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#M2_Buruli_Physiopathologie_Pluschke
After the first definite description in 1948, M. ulcerans infections have been reported from 34 countries, mainly with tropical and subtropical climates.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
l: hc.hptssiws@ekhcsulp.dreg Corresponding author. Published online: April 30, 2019. Buruli ulcer (BU) is a neglected, debilitating skin disease caused by infection with Mycobacterium ulcerans. <span>After the first definite description in 1948, M. ulcerans infections have been reported from 34 countries, mainly with tropical and subtropical climates. Following a peak of 5954 reported BU cases globally in 2004 the number of new recorded cases has been decreasing over the past years. In 2016, a total of 1952 BU cases were reported to




#M2_Buruli_Physiopathologie_Pluschke
Following a peak of 5954 reported BU cases globally in 2004 the number of new recorded cases has been decreasing over the past years. In 2016, a total of 1952 BU cases were reported to the World Health Organization (WHO) from twelve different countries.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
infection with Mycobacterium ulcerans. After the first definite description in 1948, M. ulcerans infections have been reported from 34 countries, mainly with tropical and subtropical climates. <span>Following a peak of 5954 reported BU cases globally in 2004 the number of new recorded cases has been decreasing over the past years. In 2016, a total of 1952 BU cases were reported to the World Health Organization (WHO) from twelve different countries. Underreporting is considered likely, as BU mostly affects populations in remote areas with limited access to the formal health sector. Although transmission pathways of M. ulcerans are




#M2_Buruli_Physiopathologie_Pluschke
The key event for the emergence of M. ulcerans as a species highly pathogenic for humans appears to be the acquisition of a plasmid, bearing genes encoding polyketide synthases and polyketide-modifying enzymes involved in the biosynthesis of a unique macrolide toxin, named mycolactone.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
r, infection foci are closely associated with wetlands. Considering that M. ulcerans has evolved from the fish pathogen M. marinum, involvement of an environmental niche is strongly suggestive. <span>The key event for the emergence of M. ulcerans as a species highly pathogenic for humans appears to be the acquisition of a plasmid, bearing genes encoding polyketide synthases and polyketide-modifying enzymes involved in the biosynthesis of a unique macrolide toxin, named mycolactone. The cytotoxic and immunosuppressive properties of mycolactone account for much of the pathology of BU, which is characterized by the formation of chronic, necrotizing, ulcerative skin l




#M2_Buruli_Physiopathologie_Pluschke
In the further course of its reductive evolution, M. ulcerans has diverged into at least two principal niche-adapted lineages connected with different patterns of BU case distribution. Strains of the classical lineage are responsible for BU foci in Africa and Australia that are typically characterized by high local prevalence. In contrast, scattered, sporadic BU cases recorded in Asia and the Americas are caused by strains of the ancestral lineage, which also comprises globally distributed fish and frog pathogens.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
The cytotoxic and immunosuppressive properties of mycolactone account for much of the pathology of BU, which is characterized by the formation of chronic, necrotizing, ulcerative skin lesions. <span>In the further course of its reductive evolution, M. ulcerans has diverged into at least two principal niche-adapted lineages connected with different patterns of BU case distribution. Strains of the classical lineage are responsible for BU foci in Africa and Australia that are typically characterized by high local prevalence. In contrast, scattered, sporadic BU cases recorded in Asia and the Americas are caused by strains of the ancestral lineage, which also comprises globally distributed fish and frog pathogens. Adaptation of these divergent mycolactone-producing mycobacterial lineages to different ecological habitats seems likely. Limited knowledge on definite reservoirs and potential vectors




#M2_Buruli_Physiopathologie_Pluschke
The first description of chronic skin ulcers consistent with the pathology of Mycobacterium ulcerans infection dates back to the end of the nineteenth century, when the British physician Albert Cook recorded his observations in The Mengo Hospital Notes, maintained in the library of the hospital in Kampala, Uganda [1]. In 1948, characteristics of similar skin ulcers were described by MacCallum and his colleagues in six patients from the Bairnsdale District in southeastern Australia [2], where the disease is therefore often referred to as Bairnsdale ulcer.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
entification and adequate treatment of patients are currently the most important measures to prevent the debilitating consequences of the disease. Go to: 1. History of a Mysterious Skin Disease <span>The first description of chronic skin ulcers consistent with the pathology of Mycobacterium ulcerans infection dates back to the end of the nineteenth century, when the British physician Albert Cook recorded his observations in The Mengo Hospital Notes, maintained in the library of the hospital in Kampala, Uganda [1]. In 1948, characteristics of similar skin ulcers were described by MacCallum and his colleagues in six patients from the Bairnsdale District in southeastern Australia [2], where the disease is therefore often referred to as Bairnsdale ulcer. The causative organism isolated from these ulcers was found to be an acid-fast mycobacterium, later named M. ulcerans. Noteworthy, the first isolation of the extremely slow-growing myco




#M2_Buruli_Physiopathologie_Pluschke
Noteworthy, the first isolation of the extremely slow-growing mycobacterium in culture was achieved by accidental incubation of culture plates in a faulty incubator [3], reflecting the low optimal growth temperature of the pathogen at 30–33 °C. This temperature preference is considered a major factor for the skin tropism and limited systemic dissemination of M. ulcerans infections
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
[2], where the disease is therefore often referred to as Bairnsdale ulcer. The causative organism isolated from these ulcers was found to be an acid-fast mycobacterium, later named M. ulcerans. <span>Noteworthy, the first isolation of the extremely slow-growing mycobacterium in culture was achieved by accidental incubation of culture plates in a faulty incubator [3], reflecting the low optimal growth temperature of the pathogen at 30–33 °C. This temperature preference is considered a major factor for the skin tropism and limited systemic dissemination of M. ulcerans infections. In the 1940s and 1950s a larger case series of 170 patients with necrotic skin ulcers, caused by an acid-fast mycobacterium, was recorded in the Democratic Republic of the Congo [4]. A




#M2_Buruli_Physiopathologie_Pluschke
In the 1940s and 1950s a larger case series of 170 patients with necrotic skin ulcers, caused by an acid-fast mycobacterium, was recorded in the Democratic Republic of the Congo [ 4]. A high prevalence of M. ulcerans infections was noticed in the 1950s and 1960s in a geographically very limited area of the then sparsely populated Buruli County close to the Nile River in Uganda and as a consequence, the disease became more generally known as Buruli ulcer (BU) [5, 6]
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
timal growth temperature of the pathogen at 30–33 °C. This temperature preference is considered a major factor for the skin tropism and limited systemic dissemination of M. ulcerans infections. <span>In the 1940s and 1950s a larger case series of 170 patients with necrotic skin ulcers, caused by an acid-fast mycobacterium, was recorded in the Democratic Republic of the Congo [4]. A high prevalence of M. ulcerans infections was noticed in the 1950s and 1960s in a geographically very limited area of the then sparsely populated Buruli County close to the Nile River in Uganda and as a consequence, the disease became more generally known as Buruli ulcer (BU) [5, 6]. In proximity to this initial infection focus, a second outbreak of the disease in Uganda was reported in Rwandans living in a refugee settlement that was opened in 1964 close to the Ni




