Secondary (acquired) immunodeficiency due to medical therapies

• When feasible, all indicated vaccines should be given ≥4 weeks before starting immunosuppressive medications.
• Non-live vaccines may be administered (if needed) during immunosuppressive therapy, but doses may need to be repeated when the person is no longer immunocompromised.
• Alternatively, non-live vaccine doses may be temporarily delayed (if the risk of disease exposure is low) until the person is less immunocompromised, to optimise vaccine effectiveness.
• Generally, for people receiving immunosuppressive therapies, live vaccines should be administered ≥4 weeks before starting the treatment, if feasible. Exceptions are people receiving complement inhibitors, hydroxychloroquine, sulfasalazine and low doses of azathioprine, methotrexate and mercaptopurine, which live vaccines can be safely administered any time before, during or after treatment.
• At the end of a course of immunosuppressive therapy, the length of time before live vaccines can be given varies by agent. Reconstitution of the immune system often needs to be confirmed first.
• Combinations of immunosuppressive therapies may have a cumulative immunosuppressive effect. Providers should seek expert advice if they are uncertain about the severity of immunocompromise and whether it is safe for people receiving an immunosuppressive therapy to receive a vaccine.

For more details about the immunosuppressive potential of various medications and medical conditions, see:

• Table. Types of medical conditions and immunosuppressive therapy and associated levels of immunocompromise
• Table. Immunosuppressive potential of cancer and organ rejection therapies
• Table. Immunosuppressive potential of conventional (non-biological) immunosuppressive therapies
• Table. Immunosuppressive potential of small molecule targeted therapies
• Table. Immunosuppressive potential of biological therapies
• Table. Immunosuppressive potential of corticosteroids
• Table. Immunosuppressive potential of certain medical conditions

Secondary immunodeficiency can be caused by many different types of medical therapies, including cancer chemotherapy, radiation therapy, and other immunosuppressive or immunomodulatory medications. Broad categories of immunosuppressive medical therapies include:

• conventional (non-biological) immunosuppressive therapies, chemotherapies and corticosteroids
• novel biological therapies and small molecule targeted therapies

Before and during treatment with immunosuppressive medications, it is important to consider:

• the immunosuppressive risks of the underlying disease and previous therapies
• the drug class and mechanism of action of the immunosuppressive therapy, including the therapeutic effect and the duration of effect on the immune system
• the consequences of combination therapies that can alter the extent and duration of immunocompromise (such as the use of corticosteroids at the same time as other conventional therapies or biological therapies)
• the risk of exposure to vaccine-preventable diseases and susceptibility to infection

Biological therapies

Biological therapies target specific cells or cytokines as a more precise approach to treating disease. The risks involved in the use of biological therapies depend on the type of immune cell or cytokine that is targeted.

The risks of immunosuppression differ between classes of biological therapies, and between medications within the same class. These risks are also heavily influenced by the underlying disease and by exposure to concurrent immunosuppressive therapies from other classes.¹ As biological therapies are newer classes of medication, there are limited published data to inform the risks of immunosuppression and live vaccine administration.

Biological therapies include:

• anti-T-lymphocyte therapies such as basiliximab and abatacept. These therapies are associated with a small increased risk of infection with many common infectious organisms.
• anti-B-lymphocyte therapies such as those targeting CD20 (rituximab, ocrelizumab, ofatumumab, obinutuzumab) and CD19 (inebilizumab), and belimumab. The anti-CD20 and anti-CD19 agents can cause substantial B-cell depletion, resulting in a risk of serious bacterial and viral infections (including hepatitis B, hepatitis C and herpes zoster reactivation). This risk can persist for several months or years after therapy has finished.
• antibodies targeting cellular markers such as alemtuzumab, blinatumomab, daratumumab and elotuzumab. These agents vary in their extent of immune cell depletion. Alemtuzumab carries the highest risk of bacterial and other opportunistic infections (including tuberculosis and herpes zoster virus reactivation).
• tumour necrosis factor (TNF)-alpha inhibitors such as infliximab, etanercept, adalimumab, certolizumab and golimumab. TNF-alpha inhibition results in a modest increased risk of infection with common bacteria and mycobacteria, including Mycobacterium tuberculosis.
• interleukin (IL)-1 pathway inhibitors such as anakinra, canakinumab and rilonacept. Use of these agents results in small to moderate increases in infection risk that are mainly influenced by concurrent immunosuppressive agents and underlying comorbidities.
• IL-4, IL-5 and IgE inhibitors such as dupilumab, mepolizumab, reslizumab, benralizumab and omalizumab. These agents act by targeting pathways that drive atopy (allergy), and are unlikely to cause overall immunosuppression.
• IL-6 inhibitors such as tocilizumab and sarilumab. These agents are associated with a modest increase in common bacterial and viral infections, as well as invasive fungal infections.
• IL-17 inhibitors such as secukinumab and ixekivumab. These agents reduce the release of proinflammatory cytokines and chemokines. They have been associated with a low risk of infections (predominantly yeast infections).
• IL-12/IL-23 pathway inhibitors such as ustekinumab, risankizumab, tildrakizumab and guselkumab. These agents target the IL-12 and IL-23 pathway to protect against psoriasis, inflammatory bowel disease and ankylosing spondylitis. They are associated with a modest risk of upper respiratory tract infections, possibly reactivation of tuberculosis and chronic hepatitis B infection.
• integrin inhibitors such as natalizumab and vedolizumab. These agents block the action of integrin on the surface of immune cells and endothelial cells, which inhibits the interactions between leukocytes and intestinal blood vessels. They are associated with a small risk of herpes simplex infection and herpes zoster reactivation, and upper respiratory tract infections. Natalizumab is also associated with a small risk of the infectious complication of progressive multifocal leukoencephalopathy. Vedolizumab does not have infection risks, as it is a gut-specific integrin inhibitor
• immune checkpoint inhibitors used as a treatment for cancer include CTLA-4 inhibitors (ipilimumab) and PD-1/PD-L1 inhibitors (nivolumab or pembrolizumab). These agents are directed in their anti-cancer activity, and do not appear to be associated with an increased risk of infection2,3 or vaccine-related complications.⁴
• complement inhibitors such as eculizumab and ravulizumab. These agents impair the immune response to Neisseria species, as well as other encapsulated bacteria.

