Co-infection of classic swine H1N1 influenza virus in pigs persistently infected with porcine rubulavirus.

Porcine rubulavirus (PorPV) and swine influenza virus infection causes respiratory disease in pigs. PorPV persistent infection could facilitate the establishment of secondary infections. The aim of this study was to analyse the pathogenicity of classic swine H1N1 influenza virus (swH1N1) in growing pigs persistently infected with porcine rubulavirus. Conventional six-week-old pigs were intranasally inoculated with PorPV, swH1N1, or PorPV/swH1N1. A mock-infected group was included. The co-infection with swH1N1 was at 44 days post-infection (DPI), right after clinical signs of PorPV infection had stopped. The pigs of the co-infection group presented an increase of clinical signs compared to the simple infection groups. In all infected groups, the most recurrent lung lesion was hyperplasia of the bronchiolar-associated lymphoid tissue and interstitial pneumonia. By means of immunohistochemical evaluation it was possible to demonstrate the presence of the two viral agents infecting simultaneously the bronchiolar epithelium. Viral excretion of PorPV in nasal and oral fluid was recorded at 28 and 52 DPI, respectively. PorPV persisted in several samples from respiratory tissues (RT), secondary lymphoid organs (SLO), and bronchoalveolar lavage fluid (BALF). For swH1N1, the viral excretion in nasal fluids was significantly higher in single-infected swH1N1 pigs than in the co-infected group. However, the co-infection group exhibited an increase in the presence of swH1N1 in RT, SLO, and BALF at two days after co-infection. In conclusion, the results obtained confirm an increase in the clinical signs of infection, and PorPV was observed to impact the spread of swH1N1 in analysed tissues in the early stage of co-infection, although viral shedding was not enhanced. In the present study, the interaction of swH1N1 infection is demonstrated in pigs persistently infected with PorPV.

Child homicide or natural death? A case report of unexpected death of unusual asymptomatic acute laryngotracheobronchitis.

Cases involving the unexpected deaths of children are always a concern for the police and medical examiners alike. In particular, unexpected deaths due to asphyxia without obvious injuries sometimes make decisions regarding the manner of death more difficult. In the present case, a 2-year-old boy was found dead at home, and his mother was initially believed to have killed him. A complete autopsy and forensic investigation were performed, and no injuries were found on the body; however, marked laryngeal edema was observed. Histology showed extensive inflammatory infiltration of the mucosa and submucosa of the larynx, trachea, and bronchi. The cause of death was given as respiratory failure due to acute laryngotracheobronchitis; thus, the manner of death was natural. This case helps to remind the forensic community to keep an open mind and consider a broad differential diagnosis when approaching a case rather than jumping to a conclusion based solely on a preliminary investigation.

Co-infections with respiratory viruses in dogs with bacterial pneumonia.

BACKGROUND: Bacterial pneumonia (BP) is an inflammation of the lower airways and lung parenchyma secondary to bacterial infection. The pathogenesis of BP in dogs is complex and the role of canine respiratory viruses has not been fully evaluated. OBJECTIVES: The aim of this study was to investigate the occurrence of viral co-infections in dogs with BP and to assess demographic or clinical variables as well as disease severity associated with viral co-infections. ANIMALS: Twenty household dogs with BP caused by opportunistic bacteria and 13 dogs with chronic (>30 days) tracheobronchitis caused by Bordetella bronchiseptica (BBTB). METHODS: Prospective cross-sectional observational study. Diagnosis was confirmed by clinical and laboratory findings, diagnostic imaging, and cytologic and microbiologic analysis of bronchoalveolar lavage or transtracheal wash fluid. Canine parainfluenza virus (CPIV), canine adenovirus, canine herpes virus, canine influenzavirus, canine distemper virus, canine respiratory coronavirus (CRCoV) and canine pneumovirus, as well as B. bronchiseptica and Mycoplasma spp. were analyzed in respiratory samples using PCR assays. RESULTS: CPIV was detected in 7/20 and CRCoV in 1/20 dogs with BP. Respiratory viruses were not detected in dogs with BBTB. There were no significant differences in clinical variables between BP dogs with and without a viral co-infection. CONCLUSION AND CLINICAL IMPORTANCE: Respiratory viruses were found frequently in dogs with BP and may therefore play an important role in the etiology and pathogenesis of BP. Clinical variables and disease severity did not differ between BP dogs with and without viral co-infection.

