神马文学网Lemierre's syndrome
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Lemierre's syndrome
Classification and external resources
DiseasesDB31108
Lemierre's Syndrome (or Lemierre's disease, also known as postanginal sepsis and human necrobacillosis) is a form ofthrombophlebitis[1] usually caused by the bacteriumFusobacterium necrophorum, and occasionally by other members of the genus Fusobacterium (F. nucleatum, F. mortiferum and F. varium etc.) and usually affects young, healthy adults. Lemierre syndrome develops most often after a sore throat caused by some bacterium of theStreptococcus genus, has created a peritonsillar abscess, a crater filled with pus and bacteria near the tonsils. Deep in the abscess, anaerobic bacteria (microbes that do not require oxygen) like Fusobacterium necrophorum can flourish. The bacteria penetrate from the abscess into the neighboring jugular vein in the neck and there they cause an infected clot (thrombosis) to form, from which bacteria are seeded throughout the body by the bloodstream (bacteremia). Pieces of the infected clot break off and travel to the lungs as emboli blocking branches of the pulmonary artery bringing the heart's blood to the lungs. This causes shortness of breath, chest pain and severepneumonia. Fusobacteria are normal inhabitants of the oropharyngeal flora. This is a very rare disease with only approximately 159 cases in the last 100years.[2]
Sepsis following from a throat infection was described by Scottmuller in 1918.[3] However it was Andre Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic septicemia, of whom 18 patients died.[4]
Contents
[hide]
1 Signs and symptoms2 Cause3 Pathophysiology4 Diagnosis5 Treatment6 Prognosis7 Epidemiology8 History9 References
[edit] Signs and symptoms
The symptoms vary per person, but usually start with a sore throat, fever, and general body weakness. These are followed by extreme lethargy, spiked fevers, rigors, swollen cervicallymph nodes and a swollen, tender or painful neck. Often there is abdominal pain, diarrhea, nausea and vomiting during this phase. These symptoms usually occur several days to 2 weeks after the initial symptoms.
Symptoms of pulmonary involvement can be shortness of breath, cough and painful breathing (pleuritic chest pain). Rarely there ishemoptysis. Painful or inflamed joints (arthralgia orarthritis, respectively) exist when the joints are involved.
Septic shock can occur which presents itself withhypotension,tachycardia,oliguria andtachypnea.Nuchal rigidity, headache andphotophobia occur in case there ismeningitis.
Hepatomegaly andsplenomegaly (enlarged liver and spleen, respectively) can be found, but are not always associated with hepatic or splenic abscesses.[5][6]
Other signs and symptoms that may occur:
Headache (not related to meningitis) Muscle painJaundiceTrismusCrepitations are sometimes heard over the lungsPericardial friction rubs as a sign ofpericarditis (rare)Cranial nerveparalysis andHorner's syndrome (both rare)
[edit] Cause
Fusobacterium necrophorum is the causative agent in most people with Lemierre's syndrome. However only 1 in 400 cases of Fusobacterium necrophorum results in Lemierre's syndrome.[7] and 81% of the people with Lemierres's syndrome has been infected with Fusobacterium necrophorum, while in 11% of people it was caused by other Fusobacterium species[8]. MRSA might also be an issue in Lemierre infections.[9] Rarely Lemierre's syndrome is caused by other (usuallyGram-negative) bacteria, which includeBacteroides fragilis andBacteroides melaninogenicus,Peptostreptococcus spp.,Streptococcus microaerophile,Staphylococcus aureus, andEikenella corrodens.[8][10]
[edit] Pathophysiology
Lemierre's syndrome is initiated by an infection of the head and neck region. Usually this infection is a pharyngitis (which occurred in 87,1% of patients as reported by a literature review[6]), but it can also be initiated by anotitis, amastoiditis, asinusitis or aparotitis.
