Clinicopathologic Study of Thirty-Three Fatal Cases of Asian Influenza

Oseasohn, Robert; Adelson, Lester; Kaji, Masahide

doi:10.1056/nejm195903122601101

Cited by 196 publications

(92 citation statements)

References 10 publications

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“…Although specific mutations have been associated with mouse adaptation and multiorgan spread of human isolates (62, 63), we found no conserved changes between isolates of HKx31 from the heart and brain when compared with those from the lungs. Given the well-documented ability of influenza viruses to agglutinate erythrocytes and mammalian cells (64), thrombus formation, cellular injury, and ischemia reported in patients with severe influenza infections (65,66) could also be important pathological sequelae if hemagglutination were to occur in the microvasculature of neutropenic animals.…”

Section: Discussionmentioning

confidence: 99%

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Tate

Deng

Jones

et al. 2009

The Journal of Immunology

286

308

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The clinical response to influenza infection ranges from mild disease to severe pneumonia and it remains unclear whether the inflammatory response to infection is protective or pathogenic. We have defined a novel role for neutrophils in ameliorating lung injury during influenza infection, thereby limiting development of severe disease. Infection of neutrophil-depleted mice with influenza virus HKx31 (H3N2) led to rapid weight loss, pneumonia, and death. Neutropenia was associated with enhanced virus replication in the respiratory tract; however, viral titers were declining at the time of death, leading us to investigate other factors contributing to mortality. In addition to thymic atrophy, lymphopenia, and viremic spread, depletion of neutrophils led to exacerbated pulmonary inflammation, edema, and respiratory dysfunction. Thus, while it is well established that neutrophils contribute to lung injury in a range of pathological conditions, reduced numbers or impaired neutrophil function can facilitate progression of mild influenza to severe clinical disease.

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Section: Discussionmentioning

confidence: 99%

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Tate

Deng

Jones

et al. 2009

The Journal of Immunology

286

308

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“…Las elevaciones séricas de CPK son relativamente específicas para procesos miosíticos o distróficos del músculo estriado (esquelético o miocárdico) (1,16). Aunque se han descrito alteraciones tóxicas e inflamatorias agudas en el miocardio en casos fatales de influenza (17), no se encontró evidencia de ello en nuestro paciente. Es por eso los niveles tan altos de CPK encontrados muy probablemente sean debidos al daño del músculo esquelético de los miembros inferiores.…”

Section: Discusionunclassified

Miositis aguda postinfecciosa.

Tori¹

2013

Rev Med Hered

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SUMMARYA seven year old patient in described with acute focal myositis, following an influenza-like infection, involving exclusively the gastroenemius and soleus muscles. The patient improved only with bed rest and symptomatic treatment and made a full recovery in three days. Laboratory studies showed a normal white blood count with an increase in the band forms, elevated SGOT, DHL, and CPK, all of which returned to normal after one week. The patient remains asymptomatic one month after his discharge. KEY WORDS: Acute post-infection myositis, myositis, INTRODUCCIONSe presenta un caso de miositis aguda focal transitoria, postinfecciosa, de etiología probablemente viral, en un niño de 7 años de edad, con dolor intenso en ambas pantorrillas, imposibilitándolo de mover las piernas y caminar.El objetivo de la presente comunicación es llamar la atención sobre la presencia de la asociación de miositis transitoria aguda e infecciones virales principalmente el virus de la influenza. Caso clínicoC.J.L., varón, de 7 años de edad, con antecedentes de hiperreactividad bronquial. Cuatro días antes de su ingreso había estado medicado con dicloxacilina y acetaminofén por un cuadro infeccioso respiratorio alto, caracterizado por fiebre, malestar general, coriza y tos. Siete horas antes de hospitalizarse, despierta con dolor intenso en ambas pantorrillas que le impedía mantenerse de pie y caminar El paciente estaba febril pero en buen estado general, con tos irritativa y con un dolor exquisito en ambas pantorrillas, tanto espontáneo como a la palpación. El tímpano derecho estaba congestivo. La faringe presentaba congestión sin exudados. Al examen pulmonar se encontró sibilantes y roncantes escasos en campos pulmonares. El abdomen era blando,

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“…Although several clinical reports on the occurrence of myocarditis following influenza virus infection have appeared (2,5,16), experimental studies on influenza virus-induced myocarditis still remain incomplete in regard to its reproducibility and pathogenic mechanisms (11, 18). The present study shows that in limited experimental conditions, myocarditis is induced in mice at frequency as high as 82% by inhalation of influenza A z virus.…”

Section: Discussionmentioning

confidence: 99%

“…Many viruses, for example coxsackie (9,20), echo (14), mumps (1), herpes (4,7), and influenza (11, 18) viruses, are known to be causative agents of myocarditis, and the pathogenic mechanism of some of them (4,21) has been analyzed. Myocarditis that occurs after influenza virus infection has been studied experimentally (11,18) and clinically (2,5,16), but its pathogenesis remains to be clarified.…”

mentioning

confidence: 99%

Experimental Myocarditis Induced in Mice by Infection with Influenza A₂ Virus

Sakamoto

Suzuki

Arai

et al. 1981

Microbiology and Immunology

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A mouse model was established for the study of acute myocarditis that occurs during influenza infection. Challenge with more than 10 LD50 of mouseadapted influenza A 2 virus (H2N2) induced myocarditis macroscopically discernible as white, irregularly shaped lesions which were shown by histological examination to consist of necrotic myofibers surrounded by infiltrating mononuclear inflammatory cells. After challenge with 10 LD 50 of the virus, macroscopic myocarditis was found to advance in a progressive manner up to the 7th day, while the virus titer in the heart reached its peak on the 2nd day and began to decrease on the 5th day of infection. However, development of myocarditis was significantly suppressed in mice which were irradiated with 400 R of X-rays before infection. In addition, myocarditis did not develop in congenitally athymic nude mice.These data indicate that myocarditis was not brought about by viral action directly, but that it was mediated by some function of the host against viral invasion, which was abolished by X-irradiation. The data also suggest that T cells played a key role in the development of myocarditis.

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Clinicopathologic Study of Thirty-Three Fatal Cases of Asian Influenza

Cited by 196 publications

References 10 publications

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Miositis aguda postinfecciosa.

Experimental Myocarditis Induced in Mice by Infection with Influenza A₂ Virus

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Clinicopathologic Study of Thirty-Three Fatal Cases of Asian Influenza

Cited by 196 publications

References 10 publications

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Miositis aguda postinfecciosa.

Experimental Myocarditis Induced in Mice by Infection with Influenza A2 Virus

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Product

Resources

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Experimental Myocarditis Induced in Mice by Infection with Influenza A₂ Virus