Shark fin sign: A rare EKG finding in a patient with Takotsubo cardiomyopathy from influenza A infection.

This case demonstrated the rare "shark fin" ECG pattern, an ST-segment elevation typically seen in acute myocardial infarction. We reported a case of takotsubo cardiomyopathy secondary to influenza A infection with multiple organ failure, showing the shark fin sign and resulting in in-patient mortality and various complication.

Miller-Fisher Syndrome in the Setting of Influenza A Infection.

Miller-Fisher syndrome (MFS) is a rare, and milder, variant of Guillain-Barre syndrome (GBS) that is characterized by ophthalmoplegia, areflexia, and ataxia, with the additional possibility of limb weakness. There is not a specific demographic or common situation in which MFS is usually seen. This paper details a suspected case of MFS in a 59-year-old male with a concurrent influenza infection. He had been experiencing progressive flu-like symptoms a few days prior to the onset of his neurological symptoms, presenting to the hospital with diplopia and paresthesias of his extremities. His physical exam on admission revealed areflexia and gait instability, as well as oculomotor nerve palsies that were causing his diplopia. After running tests to rule out other possible causes of his presentation, along with having a positive influenza A test, he was diagnosed with MFS and started on intravenous immunoglobulin (IVIG). His symptoms resolved by the end of the treatment course. Based on his presentation and resolution of symptoms, this would be one of the few reported cases of MFS following influenza A infection.

Sepsis Due to Haemophilus influenzae and Masked Influenza A Infection.

Haemophilus influenzae (H. influenzae) is a facultative anaerobe, pleomorphic Gram-negative coccobacillus capable of causing various respiratory and blood stream infections. Introduction of childhood immunization against H. influenza type b has decreased its prevalence. Invasive infection with non-typeable H. influenzae is increasing specially in vulnerable population. We present a case of a 69-year-old female who developed septic shock due to H. influenzae infection. She was also found to have influenza A infection in bronchoalveolar lavage (BAL) sample although initial test with nasopharyngeal swab was negative. This case report highlights the fact that in patients with high clinical suspicion, negative nasopharyngeal swab with polymerase chain reaction may not rule out influenza infection and BAL may be necessary to confirm the diagnosis and H. influenzae can be causing bacterial superinfection in such patients. She was appropriately treated with third-generation cephalosporin for H. influenzae and with oseltamivir for influenza A. Her condition improved significantly with the treatment.

Multiple Border-Zone Infarcts Triggered by Influenza A Virus Infection in a Patient With Cerebral Autosomal Dominant Arteriopathy Presenting With Subcortical Infarcts and Leukoencephalopathy.

Patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) can develop multiple border-zone infarcts due to hypotension, hypovolemia, or surgery. We report the case of a 41-year-old woman with CADASIL who developed multiple border-zone infarcts due to influenza A virus infection. The patient had no apparent history or episode of stroke or altered consciousness following the onset of respiratory symptoms, which were due to the influenza A infection. Diffusion-weighted magnetic resonance images of the brain showed multiple acute-phase infarcts in border-zone areas of both cerebral hemispheres and the corpus callosum; fluid-attenuated inversion-recovery magnetic resonance images showed increased signal in the subcortical areas of both temporal poles. Gene analysis identified a heterozygous mutation c.160C>T in exon 2 of the NOTCH3 gene (p.Arg54Cys). A diagnosis of CADASIL was established. Our case demonstrates that infectious conditions such as influenza A can trigger multiple border-zone infarctions in patients with CADASIL.

ACKR2 contributes to pulmonary dysfunction by shaping CCL5:CCR5-dependent recruitment of lymphocytes during influenza A infection in mice.

Inflammation triggered by influenza A virus (IAV) infection is important for viral clearance, induction of adaptive responses, and return to lung homeostasis. However, an exaggerated immune response, characterized by the overproduction of chemokines, can lead to intense lung injury, contributing to mortality. Chemokine scavenger receptors, such as ACKR2, control the levels of CC chemokines influencing the immune responses. Among the chemokine targets of ACKR2, CCL5 is important to recruit and activate lymphocytes. We investigated the role of ACKR2 during IAV infection in mice. Pulmonary ACKR2 expression was increased acutely after IAV infection preceding the virus-induced lung dysfunction. ACKR2-knockout (ACKR2-/-) mice were protected from IAV, presenting decreased viral burden and lung dysfunction. Mechanistically, the absence of ACKR2 resulted in augmented airway CCL5 levels, secreted by mononuclear and plasma cells in the lung parenchyma. The higher chemokine gradient led to an augmented recruitment of T and B lymphocytes, formation of inducible bronchus-associated lymphoid tissue and production of IgA in the airways of ACKR2-/- mice post-IAV. CCL5 neutralization in ACKR2-/- mice prevented lymphocyte recruitment and increased bronchoalveolar lavage fluid protein levels and pulmonary dysfunction. Finally, CCR5-/- mice presented increased disease severity during IAV infection, displaying increased neutrophils, pulmonary injury and dysfunction, and accentuated lethality. Collectively, our data showed that ACKR2 dampens CCL5 levels and the consequent recruitment of CCR5+ T helper 1 (Th1), T regulatory cells (Tregs), and B lymphocytes during IAV infection, decreasing pathogen control and promoting lung dysfunction in wild type mice. Therefore, ACKR2 is detrimental and CCR5 is protective during IAV infection coordinating innate and adaptive immune responses in mice.

