resistance' below.)
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ning or relapsing symptoms, or symptoms lasting longer than one week [77]. Those at risk for severe disease include patients who are older, pregnant, or immunocompromised [80]. Choice of drug — <span>We suggest azithromycin for treatment of Campylobacter gastroenteritis, when indicated. Fluoroquinolones are an alternative option. Although both azithromycin and fluoroquinolones are highly effective against susceptible isolates, rates of resistance to fluoroquinolones are increasing worldwide and generally exceed those for azithromycin [81-84]. (See 'Resistance' below.) In patients with uncomplicated Campylobacter infection at risk for severe disease, the dose of azithromycin is 500 mg orally daily for three days or until signs and symptoms of disease




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In patients with uncomplicated Campylobacter infection at risk for severe disease, the dose of azithromycin is 500 mg orally daily for three days or until signs and symptoms of disease have improved. A single 1 g oral dose of azithromycin may be equally effective, and is more convenient, but can be associated with gastrointestinal upset; giving it as two divided doses on the same day may limit nausea.
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re highly effective against susceptible isolates, rates of resistance to fluoroquinolones are increasing worldwide and generally exceed those for azithromycin [81-84]. (See 'Resistance' below.) <span>In patients with uncomplicated Campylobacter infection at risk for severe disease, the dose of azithromycin is 500 mg orally daily for three days or until signs and symptoms of disease have improved. A single 1 g oral dose of azithromycin may be equally effective, and is more convenient, but can be associated with gastrointestinal upset; giving it as two divided doses on the same day may limit nausea. Fluoroquinolone doses for uncomplicated infection are levofloxacin 750 mg orally daily or ciprofloxacin 750 mg orally twice daily, each for three days or until signs and symptoms of dis




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Fluoroquinolone doses for uncomplicated infection are levofloxacin 750 mg orally daily or ciprofloxacin 750 mg orally twice daily, each for three days or until signs and symptoms of disease have improved.
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g oral dose of azithromycin may be equally effective, and is more convenient, but can be associated with gastrointestinal upset; giving it as two divided doses on the same day may limit nausea. <span>Fluoroquinolone doses for uncomplicated infection are levofloxacin 750 mg orally daily or ciprofloxacin 750 mg orally twice daily, each for three days or until signs and symptoms of disease have improved. For those with complications or underlying immunosuppression, a longer course (7 to 14 days) of antibiotics may be warranted. For patients who are severely ill and cannot tolerate oral




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For those with complications or underlying immunosuppression, a longer course (7 to 14 days) of antibiotics may be warranted. For patients who are severely ill and cannot tolerate oral therapy, carbapenems are appropriate empiric therapy, but susceptibility testing should be performed to confirm that they are active. For those with life-threatening infections, the addition of an aminoglycoside to the regimen is reasonable.
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lone doses for uncomplicated infection are levofloxacin 750 mg orally daily or ciprofloxacin 750 mg orally twice daily, each for three days or until signs and symptoms of disease have improved. <span>For those with complications or underlying immunosuppression, a longer course (7 to 14 days) of antibiotics may be warranted. For patients who are severely ill and cannot tolerate oral therapy, carbapenems are appropriate empiric therapy, but susceptibility testing should be performed to confirm that they are active. For those with life-threatening infections, the addition of an aminoglycoside to the regimen is reasonable. C. jejuni and C. coli are usually sensitive to macrolides, fluoroquinolones, carbapenems, and aminoglycosides [85]; they are also typically sensitive in vitro to clindamycin, tetracycli




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C. jejuni and C. coli are usually sensitive to macrolides, fluoroquinolones, carbapenems, and aminoglycosides [85]; they are also typically sensitive in vitro to clindamycin, tetracyclines, and chloramphenicol, although there are no data indicating clinical efficacy of these agents
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rapy, but susceptibility testing should be performed to confirm that they are active. For those with life-threatening infections, the addition of an aminoglycoside to the regimen is reasonable. <span>C. jejuni and C. coli are usually sensitive to macrolides, fluoroquinolones, carbapenems, and aminoglycosides [85]; they are also typically sensitive in vitro to clindamycin, tetracyclines, and chloramphenicol, although there are no data indicating clinical efficacy of these agents. However, resistance to fluoroquinolones and macrolides has been described. C. jejuni and C. coli are inherently resistant to trimethoprim and beta-lactam antibiotics, including penicil