#M2_Buruli_Physiopathologie_Pluschke
In proximity to this initial infection focus, a second outbreak of the disease in Uganda was reported in Rwandans living in a refugee settlement that was opened in 1964 close to the Nile River. Intensive investigation of the 220 BU cases that occurred until 1969, when the community moved to a new locality, where case numbers declined, has provided much of the basic knowledge about the epidemiology of BU that is still valid today. Amongst other insights it became apparent that BU may affect individuals irrespective of sex and age, although the highest incidence was seen in children aged between 5 and 15 years. Furthermore, in contrast to a very low probability of person to person transmission, the involvement of an environmental reservoir in the transmission became obvious [ 7].
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
cally very limited area of the then sparsely populated Buruli County close to the Nile River in Uganda and as a consequence, the disease became more generally known as Buruli ulcer (BU) [5, 6]. <span>In proximity to this initial infection focus, a second outbreak of the disease in Uganda was reported in Rwandans living in a refugee settlement that was opened in 1964 close to the Nile River. Intensive investigation of the 220 BU cases that occurred until 1969, when the community moved to a new locality, where case numbers declined, has provided much of the basic knowledge about the epidemiology of BU that is still valid today. Amongst other insights it became apparent that BU may affect individuals irrespective of sex and age, although the highest incidence was seen in children aged between 5 and 15 years. Furthermore, in contrast to a very low probability of person to person transmission, the involvement of an environmental reservoir in the transmission became obvious [7]. While until then clinical attention had been concentrated on ulcerative lesions, awareness of the disease in highly endemic regions has brought attention to pre-ulcerative forms of the




#M2_Buruli_Physiopathologie_Pluschke
Until the end of the twentieth century, BU case series were reported mainly from West and Central African countries including the Congo [9], Nigeria [10], Gabon [11], Ghana [12, 13], Benin [14], and Côte d’Ivoire [15, 16] as well as from Australia [17, 18] and Papua New Guinea (PNG) [19]. Moreover, sporadic M. ulcerans infections occurred in a number of additional countries with tropical, subtropical and temperate climates [20], totalling up to 34 countries from which BU has hitherto been reported.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
n concentrated on ulcerative lesions, awareness of the disease in highly endemic regions has brought attention to pre-ulcerative forms of the infection including nodules, plaques and edema [8]. <span>Until the end of the twentieth century, BU case series were reported mainly from West and Central African countries including the Congo [9], Nigeria [10], Gabon [11], Ghana [12, 13], Benin [14], and Côte d’Ivoire [15, 16] as well as from Australia [17, 18] and Papua New Guinea (PNG) [19]. Moreover, sporadic M. ulcerans infections occurred in a number of additional countries with tropical, subtropical and temperate climates [20], totalling up to 34 countries from which BU has hitherto been reported. However, limited awareness of the disease and the fact that it often affects poor populations in remote, rural areas has hampered the detection of new infection foci and thus the contro




#M2_Buruli_Physiopathologie_Pluschke
Since 2008, a steady decline in the number of reported BU patients has been noticed (Fig. 1)
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
l Guinea, Gabon, Ghana, Guinea, Liberia, Nigeria, Sierra Leone, South Sudan, Uganda and Togo), the Americas (French Guiana), Asia (Japan), and the Western Pacific (Australia and PNG) (Table 1). <span>Since 2008, a steady decline in the number of reported BU patients has been noticed (Fig. 1). Table 1 Number of reported BU cases worldwide between 2002 and 2016. Data source: WHO Fig. 1 Number of BU cases reported worldwide between 2002 and 2016. Graph illustrating the downwar




#M2_Buruli_Physiopathologie_Pluschke
Moreover, surveillance activities in some of the highly endemic countries may have declined due to the decreased availability of specific funding. On the contrary, a steady increase in the number of BU patients has been reported from the BU endemic region of Victoria in southern Australia, with a peak incidence of 186 new BU infections in 2016.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
lishment of effective national BU control programs, underreporting is considered likely, as there is lack of data from an increasing number of countries that have reported BU cases in the past. <span>Moreover, surveillance activities in some of the highly endemic countries may have declined due to the decreased availability of specific funding. On the contrary, a steady increase in the number of BU patients has been reported from the BU endemic region of Victoria in southern Australia, with a peak incidence of 186 new BU infections in 2016. The geographic distribution of BU recorded by WHO in 2016 is illustrated in Fig. 2. Fig. 2 Worldwide distribution of BU cases in 2016. Global map illustrating countries that have report




#M2_Buruli_Physiopathologie_Pluschke
Moreover, acquisition of high-copy number insertion sequences (IS2404 and IS2606) and their expansion in the M. ulcerans genome has resulted in extensive gene loss, pseudogene formation, and modification of gene function, coining the likely adaptation to new, restricted, ecological niches [26].
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
ese mycolactones have hitherto been described [23–25]; for more information on the toxin of M. ulcerans the reader is referred to chapter “Mycolactone: More than Just a Cytotoxin” of this book. <span>Moreover, acquisition of high-copy number insertion sequences (IS2404 and IS2606) and their expansion in the M. ulcerans genome has resulted in extensive gene loss, pseudogene formation, and modification of gene function, coining the likely adaptation to new, restricted, ecological niches [26]. For more detailed information on the population genomics and molecular epidemiology of M. ulcerans the reader is referred to chapter “Population Genomics and Molecular Epidemiology of M




#M2_Buruli_Physiopathologie_Pluschke
The emergence of M. ulcerans, which has evolved from the fish and opportunistic human pathogen M. marinum [21] approximately a million years ago [22], was driven by horizontal transfer of genetic material [21]. Most notably, this included a virulence plasmid, carrying genes for the synthesis of macrolide toxins, whose cytotoxic and immunosuppressive properties account for much of the typical progressive skin necrosis and chronicity of M. ulcerans infections.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
ge) and green (ancestral lineage)) and in previous years (grey). The map was kindly created by (more...) Go to: 2. Evolution, Niche Adaptation, and Transmission of Distinct M. ulcerans Lineages <span>The emergence of M. ulcerans, which has evolved from the fish and opportunistic human pathogen M. marinum [21] approximately a million years ago [22], was driven by horizontal transfer of genetic material [21]. Most notably, this included a virulence plasmid, carrying genes for the synthesis of macrolide toxins, whose cytotoxic and immunosuppressive properties account for much of the typical progressive skin necrosis and chronicity of M. ulcerans infections. Several structural variants of these mycolactones have hitherto been described [23–25]; for more information on the toxin of M. ulcerans the reader is referred to chapter “Mycolactone:




#M2_Buruli_Physiopathologie_Pluschke
Strains of the ancestral lineage, which are closely related to M. marinum, mainly cause disease in ectotherms such as fish and frogs [25, 3133], but certain sub-groups sporadically infect humans.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
ay be transmitted by several distinct mechanisms, each enabling the entrance of a sufficient pathogen load into the susceptible layers of subcutaneous tissue. 2.1. Ancestral M. ulcerans Lineage <span>Strains of the ancestral lineage, which are closely related to M. marinum, mainly cause disease in ectotherms such as fish and frogs [25, 31–33], but certain sub-groups sporadically infect humans. Due to their distinct host range, some mycolactone-producing ancestral strains were initially given different species designations such as M. marinum for globally detected fish pathogen