During the primary infection, F. necrophorum colonizes the infection site and the infection spreads to theparapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to theinternal jugular vein.[5] In this vein, the bacteria cause the formation of athrombus containing these bacteria. Furthermore, theinternal jugular vein becomes inflamed. This septicthrombophlebitis can give rise to septicmicroemboli[11] that disseminate to other parts of the body where they can form abscesses and septic infarctions. The firstcapillaries that the emboli encounter where they can nestle themselves are the pulmonary capillaries. As a consequence, the most frequently involved site of septic metastases are the lungs, followed by the joints (knee, hip,sternoclavicular joint, shoulder and elbow[12]). In the lungs, the bacteria cause abscesses, nodulary and cavitary lesions. Pleural effusion is often present.[6] Other sites involved in septic metastasis and abscess formation are the muscles and soft tissues, liver, spleen, kidneys and nervous system (intracranial abscesses, meningitis).[5]
Production of bacterial toxins such aslipopolysaccharide leads to secretion ofcytokines by white blood cells which then both lead to symptoms ofsepsis. F. necrophorum produceshemagglutinin which causes platelet aggregation that can lead todiffuse intravascular coagulation andthrombocytopenia.[13][14]
[edit] Diagnosis
Diagnosis and the imaging (and laboratory) studies to be ordered largely depend on the patient history, signs and symptoms. If a persistent sore throat, with the symptoms are found, physicians are cautioned to screen for Lemierre's syndrome.
Laboratory investigations reveal signs of a bacterial infection with elevatedC-reactive protein,erythrocyte sedimentation rate and white blood cells (notablyneutrophils). Platelet count can be low or high. Liver function tests and renal function tests are often abnormal.
Thrombosis of the internal jugular vein can be displayed withsonography. However, thrombi that have developed recently have low echogenicity and thus will not show up on ultrasound. A CT scan or an MRI scan is more sensitive in displaying the thrombus.
Chest X-ray and chest CT may show pleural effusion, nodules, infiltrates, abscesses and cavitations.
Bacterial cultures taken from the blood,joint aspirates or other sites can identify the causative agent of the disease.
Other illnesses that can be included in thedifferential diagnosis are:
Q feverTuberculosisPneumonia
[edit] Treatment
Lemierre's syndrome is primarily treated withantibiotics given intravenously. However, because sore throats are most commonly caused byviruses, for which antibiotic treatment is unnecessary, such treatment is not usual in the first phase of the disease. Lemierre's disease proves that, rarely, antibiotics are needed for 'sore throats'.[15] Fusobacterium necrophorum is generally highly susceptible tobeta-lactam antibiotics,metronidazole,clindamycin and third generationcephalosporins while the other fusobacteria have varying degrees of resistance to beta-lactams and clindamycin[14]. Additionally, there may exist a co-infection by another bacterium. For these reasons is often advised not to use monotherapy in treating Lemierre's syndrome. Penicillin and penicillin-derived antibiotics can thus be combined with abeta-lactamase inhibitor such asclavulanic acid or with metronidazole.[10][5] Clindamycin can be given as monotherapy.
If antibiotic therapy does not improve the clinical picture, it may prove useful to drain any abscesses and/or perform ligation of the internal jugular vein where the antibiotic can not penetrate.[10][6][16]
There is no evidence to opt for or against the use of anticoagulation therapy. The low incidence of Lemierre's syndrome has not made it possible to set up clinical trials to study the disease.[10]
The disease can often be un-treatable, especially if other negative factors occur,i.e. various diseases occurring at the same time, such asmeningitis,pneumonia.
[edit] Prognosis
The mortality of Lemierre's syndrome is when diagnosed about 4.6%.[17] Since this disease is not very known and often remains undiagnosed, mortality might be much higher.