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However, resistance to fluoroquinolones and macrolides has been described. C. jejuni and C. coli are inherently resistant to trimethoprim and beta-lactam antibiotics, including penicillin and most cephalosporins [86]. A few case reports have suggested Campylobacter may be effectively treated with fosfomycin, however laboratory studies to confirm susceptibility have not been done [87]
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and aminoglycosides [85]; they are also typically sensitive in vitro to clindamycin, tetracyclines, and chloramphenicol, although there are no data indicating clinical efficacy of these agents. <span>However, resistance to fluoroquinolones and macrolides has been described. C. jejuni and C. coli are inherently resistant to trimethoprim and beta-lactam antibiotics, including penicillin and most cephalosporins [86]. A few case reports have suggested Campylobacter may be effectively treated with fosfomycin, however laboratory studies to confirm susceptibility have not been done [87]. Resistance — The rate of macrolide-resistance among Campylobacter has remained stable at <5 percent in most parts of the world [88-91]. However, in some parts of the world, such as




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The rate of macrolide-resistance among Campylobacter has remained stable at <5 percent in most parts of the world [88-91]. However, in some parts of the world, such as in Thailand and in Ireland, the macrolide-resistance rate is higher [92,93].
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rins [86]. A few case reports have suggested Campylobacter may be effectively treated with fosfomycin, however laboratory studies to confirm susceptibility have not been done [87]. Resistance — <span>The rate of macrolide-resistance among Campylobacter has remained stable at <5 percent in most parts of the world [88-91]. However, in some parts of the world, such as in Thailand and in Ireland, the macrolide-resistance rate is higher [92,93]. Despite an increase in macrolide resistance, macrolides are usually still effective in these areas. Drug susceptibility testing should be performed on isolates from patients failing the




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Drug susceptibility testing should be performed on isolates from patients failing therapy.
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e world, such as in Thailand and in Ireland, the macrolide-resistance rate is higher [92,93]. Despite an increase in macrolide resistance, macrolides are usually still effective in these areas. <span>Drug susceptibility testing should be performed on isolates from patients failing therapy. The prevalence of fluoroquinolone-resistant Campylobacter is rising. Fluoroquinolone-resistant Campylobacter is particularly prevalent in Southeast Asia, where resistance rates have bee




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The prevalence of fluoroquinolone-resistant Campylobacter is rising. Fluoroquinolone-resistant Campylobacter is particularly prevalent in Southeast Asia, where resistance rates have been reported to exceed 80 percent [92,94]. Resistance rates of greater than 50 percent have been reported in Spain, Hungary, Iran, and several resource-limited countries [95,96].
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]. Despite an increase in macrolide resistance, macrolides are usually still effective in these areas. Drug susceptibility testing should be performed on isolates from patients failing therapy. <span>The prevalence of fluoroquinolone-resistant Campylobacter is rising. Fluoroquinolone-resistant Campylobacter is particularly prevalent in Southeast Asia, where resistance rates have been reported to exceed 80 percent [92,94]. Resistance rates of greater than 50 percent have been reported in Spain, Hungary, Iran, and several resource-limited countries [95,96]. Consideration of fluoroquinolone resistance is particularly important in the setting of significant diarrhea following foreign travel and/or after failed empiric treatment with a fluoro




#Campylobacter #Infection #Traitement #Treatment
Consideration of fluoroquinolone resistance is particularly important in the setting of significant diarrhea following foreign travel and/or after failed empiric treatment with a fluoroquinolone [ 97,98].
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ce rates have been reported to exceed 80 percent [92,94]. Resistance rates of greater than 50 percent have been reported in Spain, Hungary, Iran, and several resource-limited countries [95,96]. <span>Consideration of fluoroquinolone resistance is particularly important in the setting of significant diarrhea following foreign travel and/or after failed empiric treatment with a fluoroquinolone [97,98]. The rate of resistance to fluoroquinolones is also increasing in the United States. In 1989, the rate of ciprofloxacin was 0 percent; between 2005 and 2014, it ranged from 20 to 27 perc