#M2_Buruli_Physiopathologie_Pluschke
Furthermore, ancestral strains isolated from the lesions of BU patients from Japan are often referred to as M. ulcerans subspecies shinshuense [34]. Indeed, comparative genome analysis has shown that based on the sequences of fish and frog isolates on the one hand and human disease isolates from Japan on the other hand the ancestral lineage may be subdivided into two major sub-lineages [26]
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
r mycobacteria isolated from diseased Chesapeake Bay striped bass [32], or M. liflandii for strains isolated during a mycobacteriosis outbreak in a laboratory colony of Xenopus tropicalis [31]. <span>Furthermore, ancestral strains isolated from the lesions of BU patients from Japan are often referred to as M. ulcerans subspecies shinshuense [34]. Indeed, comparative genome analysis has shown that based on the sequences of fish and frog isolates on the one hand and human disease isolates from Japan on the other hand the ancestral lineage may be subdivided into two major sub-lineages [26]. The common feature of all of these isolated pathogens is the production of mycolactone and thus it was no surprise when comparative genome analysis of ancestral and classical M. ulcera




#M2_Buruli_Physiopathologie_Pluschke
Sporadic human infections caused by ancestral strains were reported from the Americas (French Guiana [36], Suriname [38], Peru [39], Brazil [40] and Mexico [41]) and from Asia (Japan [42] and China [43]). Between 2002 and 2016, French Guiana and Japan reported to WHO 80 and 59 BU cases, respectively.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
family members was linked to a stagnant water channel in the backyard of the family’s house, in which a sample of a crayfish contained an IS2404 sequence identical to that of M. ulcerans [37]. <span>Sporadic human infections caused by ancestral strains were reported from the Americas (French Guiana [36], Suriname [38], Peru [39], Brazil [40] and Mexico [41]) and from Asia (Japan [42] and China [43]). Between 2002 and 2016, French Guiana and Japan reported to WHO 80 and 59 BU cases, respectively. No official records are available for the other South-American and Asian countries. For more detailed information on BU in French Guiana and Japan the reader is referred to chapters “My




#M2_Buruli_Physiopathologie_Pluschke
These findings suggest that certain Australian marsupials may be highly susceptible to M. ulcerans infection. In contrast, until today, surveys of small mammals in African BU endemic areas have not led to the detection of an M. ulcerans animal reservoir [48, 53]
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
in the ecology of infection as a reservoir of the pathogen [26]. In Far North Queensland (FNQ), another BU endemic area of Australia, M. ulcerans DNA was detected in excreta of bandicoots [52]. <span>These findings suggest that certain Australian marsupials may be highly susceptible to M. ulcerans infection. In contrast, until today, surveys of small mammals in African BU endemic areas have not led to the detection of an M. ulcerans animal reservoir [48, 53]. It has been suspected that in highly endemic areas of Africa, large chronic lesions of BU patients may contribute significantly to the dissemination of M. ulcerans in the environment.




#M2_Buruli_Physiopathologie_Pluschke
BU has long been considered as a disease that mainly affects children under the age of 15 years living in rural areas of Africa. A comparison of the age distribution reported for various BU case series (Table 2) shows that this assumption still holds true for African BU endemic areas and for endemic sites in PNG. However, this generalized view lapsed when larger case series were reported from Victoria in southeastern Australia, where a high average age of BU patients was observed (Table 2)
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
lia” of this book). Table 2 Demographic and clinical characteristics of BU patients 3.1. Demographic and Clinical Characteristics of M. ulcerans Infection 3.1.1. Age Distribution of BU Patients <span>BU has long been considered as a disease that mainly affects children under the age of 15 years living in rural areas of Africa. A comparison of the age distribution reported for various BU case series (Table 2) shows that this assumption still holds true for African BU endemic areas and for endemic sites in PNG. However, this generalized view lapsed when larger case series were reported from Victoria in southeastern Australia, where a high average age of BU patients was observed (Table 2). The peak incidence of BU among children in Africa and the elderly in Victoria may be partly related to the average age of the respective general populations in the affected areas. Whil




#M2_Buruli_Physiopathologie_Pluschke
But even if taking the skewed age distribution of the study populations into account, the elderly were most affected in Australia [75] and a bi-modal distribution of the age-related risk of developing BU was observed in Africa with young teenagers and the elderly being overrepresented among cases [64, 74, 76].
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
le the population in BU endemic areas in Africa is very young [64, 73, 74], the affected communities in Victoria are popular seaside holiday resorts, where many retired people have their homes. <span>But even if taking the skewed age distribution of the study populations into account, the elderly were most affected in Australia [75] and a bi-modal distribution of the age-related risk of developing BU was observed in Africa with young teenagers and the elderly being overrepresented among cases [64, 74, 76]. Increasing risk of developing BU with age may be due to the gradual deterioration of the immune system in the elderly. Interestingly, a marked underrepresentation of BU patients among c




#M2_Buruli_Physiopathologie_Pluschke
This observation was in line with subsequent sero-epidemiological studies in Ghana and Cameroon, indicating that young children are considerably less exposed to M. ulcerans than older children [77, 78].
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
h age may be due to the gradual deterioration of the immune system in the elderly. Interestingly, a marked underrepresentation of BU patients among children below 4 years of age was found [64]. <span>This observation was in line with subsequent sero-epidemiological studies in Ghana and Cameroon, indicating that young children are considerably less exposed to M. ulcerans than older children [77, 78]. In Japan, where BU disease is caused by strains of the ancestral M. ulcerans lineage, a tendency towards middle-aged adults was found [42]. In French Guiana, a marked transition of the




#M2_Buruli_Physiopathologie_Pluschke
Several studies conducted with large numbers of African BU cases revealed significant differences in the male:female ratio, when the study population was stratified by age. All of these studies have consistently reported that in children below the age of 15 years, M. ulcerans infection is more common in boys than in girls and conversely that in individuals above the age of 15 years the infection is more frequent in females than in males [7, 56, 61, 62] (Table 2). It appears likely that observed differences are due to different environmental contact patterns associated with the movement radius of children or different occupational exposure to environmental reservoirs.
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Buruli Ulcer: History and Disease Burden - Buruli Ulcer - NCBI Bookshelf
s the proportion of one of the sexes was higher than that of the other. While more female than male patients were recorded in Japan, more men than women tended to be affected in FNQ, Australia. <span>Several studies conducted with large numbers of African BU cases revealed significant differences in the male:female ratio, when the study population was stratified by age. All of these studies have consistently reported that in children below the age of 15 years, M. ulcerans infection is more common in boys than in girls and conversely that in individuals above the age of 15 years the infection is more frequent in females than in males [7, 56, 61, 62] (Table 2). It appears likely that observed differences are due to different environmental contact patterns associated with the movement radius of children or different occupational exposure to environmental reservoirs. 3.1.3. Distribution of BU Lesions on the Human Body While the mode of transmission of M. ulcerans remains unclear, it is commonly assumed that infection takes places via inoculation of




Flashcard 7682230717708

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#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Avec les sérologies de quelles autres maladies infectieuses la sérologie Tularémie peut-elle "croiser" ?
Answer

  • Brucellose
  • Légionellose
  • Mononucléose infectieuse

"Serologic assays for tularemia can cross-react with heterophile antibodies and antibodies to other gram-negative organisms such as Brucella or Legionella, but cross-reactions are typically positive at a low, non-diagnostic titer [1,51]." - UpToDate


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Serologic assays for tularemia can cross-react with heterophile antibodies and antibodies to other gram-negative organisms such as Brucella or Legionella, but cross-reactions are typically positive at a low, non-diagnostic titer [1,51].