Venous infarction mimicking top of basilar syndrome; An uncommon complication of adult influenza infection.

Influenza infection increases the risk of ischemic stroke. Here, we represent a case of a 32year-old female who presented with acutely developed altered mental status after influenza A infection. The clinical manifestation and initial lesion on brain DWI mimicked top of basilar syndrome, but without an arterial occlusion or stenosis. Follow-up neuro imaging analysis suggested cerebral venous infarction. It is valuable to report this case of venous infarction in a healthy young adult, as an uncommon complication of adult influenza infection.

Virus-neutralizing antibody response of mice to consecutive infection with human and avian influenza A viruses.

In this work we simulated in a mouse model a naturally occurring situation of humans, who overcame an infection with epidemic strains of influenza A, and were subsequently exposed to avian influenza A viruses (IAV). The antibody response to avian IAV in mice previously infected with human IAV was analyzed. We used two avian IAV (A/Duck/Czechoslovakia/1956 (H4N6) and the attenuated virus rA/Viet Nam/1203-2004 (H5N1)) as well as two human IAV isolates (virus A/Mississippi/1/1985 (H3N2) of medium virulence and A/Puerto Rico/8/1934 (H1N1) of high virulence). Two repeated doses of IAV of H4 or of H5 virus elicited virus-specific neutralizing antibodies in mice. Exposure of animals previously infected with human IAV (of H3 or H1 subtype) to IAV of H4 subtype led to the production of antibodies neutralizing H4 virus in a level comparable with the level of antibodies against the human IAV used for primary infection. In contrast, no measurable levels of virus-neutralizing (VN) antibodies specific to H5 virus were detected in mice infected with H5 virus following a previous infection with human IAV. In both cases the secondary infection with avian IAV led to a significant increase of the titer of VN antibodies specific to the corresponding human virus used for primary infection. Moreover, cross-reactive HA2-specific antibodies were also induced by sequential infection. By virtue of these results we suggest that the differences in the ability of avian IAV to induce specific antibodies inhibiting virus replication after previous infection of mice with human viruses can have an impact on the interspecies transmission and spread of avian IAV in the human population.

Intratracheal administration of influenza virus is superior to intranasal administration as a model of acute lung injury.

Infection of mice with human or murine adapted influenza A viruses results in a severe pneumonia. However, the results of studies from different laboratories show surprising variability, even in genetically similar strains. Differences in inoculum size related to the route of viral delivery (intranasal vs. intratracheal) might explain some of this variability. To test this hypothesis, mice were infected intranasally or intratracheally with different doses of influenza A virus (A/WSN/33 [H1N1]). Daily weights, a requirement for euthanasia, viral load in the lungs and brains, inflammatory cytokines, wet-to-dry ratio, total protein and histopathology of the infected mice were examined. With all doses of influenza tested, intranasal delivery resulted in less severe lung injury, as well as smaller and more variable viral loads in the lungs when compared with intratracheal delivery. Virus was not detected in the brain following either method of delivery. It is concluded that compared to intranasal infection, intratracheal infection with influenza A virus is a more reliable method to deliver virus to the lungs.

Influenza-related postinfectious encephalomyelitis complicated by a perforated peptic ulcer.

Influenza virus infection is extremely common and raises global concern due to the increasing prevalence of pandemic H1N1 infection. Influenza may occasionally be associated with neurologic complications and, also, rarely with gastrointestinal complications. Here, we report a rare case complicated with appendicitis, duodenum perforation, and transient delirious behavior after influenza A viral infection in a pediatric patient aged 14 years. The transient delirious behavior could be attributed to postinfectious encephalopathy. The perforated peptic ulcer could have resulted from influenza infection, could have been an adverse event related to oseltamivir administration, or could have been a complication of preceding gastroenteritis. Our case highlights the importance of pediatric healthcare workers to be aware of possible complications arising from both influenza infection and oseltamivir therapy, even though some of these complications may be relatively rare.