[edit] Epidemiology
Lemierre's syndrome is currently a rare, but was more common in the early 20th century before the discovery ofpenicillin. The reduced use of antibiotics for sore throats may have increased the risk of this disease, with 19 cases in 1997 and 34 cases in 1999 reported in theUK.[15] The incidence rate is currently 0.8 cases per million in the general population,[18] leading it to be termed the "forgotten disease".[19] The disease is known to affect healthy young adults. The disease is becoming less rare with many cases being reported, however it is still known as "the forgotten disease" as many doctors are unaware of its existence, therefore often not even diagnosed which might conisderably change the above mentioned statistics. The mortality rate was 90% prior to antibiotic therapy,[4] but is now generally quoted as 15% once this illness is correctly diagnosed and cured with proper medical treatment, although one series of cases reported mortality as low as 6.4%.[6]
[edit] History
Sepsis following from a throat infection was described by Scottmuller in 1918.[20] However it was Andre Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic septicemia, of whom 18 patients died.[4]
[edit] References
^Lemierre syndrome atDorland's Medical Dictionary^ O'Brien Sr, WT; Lattin GE Jr, Thompson AK (September 2006)."Lemierre syndrome: an all-but-forgotten disease". American Journal of Roentgenology 187 (3): W324.doi:10.2214/AJR.06.0096.PMID 16928914.http://www.ajronline.org/cgi/content/full/187/3/W324. ^ Schottmuller H (1918). "Ueber die Pathogenität anaërober Bazillen" (in German). Dtsch Med Wochenschr 44: 1440. ^abc Lemierre A (1936). "On certain septicemias due to anaerobic organisms". Lancet 1: 701–3.doi:10.1016/S0140-6736(00)57035-4. ^abcd Syed MI, Baring D, Addidle M, Murray C, Adams C (September 2007). "Lemierre syndrome: two cases and a review". The Laryngoscope (The American Laryngological, Rhinological & Otological Society; Lippincott Williams & Wilkins) 117 (9): 1605–1610.doi:10.1097/MLG.0b013e318093ee0e.PMID 17762792. ^abcde Chirinos JA, Lichtstein DM, Garcia J, Tamariz LJ (November 2002). "The evolution of Lemierre syndrome: report of 2 cases and review of the literature". Medicine (Baltimore) (Lippincott Williams & Wilkins) 81 (6): 458–465.PMID 12441902. ^"Sign In — Ann Intern Med".http://www.annals.org/content/151/11/812.full. ^ab Sinave CP, Hardy GJ, Fardy PW (March 1989). "The Lemierre's syndrome: suppurative thrombophlebitis of the internal jugular vein secondary to oropharyngeal infection". Medicine (Baltimore) (Williams & Wilkins) 68 (2): 85–94.PMID 2646510. ^ NCBI PubMed, Bentley TP, Brennan DF (August 2009). "Lemierre's syndrome: methicillin-resistant Staphylococcus aureus (MRSA) finds a new home.". Medicine (Orlando) (Bentley & Brennan) 37 (2): 131–4.doi:10.1016/j.jemermed.2007.07.066.PMID 18280087. ^abcd Puymirat E, Biais M, Camou F, Lefèvre J, Guisset O, Gabinski C (March 2008). "A Lemierre's syndrome variant caused by Staphylococcus aureus". American journal of emergency medicine (Elsevier) 26 (3): 380–387.doi:10.1016/j.ajem.2007.05.020.PMID 18358967. ^ Screaton NJ, Ravenel JG, Lehner PJ, Heitzman ER, Flower CD (November 1999)."Lemierre Syndrome: Forgotten but Not Extinct-Report of Four Cases". Radiology (Radiological Society of North America) 213 (2): 369–374.PMID 10551214.http://radiology.rsnajnls.org/cgi/content/full/213/2/369. "The absence of proximal thrombus at CT pulmonary angiography suggests that microemboli, rather than the macroembolic clot burden more typical of acute pulmonary embolism, are responsible for the pulmonary findings in Lemierre syndrome". ^ Beldman TF, Teunisse