Original toplevel document

UpToDate
fection, and both antibody titers may remain elevated for years after an infection. Thus, a single positive titer is supportive of the diagnosis, but may also result from an old infection [50]. <span>Serologic assays for tularemia can cross-react with heterophile antibodies and antibodies to other gram-negative organisms such as Brucella or Legionella, but cross-reactions are typically positive at a low, non-diagnostic titer [1,51]. In the United States, serologic studies are typically performed using a tube agglutination or microagglutination assay; commercially available enzyme-linked immunosorbent assays (ELISAs







Flashcard 7682235698444

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Comment définir la forme "typhoidale" de la Tularémie ?
Answer

  • Maladie systémique fébrile
  • Sans signes localisateurs francs
  • Sans adénopathie typique
  • Ne correspond pas à une autre forme de la maladie

"Typhoidal tularemia is a systemic febrile illness without prominent regional adenopathy or other localizing signs that does not fit another major form of the disease." - UpToDate


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Typhoidal tularemia is a systemic febrile illness without prominent regional adenopathy or other localizing signs that does not fit another major form of the disease. Typhoidal disease is a common presentation in certain locations.

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UpToDate
quire hospitalization, to have a longer hospital stay, to have positive cultures, and to have a higher mortality rate compared with those without pulmonary involvement [21]. Typhoidal disease — <span>Typhoidal tularemia is a systemic febrile illness without prominent regional adenopathy or other localizing signs that does not fit another major form of the disease. Typhoidal disease is a common presentation in certain locations. As an example, in the United States, it was the most common tularemia presentation among cases reported in Arkansas from 2009 through 2013 and was particularly frequent among older pati







Flashcard 7682238319884

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les formes cliniques de la Tularémie le plus souvent présentées par les patients immunodéprimés ?
Answer

  • Pneumonique
  • Typhoidale

"A review of 17 immunocompromised individuals with tularemia [...] Eight patients (48 percent) presented with pneumonic tularemia, five (29 percent) had typhoidal tularemia, and only four (24 percent) had ulceroglandular or glandular disease." - UpToDate


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emia usually have fever with or without any of the nonspecific symptoms described above (see 'Clinical syndromes' above). They may be more likely to present with pneumonic or typhoidal illness. <span>A review of 17 immunocompromised individuals with tularemia reported fever in 94 percent, sweats or fatigue in 36 percent, respiratory symptoms in 41 percent, and abdominal symptoms in 24 percent [25]. Eight patients (48 percent) presented with pneumonic tularemia, five (29 percent) had typhoidal tularemia, and only four (24 percent) had ulceroglandular or glandular disease. <span>

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UpToDate
[1]. (See 'Pneumonic disease' above.) Potential laboratory findings in severe typhoidal tularemia include elevated creatine phosphokinase (CPK), myoglobinuria, hyponatremia, and renal failure. <span>Presentation in immunocompromised patients — Immunocompromised patients with tularemia usually have fever with or without any of the nonspecific symptoms described above (see 'Clinical syndromes' above). They may be more likely to present with pneumonic or typhoidal illness. A review of 17 immunocompromised individuals with tularemia reported fever in 94 percent, sweats or fatigue in 36 percent, respiratory symptoms in 41 percent, and abdominal symptoms in 24 percent [25]. Eight patients (48 percent) presented with pneumonic tularemia, five (29 percent) had typhoidal tularemia, and only four (24 percent) had ulceroglandular or glandular disease. Other features Secondary skin manifestations — Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or ov







Flashcard 7682240941324

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Dans quelle proportion des Tularémies peut-on retrouver des manifestations cutanées ?
Answer

50 %

"Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or overlooked [3,26-28]." - UpToDate


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Secondary skin manifestations — Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or overlooked [3,26-28]. These secondary eruptions are usually maculopapular, vesiculopapular, erythema multiforme, erythema nodosum, or urticarial; some have been mistaken for varicella or drug eruptions [27].

Original toplevel document

UpToDate
]. Eight patients (48 percent) presented with pneumonic tularemia, five (29 percent) had typhoidal tularemia, and only four (24 percent) had ulceroglandular or glandular disease. Other features <span>Secondary skin manifestations — Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or overlooked [3,26-28]. These secondary eruptions are usually maculopapular, vesiculopapular, erythema multiforme, erythema nodosum, or urticarial; some have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]. More than one type of eruption can occur in the same patient [29]. The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients w







Flashcard 7682243300620

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les manifestations dermatologiques susceptibles d'être rencontrées au cours de la Tularémie ?
Answer
  • Éruptions :
    • Urticarienne
    • Maculopapuleuse
    • Vésiculopapuleuse
  • Erythème polymorphe
  • Érythème noueux
  • Syndrome de Sweet

"These secondary eruptions are usually maculopapular, vesiculopapular, erythema multiforme, erythema nodosum, or urticarial; some have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]." - UpToDate


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an> Secondary skin manifestations — Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or overlooked [3,26-28]. <span>These secondary eruptions are usually maculopapular, vesiculopapular, erythema multiforme, erythema nodosum, or urticarial; some have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]. More than one type of eruption can occur in the same patient [29]. <span>

Original toplevel document

UpToDate
]. Eight patients (48 percent) presented with pneumonic tularemia, five (29 percent) had typhoidal tularemia, and only four (24 percent) had ulceroglandular or glandular disease. Other features <span>Secondary skin manifestations — Secondary skin changes are common in all forms of tularemia, reported in up to 50 percent in some series, and are often misdiagnosed or overlooked [3,26-28]. These secondary eruptions are usually maculopapular, vesiculopapular, erythema multiforme, erythema nodosum, or urticarial; some have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]. More than one type of eruption can occur in the same patient [29]. The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients w







Flashcard 7682245659916

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les manifestations cutanées de la Tularémie plus volontiers associées à la forme pneumonique ?
Answer

Erythème noueux

"[...] whereas patients with pneumonic tularemia are more likely to have erythema nodosum." - UpToDate


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The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients with pneumonic tularemia are more likely to have erythema nodosum. In Turkey, where oropharyngeal disease is common, erythema multiforme has been reported most often with oropharyngeal or glandular tularemia [30].

Original toplevel document

UpToDate
e have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]. More than one type of eruption can occur in the same patient [29]. <span>The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients with pneumonic tularemia are more likely to have erythema nodosum. In Turkey, where oropharyngeal disease is common, erythema multiforme has been reported most often with oropharyngeal or glandular tularemia [30]. Laboratory findings — Routine laboratory tests are nonspecific. The white blood cell count may be low, normal, or elevated. Other nonspecific findings may include low platelet count, lo







Flashcard 7682248019212

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les manifestations cutanées de la Tularémie plus volontiers associées à la forme typhoidale ?
Answer
  • Erythème polymorphe
  • Erythème noueux

"Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, [...]" - UpToDate


statusnot learnedmeasured difficulty37% [default]last interval [days]               
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The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients with pneumonic tularemia are more likely to have erythema nodosum. In Turkey, where oropharyngeal disease is common, erythema multiforme has been reported most often wi

Original toplevel document

UpToDate
e have been mistaken for varicella or drug eruptions [27]. Sweet syndrome also has been reported to occur with tularemia [28]. More than one type of eruption can occur in the same patient [29]. <span>The character of the skin eruption may vary with the underlying type of tularemia. Patients with typhoidal tularemia can have erythema multiforme or erythema nodosum, whereas patients with pneumonic tularemia are more likely to have erythema nodosum. In Turkey, where oropharyngeal disease is common, erythema multiforme has been reported most often with oropharyngeal or glandular tularemia [30]. Laboratory findings — Routine laboratory tests are nonspecific. The white blood cell count may be low, normal, or elevated. Other nonspecific findings may include low platelet count, lo







Flashcard 7682251164940

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les complications d'une Tularémie non traitée ?
Answer

  • Fièvre prolongée
  • Perte de poids
  • Adénopathie
  • Handicap

"If untreated, tularemia can cause prolonged fever, weight loss, adenopathy, and debility that can last for weeks or months [15]." - UpToDate


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Complications — If untreated, tularemia can cause prolonged fever, weight loss, adenopathy, and debility that can last for weeks or months [15]. Even with appropriate treatment, some patients will have a lengthy recovery following tularemia.