#Campylobacter #Infection #Traitement #Treatment
The rate of resistance to fluoroquinolones is also increasing in the United States. In 1989, the rate of ciprofloxacin was 0 percent; between 2005 and 2014, it ranged from 20 to 27 percent [88,91]. Parallels in fluoroquinolone resistance have been observed between human isolates and strains isolated from poultry, reflecting the use of fluoroquinolones in food animals in the United States since 1995 [90,97,99-101].
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ion of fluoroquinolone resistance is particularly important in the setting of significant diarrhea following foreign travel and/or after failed empiric treatment with a fluoroquinolone [97,98]. <span>The rate of resistance to fluoroquinolones is also increasing in the United States. In 1989, the rate of ciprofloxacin was 0 percent; between 2005 and 2014, it ranged from 20 to 27 percent [88,91]. Parallels in fluoroquinolone resistance have been observed between human isolates and strains isolated from poultry, reflecting the use of fluoroquinolones in food animals in the United States since 1995 [90,97,99-101]. In one study, ciprofloxacin-resistant Campylobacter was isolated from 10 percent of 180 chicken products from grocery stores in three states [88]. Molecular subtyping has confirmed the




#Campylobacter #Infection #Traitement #Treatment
Interruption of transmission from poultry is a major factor in preventing human Campylobacter infection. Chicken should be cooked thoroughly. Utensils, cutting boards, and other items used in preparation of raw poultry should be washed thoroughly. Avoidance of unpasteurized dairy products is also an important preventive measure [103]
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lobacter species are likely to persist due to continued circulation of such organisms in poultry flocks and from acquisition of quinolone-resistant infection during foreign travel. Prevention — <span>Interruption of transmission from poultry is a major factor in preventing human Campylobacter infection. Chicken should be cooked thoroughly. Utensils, cutting boards, and other items used in preparation of raw poultry should be washed thoroughly. Avoidance of unpasteurized dairy products is also an important preventive measure [103]. Previous infection with Campylobacter is not necessarily protective of future symptomatic infections [104]. Thus, patients who have previously experienced symptomatic infections should




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Previous infection with Campylobacter is not necessarily protective of future symptomatic infections [104]. Thus, patients who have previously experienced symptomatic infections should also be advised to take such precautions
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tensils, cutting boards, and other items used in preparation of raw poultry should be washed thoroughly. Avoidance of unpasteurized dairy products is also an important preventive measure [103]. <span>Previous infection with Campylobacter is not necessarily protective of future symptomatic infections [104]. Thus, patients who have previously experienced symptomatic infections should also be advised to take such precautions. Adults with Campylobacter enteritis do not require special isolation; standard precautions are sufficient. Nosocomial infection in neonatal nurseries has been described. Infants and yo




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Adults with Campylobacter enteritis do not require special isolation; standard precautions are sufficient. Nosocomial infection in neonatal nurseries has been described. Infants and younger children in diapers with C. jejuni enteritis should be excluded from routine childcare centers until diarrhea has resolved.
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cter is not necessarily protective of future symptomatic infections [104]. Thus, patients who have previously experienced symptomatic infections should also be advised to take such precautions. <span>Adults with Campylobacter enteritis do not require special isolation; standard precautions are sufficient. Nosocomial infection in neonatal nurseries has been described. Infants and younger children in diapers with C. jejuni enteritis should be excluded from routine childcare centers until diarrhea has resolved. (See 'Children' above.) Individuals with an acute diarrheal illness should not prepare or handle food until symptoms have resolved. Antibiotic prophylaxis is occasionally used in select




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Individuals with an acute diarrheal illness should not prepare or handle food until symptoms have resolved
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eries has been described. Infants and younger children in diapers with C. jejuni enteritis should be excluded from routine childcare centers until diarrhea has resolved. (See 'Children' above.) <span>Individuals with an acute diarrheal illness should not prepare or handle food until symptoms have resolved. Antibiotic prophylaxis is occasionally used in select high-risk travelers to prevent diarrhea. However, rifaximin, the agent recommended if antibiotic prophylaxis is given, is not effe




