IRIS, also known as immune recovery syndrome.
Represents an aberrant reconstituted immunity to opportunistic pathogens on reversal of immunosuppression.
Seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
The syndrome is not restricted solely to immuno deficient patients and has been seen in tuberculosis and leprosy.
CD4 T cells are suppressed by HIV or by immunosuppressive drugs causing a decrease in the body’s normal response to certain infections.
The CD4 count rapidly increases due to treatment of HIV, or removal of other causes of immunosuppression, a sudden increase in the inflammatory response.
With suppression of CD4 T cell activity it is more difficult to fight an infection, it and that the level of infection symptoms is undetected or subclinical.
Two clinical patterns emerge: the unmasking of an occult opportunistic infection, and second is the symptomatic relapse of a prior infection despite microbiologic treatment success.
There is suspected reconstitution of antigen-specific T cell-mediated immunity with activation of the immune system following HIV therapy against persisting antigen.
If effective treatment is administered the CD4 count increases rapidly and a sudden increase in the inflammatory response produces nonspecific symptoms such as fever, and in some cases a worsening of damage to the infected tissue.
IRIS responses can lead to the unmasking of an occult opportunistic infection, or the paradoxical symptomatic relapse of a prior infection despite microbiologic treatment success.
Fever in association within flammatory tissue disease have to control of infection should arose suspicion of the diagnosis.
Treatment for this condition is unknown.
Patients spontaneously improve without any additional therapy.
The most common treatment is to administer antibiotic or antiviral drugs against the infectious organism.
In some severe cases, anti-inflammatory medications, (corticosteroids) are used to suppress inflammation.
In paradoxical IRIS reactions, the events will usually spontaneously improve without any additional therapy.
In unmasking IRIS, treatment is to administer antibiotic or antiviral drugs against the infectious organism.
In severe cases, anti-inflammatory medications, such as corticosteroids suppress inflammation.
Infections most commonly associated with IRIS include Mycobacterium tuberculosis and cryptococcal meningitis.
Patients with AIDS are more at risk for IRIS if they are starting HAART for the first time, or if they have recently been treated for an opportunistic infection.
When patients have low initial CD4 T cell count and opportunistic infection at the time of their HIV diagnosis, they should receive treatment to control the opportunistic infections before HAART is initiated approximately two weeks later r
This is true unless opportunistic infections involvethe central nervous system.
In cryptococcal meningitis IRIS can be fatal.
IRIS is common in Cryptococcal meningitis.
IRIS has been described in immunocompetent hosts who have meningitis caused by Cryptococcus gattii and Cryptococcus neoformans, as there is a sudden onset deterioration with worsening meningitis symptoms and progression or development of new neurological symptoms.
With IRIS CNS imaging shows increase in the size of brain lesions, and CSF abnormalities, while CSF culture is typically negative.
The increasing inflammation with IRIS can cause brain injury or be fatal.
Can cause an FUO.
The mechanism behind IRIS is increased inflammation as the recovering immune system recognizes the antigens of the pathogen as immunosuppression is reversed.
Patients with HIV infection, organ transplant recipients, postpartum women, neutropenic hosts, and patients that are recipients of antitumor necrosis factor therapy are at risk.
Cryptococcus, histoplasmosis, and mycobacterial infections are the most common opportunistic infections associated with immune reconstitution syndrome.
IRIS may be the cause of paradoxically worse outcomes for cryptococcal meningitis in immunocompetent compared with immunocompromised hosts.
Treatment with systemic corticosteroids during IRIS may be beneficial in preventing death or progressive disease.
Cultures are often negative in paradoxical IRIS, because reconstitution of antigen-specific T cell-mediated immunity and activation of the immune system following HIV therapy occurs against persisting antigens of intact or dead organisms, or debris.
With IRIS increased inflammation brain injury increases or can lead to fatalaties.
Mechanism behind IRIS is increased inflammation of recovering immune system recognizing the antigens of the fungus as immunosuppression is reversed.
IRIS may be the cause of paradoxically worse outcomes for cryptococcal meningitis in immunocompetent compared with immunocompromised hosts, in whom Cryptococcus neoformans is the usual pathogen.
Treatment with systemic corticosteroids may be beneficial in preventing death or progressive neurological deterioration.