Original toplevel document

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nt may be low, normal, or elevated. Other nonspecific findings may include low platelet count, low serum sodium, abnormal liver enzymes, evidence of rhabdomyolysis or myoglobinuria, and pyuria. <span>Complications — If untreated, tularemia can cause prolonged fever, weight loss, adenopathy, and debility that can last for weeks or months [15]. Even with appropriate treatment, some patients will have a lengthy recovery following tularemia. Patients with prolonged tularemia often complain of fatigue and lassitude, and may have anorexia, weakness, and weight loss. Neuropsychiatric complaints include headache, difficulty con







Flashcard 7682254048524

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Dans quelles formes de la Tularémie la survenue de méningite est classiquement rapportée ?
Answer

  • Ulcéroglandulaire
  • Typhoidale

"Meningitis, reported with ulceroglandular and typhoidal disease" - UpToDate


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Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43].

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ed with typhoidal disease [35]. F. tularensis subspecies holarctica infection of a bioprosthetic valve occurred in a patient presenting with prolonged fever and a resolving skin lesion [39,40]. <span>Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43]. Meningitis developed in a patient with fever and rash after he ran his lawn mower over a dead rabbit [43]. Other rare neurological manifestations attributed to tularemia include Guillai







Flashcard 7682256407820

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
En cas d'atteinte neuroméningée de la Tularémie, dans quels délais après les premiers signes cliniques se déclare généralement les signes de méningite ?
Answer

Dans les 3 à 30 jours

"Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness" - UpToDate


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Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43].

Original toplevel document

UpToDate
ed with typhoidal disease [35]. F. tularensis subspecies holarctica infection of a bioprosthetic valve occurred in a patient presenting with prolonged fever and a resolving skin lesion [39,40]. <span>Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43]. Meningitis developed in a patient with fever and rash after he ran his lawn mower over a dead rabbit [43]. Other rare neurological manifestations attributed to tularemia include Guillai







Flashcard 7682258767116

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont généralement la formule et la composition du LCS en cas de méningite tularémique ?
Answer

  • Pléiocytose mononucléée
  • Hyperprotéinorachie
  • Hypoglycorachie

"Meningitis, [...] causes a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43]." - UpToDate


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Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43].

Original toplevel document

UpToDate
ed with typhoidal disease [35]. F. tularensis subspecies holarctica infection of a bioprosthetic valve occurred in a patient presenting with prolonged fever and a resolving skin lesion [39,40]. <span>Meningitis, reported with ulceroglandular and typhoidal disease, can develop 3 to 30 days after the onset of illness and cause a cerebrospinal fluid mononuclear cell pleocytosis with low glucose and high protein [41-43]. Meningitis developed in a patient with fever and rash after he ran his lawn mower over a dead rabbit [43]. Other rare neurological manifestations attributed to tularemia include Guillai







Flashcard 7682261912844

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Citer deux présentations / contextes pneumologiques qui doivent faire évoquer une Tularémie ?
Answer

  • Clinique : Pneumonie aiguë communautaire résistante aux Beta-Lactamines et sans diagnostic après tests standards
  • Radiographique : Infiltrats parenchymateux nodulaires et épanchement pleural

"● Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing
● Nodular infiltrates plus a pleural effusion on chest imaging" - UpToDate


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cal lymphadenopathy ● Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ● Persistent systemic febrile illness that is undiagnosed after routine testing <span>● Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ● Nodular infiltrates plus a pleural effusion on chest imaging <span>

Original toplevel document

UpToDate
e delayed, the initial diagnosis of tularemia is often made presumptively, when the patient's presentation is both clinically and epidemiologically consistent and there is no more likely cause. <span>Specific clinical features that should prompt consideration for tularemia include: ●Regional lymphadenopathy, particularly if associated with an inoculation site ●Conjunctivitis accompanied by local lymphadenopathy ●Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ●Persistent systemic febrile illness that is undiagnosed after routine testing ●Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ●Nodular infiltrates plus a pleural effusion on chest imaging When these clinical features are observed in the setting of a history of animal (particularly wild animal) exposure or insect bites, the possibility of tularemia is greater, and making







Flashcard 7682264272140

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Donner une présentation clinique générale aspécifique / situation devant faire évoquer une Tularémie ?
Answer

Maladie systémique fébrile non diagnsotiquée après des tests standards

"● Persistent systemic febrile illness that is undiagnosed after routine testing" - UpToDate


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ularly if associated with an inoculation site ● Conjunctivitis accompanied by local lymphadenopathy ● Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing <span>● Persistent systemic febrile illness that is undiagnosed after routine testing ● Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ● Nodular infiltrates plus a pleural effusion on chest imaging <

Original toplevel document

UpToDate
e delayed, the initial diagnosis of tularemia is often made presumptively, when the patient's presentation is both clinically and epidemiologically consistent and there is no more likely cause. <span>Specific clinical features that should prompt consideration for tularemia include: ●Regional lymphadenopathy, particularly if associated with an inoculation site ●Conjunctivitis accompanied by local lymphadenopathy ●Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ●Persistent systemic febrile illness that is undiagnosed after routine testing ●Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ●Nodular infiltrates plus a pleural effusion on chest imaging When these clinical features are observed in the setting of a history of animal (particularly wild animal) exposure or insect bites, the possibility of tularemia is greater, and making







Flashcard 7682266631436

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Donner une présentation clinique ophtalmologique pouvant faire évoquer une Tularémie ?
Answer

Conjonctivite et adénopathie locale (syndrome de Parinaud)

"● Conjunctivitis accompanied by local lymphadenopathy" - UpToDate


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Specific clinical features that should prompt consideration for tularemia include: ● Regional lymphadenopathy, particularly if associated with an inoculation site ● Conjunctivitis accompanied by local lymphadenopathy ● Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ● Persistent systemic febrile illness that is undiagnosed after routine testing ● Community

Original toplevel document

UpToDate
e delayed, the initial diagnosis of tularemia is often made presumptively, when the patient's presentation is both clinically and epidemiologically consistent and there is no more likely cause. <span>Specific clinical features that should prompt consideration for tularemia include: ●Regional lymphadenopathy, particularly if associated with an inoculation site ●Conjunctivitis accompanied by local lymphadenopathy ●Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ●Persistent systemic febrile illness that is undiagnosed after routine testing ●Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ●Nodular infiltrates plus a pleural effusion on chest imaging When these clinical features are observed in the setting of a history of animal (particularly wild animal) exposure or insect bites, the possibility of tularemia is greater, and making







Flashcard 7682268990732

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Donner une présentation ORL pouvant faire évoquer une Tularémie ?
Answer