#Campylobacter #Infection #Traitement #Treatment
For patients with severe disease or risk for severe disease, we suggest treatment with azithromycin (Grade 2C). A fluoroquinolone is an alternative, but susceptibility should be confirmed.
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on of electrolyte abnormalities should be the focus of therapy. Antibiotics are not needed for most cases of C. jejuni gastroenteritis. (See 'Treatment' above.) •Role of antimicrobial therapy − <span>For patients with severe disease or risk for severe disease, we suggest treatment with azithromycin (Grade 2C). A fluoroquinolone is an alternative, but susceptibility should be confirmed. For uncomplicated infections in patients at risk for severe disease, we typically use azithromycin 500 mg orally daily for three days or until signs and symptoms of disease have improve




#Campylobacter #Infection #Traitement #Treatment
Campylobacter resistance to macrolides and fluoroquinolones has been described. The rate of macrolide resistance among Campylobacter has remained stable at <5 percent in most parts of the world; the prevalence of fluoroquinolone-resistant Campylobacter is rising in many areas, particularly in Southeast Asia.
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d symptoms of disease have improved. For patients who cannot tolerate oral therapy, a carbapenem or an aminoglycoside are appropriate options. (See 'Antimicrobial therapy' above.) •Resistance − <span>Campylobacter resistance to macrolides and fluoroquinolones has been described. The rate of macrolide resistance among Campylobacter has remained stable at <5 percent in most parts of the world; the prevalence of fluoroquinolone-resistant Campylobacter is rising in many areas, particularly in Southeast Asia. (See 'Resistance' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES Kapperud G, Lassen J, Ostroff SM, Aasen S. Clinical features of sporadic Campylobacter infections in




#Campylobacter #Clinical #Clinique #Diagnosis #Diagnostic #Infection
Common features − The mean incubation period is three days (range one to seven days) (figure 1). Early symptoms include abrupt onset of abdominal pain and diarrhea. The acute illness is characterized by cramping periumbilical abdominal pain and diarrhea. Patients frequently report ten or more bowel movements per day. Bloody stools are observed on the second or third day of diarrhea in about 15 percent of adults; in children bloody stools may be present in more than half of cases. Diarrhea is self-limited and lasts for a mean of seven days.
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orne disease. Campylobacter infection can also be transmitted via water-borne outbreaks and direct contact with animals or animal products. (See 'Introduction' above.) ●Clinical manifestations •<span>Common features − The mean incubation period is three days (range one to seven days) (figure 1). Early symptoms include abrupt onset of abdominal pain and diarrhea. The acute illness is characterized by cramping periumbilical abdominal pain and diarrhea. Patients frequently report ten or more bowel movements per day. Bloody stools are observed on the second or third day of diarrhea in about 15 percent of adults; in children bloody stools may be present in more than half of cases. Diarrhea is self-limited and lasts for a mean of seven days. (See 'Common presenting features' above.) •Unique manifestations and complications − Patients with Campylobacter infection can present with clinical manifestations mimicking other disea




#Campylobacter #Clinical #Clinique #Diagnosis #Diagnostic #Infection
Unique manifestations and complications − Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis). A variety of acute complications can occur. There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS).
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5 percent of adults; in children bloody stools may be present in more than half of cases. Diarrhea is self-limited and lasts for a mean of seven days. (See 'Common presenting features' above.) •<span>Unique manifestations and complications − Patients with Campylobacter infection can present with clinical manifestations mimicking other diseases (eg, "pseudoappendicitis" and colitis). A variety of acute complications can occur. There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS). (See 'Unique manifestations' above and 'Complications' above.) ●Diagnosis − The diagnosis of Campylobacter enteritis is established by stool culture. Patients with late onset reactive a




#Campylobacter #Clinical #Clinique #Diagnosis #Diagnostic #Infection
Diagnosis − The diagnosis of Campylobacter enteritis is established by stool culture. Patients with late onset reactive arthritis or GBS may have negative stool studies; serologic tests can be used to detect recent Campylobacter infection in these patients.
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r. There are two major late onset complications of Campylobacter infection: reactive arthritis and Guillain-Barré syndrome (GBS). (See 'Unique manifestations' above and 'Complications' above.) ●<span>Diagnosis − The diagnosis of Campylobacter enteritis is established by stool culture. Patients with late onset reactive arthritis or GBS may have negative stool studies; serologic tests can be used to detect recent Campylobacter infection in these patients. (See 'Diagnosis' above.) ●Management •Supportive care − Campylobacter infection is usually a mild, self-limited infection. Maintenance of proper hydration and correction of electrolyte