Week of Feb 8-12 - 16 outbreaks total reported to DHMH: 11 influenza-like illness outbreaks in nursing homes, 1 outbreak of influenza-like illness with pneumonia in a nursing home, 1 confirmed influenza A outbreak in a N.H., 1 gastroenteritis in a food-service facility, and 2 gastroenteritis outbreaks in nursing homes
Week of Feb 15-19 - 32 outbreaks reported to DHMH: 18 outbreaks of influenza-like
illness in nursing homes, 3 gastroenteritis outbreaks in nursing homes/health
care facilities, 1 case investigation of Legionella, 2 outbreaks of scabies
in nursing homes, 4 outbreaks of foodborne gastroenteritis, 1 outbreak
of pneumonia at a nursing home, 2 influenza-like illness with pneumonia
outbreak in a nursing home, and 1 outbreak of rash illness reported in
a middle school
Cytomegalovirus
Cytomegalovirus (CMV) is an enveloped DNA virus that is a family of species-specific viruses. As a member of the herpesvirus group, CMV is capable of establishing latency after primary infection. CMV is rarely pathogenic in healthy adults, but when host resistance falls below a critical threshold. CMV can reactivate.
CMV is a pathogen in a variety of patients. In immunocompetent individuals, it can occasionally cause a mononucleosis-like infection. In pregnant women, primary infection can cause severe generalized organ manifestations with high mortality and vertical transmission can cause congenital infection manifested as mental retardation. CMV is an important pathogen in immunocompromised patients, in particular, in transplant recipients and HIV positive patients.
CMV in HIV infection
Epidemiology: CMV is present in 90% to 99% of HIV positive patients. However, in most of these patients the virus is latent. Approximately 30% to 40% of HIV positive patient will develop serious CMV disease. The incidence of CMV disease appears to be increasing as patients with HIV live longer with more profound degrees of immunosuppression.
Clinical Features: Reactivation typically does not occur until the CD4 count drops below 100. The most common manifestation is retinitis. Other frequent manifestations include esophagitis, colitis, polyradiculopathy and disseminated (multiple organ) infection.
Diagnosis: Although the documentation of past CMV infection is relatively straightforward by detection if IgG antibodies to CMV, the diagnosis of active disease is more complicated. As most infection in this patient population is reactivation and not primary, the correlation between IgM antibodies and symptomatic disease is poor, and therefore serology is not a reliable indicator of disease. Excretion in the urine for months after infection means a positive urine culture is an unreliable indicator of infection. CMV can be culture from blood or tissue specimens on human fibroblasts, but cytopathic changes may not be detected for one to four weeks and sensitivity is low. A more rapid detection can be achieved by culturing the specimen on monolayers and staining with a fluorescein labeled antibody directed to a CMV protein expressed early in replication' results can be achieved in 3 days but sensitivity is still low. Polymerase chain reaction (PCR) can be performed in the laboratory on cerebrospinal fluid, amniotic fluid and vitreous humor and has an analytical sensitivity of 20-200 copies. In sites not amenable to PCR, culture and histologic examination can be performed. Characteristic histopathologic findings include markedly enlarged cells with large purple intranuclear inclusions surrounded by a halo with smaller basophilic cytoplasmic inclusions. An immunohistochemical stain for CMV is also available for cases where routine (H&E) stains are equivocal. Of note, the diagnosis of CMV retinitis remains a clinical diagnosis based on characteristic appearance on fundoscopic examination, although the use of CMV PCR is increasingly performed.
Therapy: CMV retinitis can be treated with oral ganciclovir, intraocular ganciclovir implant, intravitreal ganciclovir injection, foscarnet or cidofovir. Unfortunately, most patients with CMV retinitis relapse. Disseminated infection is typically treated with 3 to 6 weeks of induction therapy with ganciclovir followed by lifelong maintenance therapy with ganciclovir. Ganciclovir has serious marrow toxicity, including granulocytopenia and thrombocytopenia; these effects are usually reversible.
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