Pharyngite sévère d'évolution non favorable sous Beta-Lactamines

"● Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing" - UpToDate


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res that should prompt consideration for tularemia include: ● Regional lymphadenopathy, particularly if associated with an inoculation site ● Conjunctivitis accompanied by local lymphadenopathy <span>● Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ● Persistent systemic febrile illness that is undiagnosed after routine testing ● Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after

Original toplevel document

UpToDate
e delayed, the initial diagnosis of tularemia is often made presumptively, when the patient's presentation is both clinically and epidemiologically consistent and there is no more likely cause. <span>Specific clinical features that should prompt consideration for tularemia include: ●Regional lymphadenopathy, particularly if associated with an inoculation site ●Conjunctivitis accompanied by local lymphadenopathy ●Severe pharyngitis that is unresponsive to penicillin and undiagnosed after routine testing ●Persistent systemic febrile illness that is undiagnosed after routine testing ●Community-acquired pneumonia that is unresponsive to standard antibiotic therapy and undiagnosed after routine testing ●Nodular infiltrates plus a pleural effusion on chest imaging When these clinical features are observed in the setting of a history of animal (particularly wild animal) exposure or insect bites, the possibility of tularemia is greater, and making







Flashcard 7682271612172

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Dans quelles régions du monde la Tularémie est-elle moins fréquente ?
Answer
  • Amérique du Sud
  • Afrique
  • Australie
  • Angleterre

"It has been reported globally, but is less common in Africa, South America, Australia, and England." - UpToDate


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The patient's location, activities, and travel history also should inform the likelihood of tularemia. It has been reported globally, but is less common in Africa, South America, Australia, and England.

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reasonable. In particular, people who are farmers, veterinarians, hunters, national park service employees, landscapers, meat handlers, or laboratory workers are at increased risk for exposure. <span>The patient's location, activities, and travel history also should inform the likelihood of tularemia. It has been reported globally, but is less common in Africa, South America, Australia, and England. In the United States, it is most commonly reported in the south-central states, the Pacific Northwest, and parts of Massachusetts (figure 1). Clusters of cases, particularly of infectio







Flashcard 7682277117196

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelle proportion de mortalité dans la Tularémie en général depuis l'introduction d'antibiotiques efficaces (Streptomycine) ?
Answer

Mortalité 5 %

"Since the introduction of effective antibiotics (in particular streptomycin), historical mortality rates from tularemia have decreased from as high as 60 percent in severely ill patients with pneumonic or typhoidal disease to less than 5 percent overall [16,21,47,50]." - UpToDate


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Since the introduction of effective antibiotics (in particular streptomycin), historical mortality rates from tularemia have decreased from as high as 60 percent in severely ill patients with pneumonic or typhoidal disease to less than 5 percent overall [16,21,47,50].

Original toplevel document

UpToDate
ted or confirmed tularemia. Although spontaneous resolution of infection in the absence of specific treatment has been recorded [2], early effective treatment is associated with less morbidity. <span>Since the introduction of effective antibiotics (in particular streptomycin), historical mortality rates from tularemia have decreased from as high as 60 percent in severely ill patients with pneumonic or typhoidal disease to less than 5 percent overall [16,21,47,50]. Effective antibiotics — Antimicrobials with well-established clinical efficacy include the aminoglycosides streptomycin and gentamicin, tetracycline, doxycycline, the fluoroquinolones,







Flashcard 7682280262924

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelles sont les familles d'antibiotiques généralement utilisées pour traiter une Tularémie ?
Answer

  • Aminosides
  • Fluoroquinolones
  • Cyclines
  • (Chloramphénicol)

"Antimicrobials with well-established clinical efficacy include the aminoglycosides streptomycin and gentamicin, tetracycline, doxycycline, the fluoroquinolones, and chloramphenicol." - UpToDate


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Antimicrobials with well-established clinical efficacy include the aminoglycosides streptomycin and gentamicin, tetracycline, doxycycline, the fluoroquinolones, and chloramphenicol.

Original toplevel document

UpToDate
rates from tularemia have decreased from as high as 60 percent in severely ill patients with pneumonic or typhoidal disease to less than 5 percent overall [16,21,47,50]. Effective antibiotics — <span>Antimicrobials with well-established clinical efficacy include the aminoglycosides streptomycin and gentamicin, tetracycline, doxycycline, the fluoroquinolones, and chloramphenicol. These agents exhibit achievable minimal inhibitory concentrations (MICs) when tested using a standardized in vitro method against F. tularensis [60-62]. Resistance to aminoglycosides, f







Flashcard 7682282884364

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Quelle est la fréquence de la résistance de F.tularensis subsp holarctica dans une étude française ? (qualitatif)
Answer

Inexistante

"In a study from France, there was no fluoroquinolone resistance among 42 F. tularensis subspecies holarctica isolates and no molecular evidence of DNA gyrase mutations (which would confer fluoroquinolone resistance) among 82 tissue samples from patients with tularemia, including those who had a suboptimal outcome with fluoroquinolone treatment [64]" - UpToDate


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In a study from France, there was no fluoroquinolone resistance among 42 F. tularensis subspecies holarctica isolates and no molecular evidence of DNA gyrase mutations (which would confer fluoroquinolone resistance) among 82 tissue samples from patients with tularemia, including those who had a suboptimal outcome with fluoroquinolone treatment [64]

Original toplevel document

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nolones, or tetracycline in human isolates has been uncommon [63]. However, the majority of 29 human isolates of F. tularensis subspecies holarctica in Spain were resistant to tigecycline [63]. <span>In a study from France, there was no fluoroquinolone resistance among 42 F. tularensis subspecies holarctica isolates and no molecular evidence of DNA gyrase mutations (which would confer fluoroquinolone resistance) among 82 tissue samples from patients with tularemia, including those who had a suboptimal outcome with fluoroquinolone treatment [64]. Beta-lactams have been associated with clinical failure despite favorable in vitro susceptibilities [65]. Although successful use of erythromycin has been reported, it is not considere







Flashcard 7682287865100

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
Au cours de la Tularémie, pourquoi les traitements par DOXYCYCLINE sont plus longs ?
Answer

Risque de rechute

"Doxycycline is administered for a longer duration than other agents because of a higher risk of relapse with shorter courses." - UpToDate


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¥ Doxycycline is administered for a longer duration than other agents because of a higher risk of relapse with shorter courses. ‡ Levofloxacin has also been used successfully, although there is more clinical experience with ciprofloxacin, and the optimal dose is uncertain.

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lete the prescribed course of treatment. The duration of gentamicin in children with mild disease may be shortened to 5 to 7 days if there is an adequate clinical response and no complications. <span>¥ Doxycycline is administered for a longer duration than other agents because of a higher risk of relapse with shorter courses. ‡ Levofloxacin has also been used successfully, although there is more clinical experience with ciprofloxacin, and the optimal dose is uncertain. References: Dennis, DT, Inglesby, TV, Henderson, DA, et al. Tularemia as a biological weapon: medical and public health management. JAMA 2001; 285:2763. American Academy of Pediatrics.







Flashcard 7682294680844

Tags
#Clinical #Cliniques #Diagnosis #Diagnostic #Maladies-infectieuses-et-tropicales #Manifestations #Tularemia #Tularemie
Question
[VoF] - Il n'existe pas de transmission interpersonnelle de la Tularémie
Answer

VRAI

"Standard precautions are adequate for hospitalized patients with tularemia; person-to-person transmission does not occur." - UpToDate


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Standard precautions are adequate for hospitalized patients with tularemia; person-to-person transmission does not occur.