HA, Schouten TJ (November 1997). "Septic arthritis of the hip by Fusobacterium necrophorum after tonsillectomy: a form of Lemierre syndrome?". European journal of pediatrics (Springer-Verlag) 156 (11): 856–857.PMID 9392400. ^ Kanoe M, Yamanaka M, Inoue M (1989). "Effects of Fusobacterium necrophorum on the mesenteric microcirculation of guinea pigs". Medical Microbiology and Immunology (Springer Berlin / Heidelberg) 178 (2): 99–104.PMID 2659950. ^ab Hagelskjaer Kristensen L, Prag J (Aug 2000). "Human necrobacillosis, with emphasis on Lemierre's syndrome". Clinical Infectious Diseases 31 (2): 524–532.doi:10.1086/313970.PMID 10987717. ^ab UK Chief Medical Officer Update 29 Feb 2001 (CMO Update29 Feb 2001)^ Aspesberro F, Siebler T, Van Nieuwenhuyse JP, Panosetti E, Berthet F (September 2008). "Lemierre syndrome in a 5-month-old male infant: Case report and review of the pediatric literature". Pediatric critical care medicine (The Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies) 9 (5): e35-37.doi:10.1097/PCC.0b013e31817319fa.PMID 18779698. ^"Sign In — Ann Intern Med".http://www.annals.org/content/151/11/812.full. ^ Sibai K, Sarasin F (2004). "[Lemierre syndrome: a diagnosis to keep in mind]" (in French). Revue médicale de la Suisse romande 124 (11): 693–5.PMID 15631168. ^ Weesner CL, Cisek JE (1993). "Lemierre syndrome: the forgotten disease". Annals of emergency medicine 22 (2): 256–8.doi:10.1016/S0196-0644(05)80216-1.PMID 8427443. ^ Schottmuller H (1918). "Ueber die Pathogenität anaërober Bazillen" (in German). Dtsch Med Wochenschr 44: 1440.
Jump to:navigation,search
Lemierre's syndrome
Classification and external resources
DiseasesDB31108
Lemierre's Syndrome (or Lemierre's disease, also known as postanginal sepsis and human necrobacillosis) is a form ofthrombophlebitis[1] usually caused by the bacteriumFusobacterium necrophorum, and occasionally by other members of the genus Fusobacterium (F. nucleatum, F. mortiferum and F. varium etc.) and usually affects young, healthy adults. Lemierre syndrome develops most often after a sore throat caused by some bacterium of theStreptococcus genus, has created a peritonsillar abscess, a crater filled with pus and bacteria near the tonsils. Deep in the abscess, anaerobic bacteria (microbes that do not require oxygen) like Fusobacterium necrophorum can flourish. The bacteria penetrate from the abscess into the neighboring jugular vein in the neck and there they cause an infected clot (thrombosis) to form, from which bacteria are seeded throughout the body by the bloodstream (bacteremia). Pieces of the infected clot break off and travel to the lungs as emboli blocking branches of the pulmonary artery bringing the heart's blood to the lungs. This causes shortness of breath, chest pain and severepneumonia. Fusobacteria are normal inhabitants of the oropharyngeal flora. This is a very rare disease with only approximately 159 cases in the last 100years.[2]
Sepsis following from a throat infection was described by Scottmuller in 1918.[3] However it was Andre Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic septicemia, of whom 18 patients died.[4]
Contents
[hide]
1 Signs and symptoms2 Cause3 Pathophysiology4 Diagnosis5 Treatment6 Prognosis7 Epidemiology8 History9 References
[edit] Signs and symptoms
The symptoms vary per person, but usually start with a sore throat, fever, and general body weakness. These are followed by extreme lethargy, spiked fevers, rigors, swollen cervicallymph nodes and a swollen, tender or painful neck. Often there is abdominal pain, diarrhea, nausea and vomiting during this phase. These symptoms usually occur several days to 2 weeks after the initial symptoms.
