Clinical Manifestations of Cytomegalovirus
المؤلف:
Baijayantimala Mishra
المصدر:
Textbook of Medical Virology
الجزء والصفحة:
2nd Edition , p39-41
2025-07-21
530
Infection in immunocompetent host usually does not lead to clinically apparent manifestation. Occasionally it may lead to mononucleosis like features with fever, cervical lymphadenopathy, and sore throat with or without hepatosplenomegaly.
CMV infection in immunocompromised individuals and congenital CMV infection are the two most important clinical entities due to CMV infection.
At this stage, it is important to understand the difference between CMV infection and CMV disease.
CMV infection: Evidence of CMV replication regardless of symptoms (differs from latent CMV).
CMV disease: When CMV infection is accompanied by clinical symptoms and sign, CMV disease is characterized with fever, malaise, leukopenia, and/or thrombocytopenia or as tissue-invasive disease.
Asymptomatic CMV infection is defined as CMV replication without sign and symptoms of CMV disease.
Congenital infection: Around 90% of congenitally infected babies are asymptomatic at birth and 10% present with clinically apparent disease. Amongst the symptomatic neonates, death occurs in around 10% within a few weeks of birth.
Two-thirds of symptomatic neonates show the evidences of neural involvement in the form of microcephaly, lethargy-generalized hypotonia, poor feeding, and seizure. Cranial imaging shows abnormality in about 75% of symptomatic neonates where periventricular calcification is the most common, and other abnormalities can be ventriculomegaly, lissencephaly and cortical atrophy. Sensorineural hearing loss is reported in around 50% symptomatic newborns and chorioretinitis in around 10%. Clinical findings of congenital CMV infection are given in Table 1. The risk of developing sequelae is higher in neonates who were symptomatic at birth as compared to those who were asymptomatic. Hearing loss, mental retar dation and retinitis are the common sequelae.
Table1. Clinical manifestations of congenital CMV infection
Primary maternal infection, infection at early age of gestation, high level of viremia at birth and infection due to CMV gN4 genotype are associated with the severity of congenital disease.
Infection in immunocompromised hosts:
Incidence of CMV infection or disease in transplant recipients depends on the:
• CMV infection status of the donor (D) and recipient (R).
• Degree of immunosuppressive therapy.
• Viral load.
CMV infection in solid organ transplant (SOT) recipients: According to the CMV immune status, donor (D)/recipient (R) combination has been stratified into four groups. According to the level of risk involved, these are:
1. D+/R–: Donor seropositive/recipient seronegative: Donor can transmit the infection to the recipient leading to primary CMV infection in the recipient and as recipient has no previous CMV antibody to fight, the disease severity can also be high. Thus, this group is considered to carry the highest risk for CMV disease in recipient.
2. D+/R+: Both donor and recipient seropositive: As recipient is already seropositive, the chance of infection is mostly due to reactivation of the latent virus than due to transmitted infection from donor.
3. D–/R+: Donor seronegative and recipient seropositive: In this case, most common cause of infection is reactivation of latent virus in the recipient.
4. D–/R–: Both donor and recipients are CMV seronegative. So, the only chance of acquiring infection is from sources other than donor. But if infection will be acquired, it will be primary infection in the recipient which may cause severe disease.
The most common manifestation of CMV disease in SOT recipients is termed CMV syndrome:
• This is characterized by general symptoms like fever, malaise, anorexia and arthralgia. Blood count shows, leukopenia, thrombocytopenia and raised hepatic transaminase.
• In severe cases, tissue invasion can occur affecting various organs. The involvement of gastrointestinal system is the most common amongst them; however, any organ can be affected leading to hepatitis, pneumonitis, nephritis, retinitis, etc.
Indirect effect of HCMV infection can also occur which includes graft rejection, accelerated coronary artery vasculopathy in heart transplant patients and opportunistic infections.
Transplant organ is usually affected in case of primary infection in these patients. This is manifested as renal impairment in kidney transplant, pneumonitis in lung transplant, vasculopathy in heart transplant, etc. In SOT recipients, most of the HCMV infections occur within 4–8 weeks post-transplant. Prophylactic or pre-emptive therapy is given early to prevent the development of CMV disease.
HCMV infection in HSCT recipients: In contrast to SOT recipients, the level of risk according to the donor–recipient CMV serostatus is D–/R+, D+/R+, D+/R– and D–/R–. The risk gets enhanced in case of histocompatibility mismatch.
Gastrointestinal disease and interstitial pneumonitis are the common manifestations in allogenic HSCT recipients. The widespread use of prophylactic or pre-emptive therapy based on pp65 antigenemia or CMV DNA load by real-time PCR has reduced the incidence of CMV disease to a great extent.
The clinical manifestations and diagnosis of CMV disease involving various organs are same in all types of immunocompromised patients.
Gastrointestinal (GI) CMV disease commonly involves the lower GI tract than upper GI tract. It is clinically presented as diarrhea, vomiting, bleeding, anorexia and abdominal pain and often indistinguishable from GI GVHD.
CMV pneumonia is another common clinical entity in transplant recipients. It presents with the features of pneumonia such as hypoxia, tachypnea, dyspnea, appearance of new infiltrates in imaging, etc.
CMV hepatitis, retinitis, encephalitis and disseminated CMV disease are other manifestations.
HCMV infection in HIV patients: Cytomegalo virus disease is one of the AIDS defining illnesses. High HIV viral load and low CD4 counts are the two most important risk factors for HCMV infection in HIV patients. Majority of HCMV infection occurs in HIV positive patients with CD4 count
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