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and ankles ●Using insect repellents that are also effective against ticks ●Removing ticks promptly ●Only drinking potable water ●Adequately cooking wild meats Institutional infection control — <span>Standard precautions are adequate for hospitalized patients with tularemia; person-to-person transmission does not occur. Whenever tularemia is suspected or proven, microbiology laboratory and autopsy personnel handling patient specimens should be notified so that they can take precautions to minimize the







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Question
Après une exposition potentielle à F.tularensis, dans quels contextes ne PAS prescrire de prophylaxie ?
Answer

  • Délai depuis contact supérieur à la période d'incubation (> 1 semaine)
  • Individus vaccinés
  • Exposition à bas risque de contamination

> Surveillance simple

"Watchful waiting without antibiotics while monitoring for fever or other symptoms of tularemia is an appropriate strategy for individuals with lower-risk exposures, those identified later in the incubation period (eg, more than a week after exposure), and in vaccinated individuals." - UpToDate


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Watchful waiting without antibiotics while monitoring for fever or other symptoms of tularemia is an appropriate strategy for individuals with lower-risk exposures, those identified later in the incubation period (eg, more than a week after exposure), and in vaccinated individuals. As examples, prophylaxis is not indicated following a tick bite [1,2] or if the only risk was close contact with a patient with tularemia [1,47].

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nnel, and others exposed through nonintact skin, mucosal surfaces, or aerosols to materials contaminated with F. tularensis, as well as persons exposed to F. tularensis in a bioterrorism event. <span>Watchful waiting without antibiotics while monitoring for fever or other symptoms of tularemia is an appropriate strategy for individuals with lower-risk exposures, those identified later in the incubation period (eg, more than a week after exposure), and in vaccinated individuals. As examples, prophylaxis is not indicated following a tick bite [1,2] or if the only risk was close contact with a patient with tularemia [1,47]. Management without antibiotics following exposure to a bioterrorism event is also recommended for persons identified after others have become symptomatic (ie, later in the incubation pe







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There are five basic abnormalities of the pulse rhythm: the pause, regular brady- cardia, regular tachycardia, irregular rhythm varying with respiration, and cha- otic rhythm (irregularly irregular rhythm)
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Regular tachycardia is caused by sinus tachycardia, atrial flutter, paroxysmal supraventricular tachycardia, or ventricular tachycardia.
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Regular bradycardia is caused by sinus bradycardia, complete heart block, or halved pulse.
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The pause is caused by premature beats or second-degree heart block. It is named by the number of regular beats before each pause (i.e., bigeminal, trigeminal, or group beating)
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An irregular rhythm varying with respiration is sinus arrhythmia, a common rhythm of young, healthy patients.
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The chaotic rhythm is caused by atrial fibrillation or multifocal extrasystoles
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These arrhythmias may be distinguished by examination of the venous wave- forms, heart tones, and response to vagal maneuvers. Even so, all arrhythmias require electrocardiography for confirmation and monitoring
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Question
Devant une suspicion d'arythmie à l'examen cardiovasculaire, que dois-je : regarder, écouter et demander au patient de faire ?
Answer

  • Regarder : Pouls veineux (jugulaire)
  • Ecouter : Bruits du coeur (intensité / rythme)
  • Demander : Manoeuvres vagales

"These arrhythmias may be distinguished by examination of the venous wave- forms, heart tones, and response to vagal maneuvers." - McGee


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These arrhythmias may be distinguished by examination of the venous wave- forms, heart tones, and response to vagal maneuvers. Even so, all arrhythmias require electrocardiography for confirmation and monitoring

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Question
Quelles sont les 5 perturbations de bases du rythme cardiaque objectivables à la prise du pouls ?
[unknown IMAGE 7682360741132]
Answer

  • La pause
  • La tachycardie régulière
  • La bradycardie régulière
  • Le rythme variant avec la respiration
  • La tachycardie irrégulièrement irrégulière (rythme chaotique)

"There are five basic abnormalities of the pulse rhythm: the pause, regular brady- cardia, regular tachycardia, irregular rhythm varying with respiration, and cha- otic rhythm (irregularly irregular rhythm)" - McGee


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There are five basic abnormalities of the pulse rhythm: the pause, regular brady- cardia, regular tachycardia, irregular rhythm varying with respiration, and cha- otic rhythm (irregularly irregular rhythm)

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In the late 19th and early 20th centuries, before the introduction of electrocar- diography, clinicians could examine the patient’s arterial pulse, heart tones, and jugular venous waveforms and, from these observations alone, diagnose atrial and ventricular premature contractions, atrial flutter, atrial fibrillation, complete heart block, Mobitz 1 and 2 atrioventricular block, and sinoatrial block.1-3
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In fact, clini- cians were familiar enough with the bedside findings of these arrhythmias that early textbooks of electrocardiography included tracings of the arterial and venous pulse to help explain the electrocardiogram (ECG; Fig. 16.1).4
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The bedside diagnosis of arrhythmias today is probably little more than a intel- lectual game, because all significant arrhythmias require electrocardiography for confirmation and monitoring. Nonetheless, bedside diagnosis of arrhythmias is still possible, using principles discovered 100 years ago by Mackenzie, Wenckebach, and Lewis. These principles, based on extensive investigation and many polygraph recordings of the arterial and venous pulse,1-4 allow diagnosis of simple arrhythmias when the electrocardiograph is not immediately nearby
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The first step in diagnosing arrhythmias is to determine the basic rhythm of the patient’s radial pulse.
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The radial pulse may not correspond to the ventricular pulse (or apical pulse), as determined by auscultation of the heart tones or palpation of the cardiac impulse because some ventricular contractions are too weak to propel blood to the radial artery.
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Although the clinician must compare the radial pulse with the ventricular pulse to diagnose arrhythmias, the difference in rate between the two by itself indi- cates no particular diagnosis.
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The pause has two important causes: premature contractions (common) and heart block (uncommon).
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When the radial pulse consists of the regular repetition of two beats followed by a pause, the term bigeminal pulse or bigeminal rhythm is used
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The finding of several beats between each pause is usually called group beating, and even longer periods of regular rhythm interrupted by the rare pause are sometimes referred to as pulse intermissions
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The basic mechanism for all these rhythm disturbances is the same; only the frequency of premature beats or heart block differs among them.
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Because the cadence of these rhythms becomes predictable after short periods of observation, the term regularly irregular is sometimes used. This term, however, inaccurately conveys to others what is actually going on and is best discarded.
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Question
Donner la cause fréquente de pause dans le rythme cardiaque à la palpation du pouls
Answer

Extrasystole (contraction prématurée)

"The pause has two important causes: premature contractions (common) [...]" - McGee


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The pause has two important causes: premature contractions (common) and heart block (uncommon).

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BASIC MECHANISM OF THE PAUSE The pause has three basic mechanisms, illustrated in Fig. 16.3. The two most impor- tant questions that distinguish these mechanisms are the following: (1) Is there a premature radial pulse immediately preceding the pause? (2) Do additional ventric- ular beats (identified by listening to the heart tones or palpating the apical pulse) occur during the pause?
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Question
Quelles sont les deux questions à se poser devant une pause dans le rythme cardiaque à la palpation du pouls afin de différencier parmi les mécanismes à l'oeuvre dans cette pause ?
[unknown IMAGE 7682379877644]
Answer

  • Présence d'un battement radial prématuré avant la pause ?
  • Présence de battements ventriculaires surajoutés (auscultés ou palpés à l'apex) pendant la pause ?