Symptoms of pulmonary involvement can be shortness of breath, cough and painful breathing (pleuritic chest pain). Rarely there ishemoptysis. Painful or inflamed joints (arthralgia orarthritis, respectively) exist when the joints are involved.
Septic shock can occur which presents itself withhypotension,tachycardia,oliguria andtachypnea.Nuchal rigidity, headache andphotophobia occur in case there ismeningitis.
Hepatomegaly andsplenomegaly (enlarged liver and spleen, respectively) can be found, but are not always associated with hepatic or splenic abscesses.[5][6]
Other signs and symptoms that may occur:
Headache (not related to meningitis) Muscle painJaundiceTrismusCrepitations are sometimes heard over the lungsPericardial friction rubs as a sign ofpericarditis (rare)Cranial nerveparalysis andHorner's syndrome (both rare)
[edit] Cause
Fusobacterium necrophorum is the causative agent in most people with Lemierre's syndrome. However only 1 in 400 cases of Fusobacterium necrophorum results in Lemierre's syndrome.[7] and 81% of the people with Lemierres's syndrome has been infected with Fusobacterium necrophorum, while in 11% of people it was caused by other Fusobacterium species[8]. MRSA might also be an issue in Lemierre infections.[9] Rarely Lemierre's syndrome is caused by other (usuallyGram-negative) bacteria, which includeBacteroides fragilis andBacteroides melaninogenicus,Peptostreptococcus spp.,Streptococcus microaerophile,Staphylococcus aureus, andEikenella corrodens.[8][10]
[edit] Pathophysiology
Lemierre's syndrome is initiated by an infection of the head and neck region. Usually this infection is a pharyngitis (which occurred in 87,1% of patients as reported by a literature review[6]), but it can also be initiated by anotitis, amastoiditis, asinusitis or aparotitis.
During the primary infection, F. necrophorum colonizes the infection site and the infection spreads to theparapharyngeal space. The bacteria then invade the peritonsillar blood vessels where they can spread to theinternal jugular vein.[5] In this vein, the bacteria cause the formation of athrombus containing these bacteria. Furthermore, theinternal jugular vein becomes inflamed. This septicthrombophlebitis can give rise to septicmicroemboli[11] that disseminate to other parts of the body where they can form abscesses and septic infarctions. The firstcapillaries that the emboli encounter where they can nestle themselves are the pulmonary capillaries. As a consequence, the most frequently involved site of septic metastases are the lungs, followed by the joints (knee, hip,sternoclavicular joint, shoulder and elbow[12]). In the lungs, the bacteria cause abscesses, nodulary and cavitary lesions. Pleural effusion is often present.[6] Other sites involved in septic metastasis and abscess formation are the muscles and soft tissues, liver, spleen, kidneys and nervous system (intracranial abscesses, meningitis).[5]
Production of bacterial toxins such aslipopolysaccharide leads to secretion ofcytokines by white blood cells which then both lead to symptoms ofsepsis. F. necrophorum produceshemagglutinin which causes platelet aggregation that can lead todiffuse intravascular coagulation andthrombocytopenia.[13][14]
[edit] Diagnosis
Diagnosis and the imaging (and laboratory) studies to be ordered largely depend on the patient history, signs and symptoms. If a persistent sore throat, with the symptoms are found, physicians are cautioned to screen for Lemierre's syndrome.
Laboratory investigations reveal signs of a bacterial infection with elevatedC-reactive protein,erythrocyte sedimentation rate and white blood cells (notablyneutrophils). Platelet count can be low or high. Liver function tests and renal function tests are often abnormal.
Thrombosis of the internal jugular vein can be displayed withsonography. However, thrombi that have developed recently have low echogenicity and thus will not show up on ultrasound. A CT scan or an MRI scan is more sensitive in displaying the thrombus.
Chest X-ray and chest CT may show pleural effusion, nodules, infiltrates, abscesses and cavitations.
