Idiopathic CD4 lymphocytopenia (ICL) is a rare entity of immune deficit of CD4+ T cells (below 300/mm³) which was first defined in 1992, unrelated to human immunodeficiency virus (HIV) syndrome without predefined clinical presentation and natural history. The etiology, pathogenesis, and management of ICL remains poorly understood and inadequately defined. The clinical presentation can range from serious opportunistic infections to incidentally diagnosed asymptomatic individuals. Cryptococcal and nontuberculous mycobacterial infections and progressive multifocal leukoencephalopathy are the most significant presenting infections, although the spectrum of opportunistic diseases can be similar to that in patients with lymphopenia and HIV infection. The prognosis is influenced by the accompanying opportunistic infections and response to the treatment. This rare disease invites uncountable opportunistic infections sometimes leading to lethal outcome. We report a case of ICL in an immunocompetent 18-year-old male with a history of intermittent epistaxis, fungal nasal polyp diagnosed to have Rhizopus with drug-induced acute kidney injury during the course of treatment, a rarest diagnosis as underlying main disease entity. To the best of our knowledge, ICL presenting with opportunistic infection of Rhizopus is the first case to be reported here from a tertiary care center of India, a developing country where a major population lives with poor hygiene and low socioeconomic status.

In human history, there have been several times of influenza raging, which have caused tens of millions of deaths and brought serious social and economic burdens. Although with the development of science, the emergence of vaccines has significantly reduced the incidence and mortality of influenza, due to the high variability of viruses, there is still a lack of effective treatment. More and more studies have found that bacterial pneumonia secondary to influenza was an important cause of the progression to critical illness or even death. Hence, diagnosis and treatment timely of secondary bacterial pneumonia are valuable. Therefore, we discuss the pathogens of bacterial pneumonia secondary to influenza, associated morbidity, mortality, and risk factors. Hopefully, it can provide some valuable references for clinical practice. Since some clinical studies have not separated pneumonia from lower respiratory tract infections, we will discuss these two situations together.

H1N1 pneumonia is one of the most common causes of community-acquired pneumonia in India. It occurs throughout the year without any seasonal variation. The clinical presentation of the disease varies in severity each year and complications associated with it are most unusual. We recently reported a case of recurrent pneumomediastinum associated with H1N1. Here, we want to report another patient who was diagnosed with severe H1N1 pneumonia complicated by a cardiac tamponade. Cardiac tamponade is a life threatening complication of viral pneumonia and needs to addressed immediately. Ours is the first case report with cardiac tamponade associated with H1N1 pneumonia.

A secondary bacterial infection of the influenza virus in the lungs is a key cause of exacerbation and death. The pathogenesis is characterized by complex interactions between co-infecting pathogens and the host, leading to the destruction of the physical barrier of the airways and the dysregulation of the immune response. This article will review the progress of the mechanism of secondary bacterial infection of influenza virus and provide strategies for preventing the co-infection of influenza virus and bacteria.

H9N2 avian influenza viruses cause worldwide infections in animals including humans and show a threat as a pandemic infection. Since 1998 more than 59 cases including one death due to H9N2 infection had been reported worldwide and the majority of confirmed cases were young children. Due to the large host variety, tolerance to both poultry and mammals and widespread gene reassortment, H9N2 viruses played a crucial role in worldwide infection. In this review, we discuss the current worldwide infection of H9N2 avian influenza viruses as well as their host range, pathogenesis, epidemiology, diagnosis, control, and its pandemic potential.

Background: Mono-infections of Plasmodium spp., hepatitis B virus (HBV), and Mycobacterium tuberculosis could elicit activation of complements for innate immunity leading to inflammatory responses. Objective: This work was designed to determine host immune responses to mono-infections of Plasmodium spp., HBV, and M. tuberculosis in blood complement 3 (C3), complement 5 (C5), tumor necrosis factor-alpha (TNF-α), and interleukin 10 (IL-10). Materials and Methods: Of 200 volunteers 66 Plasmodium spp., mono-infected, 28 HBV mono-infected, 12 M. tuberculosis mono-infected and 62 noninfected volunteers were studied as test and controls. ELISA was used to determine HBV, hepatitis C virus (HCV), HIV, plasma C3, C5, IL-10, and TNF-α while Plasmodium spp., was identified by Geimsha thick-film microscopy and M. tuberculosis by immunofluorescence microscopy. Results: The results obtained in the 200 volunteers showed. 69% (138) were infected with one or more of Plasmodium, HBV, HCV, HIV, and M. tuberculosis; 31% (62) were not infected; 16% (32) had co-infections of at least two of Plasmodium, HBV, HCV, HIV, and M. tuberculosis; 33% (66) were Plasmodium spp., mono-infected 14% (28) were HBV mono-infected while 6% (12) were M. tuberculosis. mono-infected. There was a significant increase in the plasma C3 in M. tuberculosis mono-infection compared with Plasmodium mono-infection; HBV mono-infection and control (P < 0.05). There was a significant increase in the plasma C3 in Plasmodium mono-infection compared with HBV mono-infection and control (P < 0.05) There was a significant decrease in the plasma C3 in the results obtained in HBV mono-infection compared with the control (P < 0.05). There was a significant increase in the plasma C5 in M. tuberculosis mono-infection compared with Plasmodium mono-infection; HBV mono-infection and control (P < 0.05). There was a significant increase in the plasma C5 in Plasmodium mono-infection compared with HBV mono-infection (P < 0.05). There was a significant decrease in plasma IL-10 and increased plasma TNF-α in Plasmodium, M. tuberculosis, and HBV mono-infections compared with the control (P < 0.05). There was also a significant increase in plasma TNF-α in M. tuberculosis mono-infection compared with Plasmodium mono-infection (P < 0.05). Conclusion: There was an evidence of host immune responses as evidenced by a significant increase in plasma C3, C5, and TNF-α including a decrease in IL-10 in mono-infections of Plasmodium spp., HBV and M. tuberculosis.