"The two most important questions that distinguish these mechanisms are the following:
(1) Is there a premature radial pulse immediately preceding the pause?
(2) Do additional ventricular beats (identified by listening to the heart tones or palpating the apical pulse) occur during the pause?" - McGee


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BASIC MECHANISM OF THE PAUSE The pause has three basic mechanisms, illustrated in Fig. 16.3. The two most impor- tant questions that distinguish these mechanisms are the following: (1) Is there a premature radial pulse immediately preceding the pause? (2) Do additional ventric- ular beats (identified by listening to the heart tones or palpating the apical pulse) occur during the pause?

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If the premature contraction is too weak to open the aortic valve (second example in Fig. 16.3), the clinician palpating the pulse will not detect the quick beat but only feel the pause. Listening to the heart, he or she will only hear the first sound of the premature beat (S2 is absent because the aortic valve never opens)
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Some premature contractions are strong enough to open the aortic valve (first example in Fig. 16.3). If so, the clinician will feel a quick beat in the radial pulse just preceding the pause, although the quick beat is usually not as strong as a normal sinus beat. When listening to the heart tones, the clinician will hear both the first and second heart sounds of the early beat
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Patients with premature contractions (the first two examples in Fig. 16.3) have evidence of a premature ventricular beat during or immediately preceding the pause in the radial pulse. This early beat is always evident in the form of a pal- pable apical impulse or additional heart tones, although it may not be felt in the radial artery
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Patients with heart block (third example in Fig. 16.3), whether sinoatrial or atrio- ventricular, lack a palpable apical impulse or extra heart tones during the pause
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Question
Combien de déflexion ressenties à la palpation du pouls radial dans un rythme bigéminal entre chaque pause ?
Answer

DEUX

"When the radial pulse consists of the regular repetition of two beats followed by a pause, the term bigeminal pulse or bigeminal rhythm is used" - McGee

et

"When there are three radial pulse beats between each pause, the appropriate term is trigeminal pulse or trigeminal rhythm" - McGee


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When the radial pulse consists of the regular repetition of two beats followed by a pause, the term bigeminal pulse or bigeminal rhythm is used

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Based upon the mechanisms previously discussed, there are three causes of the bigeminal pulse rhythm: (1) alternating normal and premature contractions; (2) premature contractions occurring every third beat, although the premature con- traction is too weak to open the aortic valve; and (3) 3:2 heart block (atrioven- tricular or sinoatrial). In causes 2 and 3, both beats of the couplet are strong, but cause 2 has evidence of a ventricular contraction during the pause, whereas cause 3 does not.
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The same analysis is used for trigeminal rhythms and grouped beating (i.e., in trigeminal rhythms, possible causes are premature contractions after every two or three normal beats or 4:3 heart block).
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Two helpful bedside findings distinguish atrial premature contractions from ventricular ones: compensatory pause and "cannon a waves"
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Question
Quelles sont les deux trouvailles cliniques qui peuvent orienter vers l'origine atriale ou ventriculaire d'une extrasystole (battement prématuré) ?
Answer
  • Pause compensatoire
  • Ondes A en "coup de canon"
"Two helpful bedside findings distinguish atrial premature contractions from ventricular ones: compensatory pause and "cannon a waves"" - McGee

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Two helpful bedside findings distinguish atrial premature contractions from ventricular ones: compensatory pause and "cannon a waves"

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Beats that originate in the ventricle usually do not upset the underlying sinus rhythm, causing the beat immediately following the pause to fall exactly when the clinician anticipates it. Tapping the foot during the normal regular rhythm helps determine this. In Fig. 16.3, the distance “b” equals “a,” meaning there is a “com- plete compensatory pause.”
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Beats that originate in the atria, in contrast, often reset the sinus node, causing the next beat to appear earlier than expected. In Fig. 16.3, “b” would be less than “a,” and the clinician tapping the foot would find that the basic meter of rhythm changes. This rule is more helpful when the pause is not compensatory (i.e., b < a, indi- cating the beat is atrial), because many atrial premature contractions also seem to have a complete compensatory pause at the bedside.
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The appearance of a sudden prominent venous wave in the neck (cannon A wave) during the pause indicates that the premature beat was ventricular (see also Chapter 36). This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricuspid valve.
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Rarely, extremely premature ectopic atrial beats may also produce cannon A waves, but these waves precede the first heart sound of the premature contraction, whereas cannon A waves from ventricular premature con- tractions always follow the first heart sound of the premature beat.
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Question
Laquelle de ce deux extrasystoles entraîne une pause compensatoire : atriale ou ventriculaire ?
[unknown IMAGE 7682379877644]
Answer

Ventriculaire

"Beats that originate in the ventricle usually do not upset the underlying sinus rhythm, causing the beat immediately following the pause to fall exactly when the clinician anticipates it. [...] In Fig. 16.3, the distance “b” equals “a,” meaning there is a “complete compensatory pause.”" - McGee


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Beats that originate in the ventricle usually do not upset the underlying sinus rhythm, causing the beat immediately following the pause to fall exactly when the clinician anticipates it. Tapping the foot during the normal regular rhythm helps determine this. In Fig. 16.3, the distance “b” equals “a,” meaning there is a “com- plete compensatory pause.”

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Question
En faveur de quelle origine de l'extrasystole plaide une onde A en coup de canon visible à l'examen du pouls veineux jugulaire ?
Answer

Ventriculaire

"The appearance of a sudden prominent venous wave in the neck (cannon A wave) [...] indicates that the premature beat was ventricular (see also Chapter 36)" - McGee


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The appearance of a sudden prominent venous wave in the neck (cannon A wave) during the pause indicates that the premature beat was ventricular (see also Chapter 36). This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricus

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Question
À quelle moment de l'irrégularité du cycle cardiaque apparaît l'onde A en coup de canon ?
Answer

Pendant la pause

"The appearance of a sudden prominent venous wave in the neck (cannon A wave) during the pause indicates that the premature beat [...]." - McGee


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The appearance of a sudden prominent venous wave in the neck (cannon A wave) during the pause indicates that the premature beat was ventricular (see also Chapter 36). This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricusp

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#Chapter-16 #McGee-EBPD-Arrythmias #McGee-EBPD-Arythmies #Semio-Cardio #Semio-Cardio-Palpation #Semiologie #Semiology
Question
Quelle est l'explication physiopathologique à la survenue des ondes A en coup de canon pendant les extrasystoles ?
Answer

Contraction auriculaire contre des valves auriculo-ventriculaires fermées par la contraction ventriculaire prématurée

"This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricuspid valve." - Mcgee


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The appearance of a sudden prominent venous wave in the neck (cannon A wave) during the pause indicates that the premature beat was ventricular (see also Chapter 36). This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricuspid valve.

Original toplevel document (pdf)

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#Chapter-16 #McGee-EBPD-Arrythmias #McGee-EBPD-Arythmies #Semio-Cardio #Semio-Cardio-Palpation #Semiologie #Semiology
Regular bradycardia is a heart rate of less than 50 beats/minute.
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There are three causes of regular bradycardia that are recognizable at the bedside: sinus bradycardia, complete heart block, and halved pulse
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