Bacterial cultures taken from the blood,joint aspirates or other sites can identify the causative agent of the disease.
Other illnesses that can be included in thedifferential diagnosis are:
Q feverTuberculosisPneumonia
[edit] Treatment
Lemierre's syndrome is primarily treated withantibiotics given intravenously. However, because sore throats are most commonly caused byviruses, for which antibiotic treatment is unnecessary, such treatment is not usual in the first phase of the disease. Lemierre's disease proves that, rarely, antibiotics are needed for 'sore throats'.[15] Fusobacterium necrophorum is generally highly susceptible tobeta-lactam antibiotics,metronidazole,clindamycin and third generationcephalosporins while the other fusobacteria have varying degrees of resistance to beta-lactams and clindamycin[14]. Additionally, there may exist a co-infection by another bacterium. For these reasons is often advised not to use monotherapy in treating Lemierre's syndrome. Penicillin and penicillin-derived antibiotics can thus be combined with abeta-lactamase inhibitor such asclavulanic acid or with metronidazole.[10][5] Clindamycin can be given as monotherapy.
If antibiotic therapy does not improve the clinical picture, it may prove useful to drain any abscesses and/or perform ligation of the internal jugular vein where the antibiotic can not penetrate.[10][6][16]
There is no evidence to opt for or against the use of anticoagulation therapy. The low incidence of Lemierre's syndrome has not made it possible to set up clinical trials to study the disease.[10]
The disease can often be un-treatable, especially if other negative factors occur,i.e. various diseases occurring at the same time, such asmeningitis,pneumonia.
[edit] Prognosis
The mortality of Lemierre's syndrome is when diagnosed about 4.6%.[17] Since this disease is not very known and often remains undiagnosed, mortality might be much higher.
[edit] Epidemiology
Lemierre's syndrome is currently a rare, but was more common in the early 20th century before the discovery ofpenicillin. The reduced use of antibiotics for sore throats may have increased the risk of this disease, with 19 cases in 1997 and 34 cases in 1999 reported in theUK.[15] The incidence rate is currently 0.8 cases per million in the general population,[18] leading it to be termed the "forgotten disease".[19] The disease is known to affect healthy young adults. The disease is becoming less rare with many cases being reported, however it is still known as "the forgotten disease" as many doctors are unaware of its existence, therefore often not even diagnosed which might conisderably change the above mentioned statistics. The mortality rate was 90% prior to antibiotic therapy,[4] but is now generally quoted as 15% once this illness is correctly diagnosed and cured with proper medical treatment, although one series of cases reported mortality as low as 6.4%.[6]
[edit] History
Sepsis following from a throat infection was described by Scottmuller in 1918.[20] However it was Andre Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic septicemia, of whom 18 patients died.[4]
[edit] References