Successful clearance of human parainfluenza virus type 2 viraemia with intravenous ribavirin and immunoglobulin in a patient with acute myocarditis.

Human parainfluenza virus (HPIV) infection as an aetiology of acute viral myocarditis is rare, with only few cases reported in the literature to date. Here we report a case of fulminant HPIV-2 myocarditis in a 47 year-old man with viraemia who was successfully treated with intravenous ribavirin and intravenous immunoglobulin (IVIG). There are currently no recommendations on the treatment of HPIV myocarditis. We are, to our knowledge, the first to report a patient with a documented HPIV-2 viraemia that subsequently cleared after the initiation of antiviral therapy. Although it is difficult to definitively attribute the patient's clinical improvement to ribavirin or IVIG alone, our case does suggest that clinicians may wish to consider initiating ribavirin and IVIG in patients with HPIV myocarditis and persistent viraemia not responding to supportive measures alone.

Sudden infant death syndrome due to parainfluenza virus 2 associated with hemophagocytic syndrome.

We report a child with Sudden Infant Death Syndrome (SIDS), aged 16 months. The histological findings of tonsils, spleen, and bone marrow revealed many hemophagocytic cells. Parainfluenza virus type 2 (PIV2) was cultured in the nasopharynx and detected by reverse-transcription (RT)-PCR in liver tissue and bone marrow. His laboratory data of elevated level of ferritin and IL-6 suggested hemophagocytic syndrome (HPS). It is suspected that PIV2 infection in infants is a risk factor for SIDS.

Fatal hemorrhagic pneumonia concomitant with Chlamydia pneumoniae and parainfluenza virus 4 infection.

CONTEXT: Cases of fatal hemorrhagic pneumonia need to be investigated for highly contagious viral causes. While not all hemorrhagic pneumonias are caused by very contagious agents, the etiology must be correctly determined in order to administer appropriate patient care. OBJECTIVE: To determine whether chlamydia, paramyxovirus, or mycoplasma was the causative agent in a case of fatal hemorrhagic pneumonia, and to evaluate the possibility that this was the first case of hantavirus pulmonary syndrome in Illinois. DESIGN: Nonroutine virological and molecular analyses were performed on lung tissue taken during an unrestricted autopsy of a patient who died in 2002. SETTING AND PATIENT: An elderly, male, Chicago-area resident with a 3-week history of nonspecific, mild upper respiratory tract infection was admitted for hospital treatment of the respiratory infection and viral myositis without cardiac involvement. The patient became febrile, hypoxic, developed hemorrhagic pneumonia, and died. Because he had proven exposure to mice and had developed hemorrhagic pneumonia, hantavirus pulmonary syndrome was suspected as the cause of death. Mice known to carry hantaviruses live in Illinois, including the Chicago area. INTERVENTIONS: Gatifloxacin and heparin anticoagulation were initiated because community-acquired pneumonia and pulmonary embolism were considered likely etiologies for an acute exacerbation of hypoxemia. RESULTS: Two respiratory pathogens were isolated and identified: Chlamydia pneumoniae and human parainfluenza virus 4a. CONCLUSIONS: A mixed (polymicrobial) infection contributed to the patient's death. Hemorrhage was likely a result of anticoagulation therapy superimposed on lung tissues damaged by pneumonia. The uncommon nature of this case and the pathogens involved underscore the challenges in infection control and clinical evaluation that hospitals will face when confronted with possibly new and potentially deadly communicable diseases.