^Lemierre syndrome atDorland's Medical Dictionary^ O'Brien Sr, WT; Lattin GE Jr, Thompson AK (September 2006)."Lemierre syndrome: an all-but-forgotten disease". American Journal of Roentgenology 187 (3): W324.doi:10.2214/AJR.06.0096.PMID 16928914.http://www.ajronline.org/cgi/content/full/187/3/W324. ^ Schottmuller H (1918). "Ueber die Pathogenität anaërober Bazillen" (in German). Dtsch Med Wochenschr 44: 1440. ^abc Lemierre A (1936). "On certain septicemias due to anaerobic organisms". Lancet 1: 701–3.doi:10.1016/S0140-6736(00)57035-4. ^abcd Syed MI, Baring D, Addidle M, Murray C, Adams C (September 2007). "Lemierre syndrome: two cases and a review". The Laryngoscope (The American Laryngological, Rhinological & Otological Society; Lippincott Williams & Wilkins) 117 (9): 1605–1610.doi:10.1097/MLG.0b013e318093ee0e.PMID 17762792. ^abcde Chirinos JA, Lichtstein DM, Garcia J, Tamariz LJ (November 2002). "The evolution of Lemierre syndrome: report of 2 cases and review of the literature". Medicine (Baltimore) (Lippincott Williams & Wilkins) 81 (6): 458–465.PMID 12441902. ^"Sign In — Ann Intern Med".http://www.annals.org/content/151/11/812.full. ^ab Sinave CP, Hardy GJ, Fardy PW (March 1989). "The Lemierre's syndrome: suppurative thrombophlebitis of the internal jugular vein secondary to oropharyngeal infection". Medicine (Baltimore) (Williams & Wilkins) 68 (2): 85–94.PMID 2646510. ^ NCBI PubMed, Bentley TP, Brennan DF (August 2009). "Lemierre's syndrome: methicillin-resistant Staphylococcus aureus (MRSA) finds a new home.". Medicine (Orlando) (Bentley & Brennan) 37 (2): 131–4.doi:10.1016/j.jemermed.2007.07.066.PMID 18280087. ^abcd Puymirat E, Biais M, Camou F, Lefèvre J, Guisset O, Gabinski C (March 2008). "A Lemierre's syndrome variant caused by Staphylococcus aureus". American journal of emergency medicine (Elsevier) 26 (3): 380–387.doi:10.1016/j.ajem.2007.05.020.PMID 18358967. ^ Screaton NJ, Ravenel JG, Lehner PJ, Heitzman ER, Flower CD (November 1999)."Lemierre Syndrome: Forgotten but Not Extinct-Report of Four Cases". Radiology (Radiological Society of North America) 213 (2): 369–374.PMID 10551214.http://radiology.rsnajnls.org/cgi/content/full/213/2/369. "The absence of proximal thrombus at CT pulmonary angiography suggests that microemboli, rather than the macroembolic clot burden more typical of acute pulmonary embolism, are responsible for the pulmonary findings in Lemierre syndrome". ^ Beldman TF, Teunisse HA, Schouten TJ (November 1997). "Septic arthritis of the hip by Fusobacterium necrophorum after tonsillectomy: a form of Lemierre syndrome?". European journal of pediatrics (Springer-Verlag) 156 (11): 856–857.PMID 9392400. ^ Kanoe M, Yamanaka M, Inoue M (1989). "Effects of Fusobacterium necrophorum on the mesenteric microcirculation of guinea pigs". Medical Microbiology and Immunology (Springer Berlin / Heidelberg) 178 (2): 99–104.PMID 2659950. ^ab Hagelskjaer Kristensen L, Prag J (Aug 2000). "Human necrobacillosis, with emphasis on Lemierre's syndrome". Clinical Infectious Diseases 31 (2): 524–532.doi:10.1086/313970.PMID 10987717. ^ab UK Chief Medical Officer Update 29 Feb 2001 (CMO Update29 Feb 2001)^ Aspesberro F, Siebler T, Van Nieuwenhuyse JP, Panosetti E, Berthet F (September 2008). "Lemierre syndrome in a 5-month-old male infant: Case report and review of the pediatric literature". Pediatric critical care medicine (The Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies) 9 (5): e35-37.doi:10.1097/PCC.0b013e31817319fa.PMID 18779698. ^"Sign In — Ann Intern Med".http://www.annals.org/content/151/11/812.full. ^ Sibai K, Sarasin F (2004). "[Lemierre syndrome: a diagnosis to keep in mind]" (in French). Revue médicale de la Suisse romande 124 (11): 693–5.PMID 15631168. ^ Weesner CL, Cisek JE (1993). "Lemierre syndrome: the forgotten disease". Annals of emergency medicine 22 (2): 256–8.doi:10.1016/S0196-0644(05)80216-1.PMID 8427443. ^ Schottmuller H (1918). "Ueber die Pathogenität anaërober Bazillen" (in German). Dtsch Med Wochenschr 44: 1440.