Some biological therapies have a mechanism of action that does not result in immunosuppression. Examples are monoclonal antibodies used for treating osteoporosis that target the calcitonin gene-related peptide (CGRP) pathway or inhibit the receptor activator of nuclear factor kappa Β (RANK) ligand.

For more details, see Table. Immunosuppressive potential of biological therapies.

Small molecule targeted therapies

Small molecule targeted therapies work by entering cells and acting on secondary messenger systems. Different types of therapies have different immunosuppressive effects, but they are generally associated with a moderately increased risk of infection.

Small molecule targeted therapies include:

• anaplastic lymphoma kinase (ALK) inhibitors, such as crizotinib, ceritinib, alectinib and brigatinib
• BCR-ABL tyrosine kinase inhibitors (such as imatinib, dasatinib, nilotinib, ponatinib and bosutinib)
• Bruton’s tyrosine kinase inhibitors (such as ibrutinib and acalabrutinib)
• cyclin-dependent kinase (CDK) inhibitors (such as palbociclib, ribociclib and abemaciclib)
• Janus kinase (JAK) inhibitors (such as tofacitinib, baricitinib and ruxolitinib)
• phosphoinositide 3-kinase (PI3K) inhibitors (such as idelalisib)

For more details, see Table. Immunosuppressive potential of small molecule targeted therapies.

People with secondary immunodeficiency due to medical therapies can safely receive non-live vaccines, including seasonal influenza and COVID-19 vaccines.

An exception is Q fever vaccine. At present, this vaccine is contraindicated because there are no published data on its efficacy and safety in people who are immunocompromised (see Q fever).

When feasible, people who are immunocompromised due to medical therapies should receive all age-recommended vaccines ≥4 weeks before starting immunosuppressive therapies.

However, they may receive routine non-live vaccines during immunosuppressive therapy if needed. Doses may need to be repeated when the person is no longer immunocompromised, unless an antibody response can be demonstrated using a known correlate of protection.

Some people who are immunocompromised due to medical therapies may need altered primary vaccination schedules or additional doses of some routine non-live vaccines to optimise disease protection. See Table. Recommendations for non-live vaccine administration in people who are immunocompromised due to immunosuppressive therapies.

Live vaccines are generally contraindicated during immunosuppressive therapy due to the risk of disseminated disease. Exceptions are for people receiving the following as monotherapy:

• complement inhibitors
• single immune checkpoint inhibitor used as anti-neoplastic agents (although data is limited in this population) – see Immune checkpoint inhibitors
• low doses of certain conventional immunosuppressive therapies — see Conventional (non-biological) immunosuppressive therapies
• certain targeted biological or small molecular therapies — see Biological therapies and Small molecule targeted therapies

People receiving other medications should receive any recommended live vaccines ≥4 weeks before starting the immunosuppressive treatment.

After therapy, the length of time before live vaccines can be given varies by agent. Immune reconstitution should be confirmed before giving live vaccines.

For therapies that are not included in this section or related tables, seek advice from the treating specialist about infection risk and safety of live vaccines.

See Table. Recommended timing of live vaccine administration for people receiving immunosuppressive therapies. If combinations of immunosuppressive therapies have been prescribed, seek specialist advice.

Overview

People receiving low-dose corticosteroids (<2 mg/kg/day for children, or <20 mg/day for adults, prednisolone-equivalent dosing) over a short time (<14 days) can safely receive non-live and live vaccines.

People receiving corticosteroids at a higher dose (≥2 mg/kg/day for children, or ≥20 mg/day for adults, prednisolone-equivalent dosing) or over a longer time (≥14 days) can safely receive non-live and live vaccines, either:

• 4 weeks before starting high-dose corticosteroids, or
• ≥4 weeks after treatment ends, or
• during a period when corticosteroids are weaned (to <20 mg/day for adults, or <2 mg/kg/day for children, prednisolone-equivalent dosing) for at least 1 month

Specialist guidance should be sought on administration of live vaccines in people taking prolonged or high-dose corticosteroids alongside other immunosuppressive therapies.

Introduction

Corticosteroids have anti-inflammatory and immunosuppressive effects that are reversible when the medication is discontinued. Several topical, inhaled and systemic corticosteroids are available in Australia. These agents differ with respect to their potency and duration of action, which determines the corticosteroid’s efficacy and therapeutic use.

The level of immunosuppression caused by corticosteroids is affected by the specific corticosteroid prescribed, the dose, therapy duration and route of administration. The minimum dose of corticosteroid therapy that causes immunosuppression is not well defined.

In this Handbook, corticosteroid doses are defined against prednisolone as a standard.^5-7 Prednisolone is one of the most widely used systemic corticosteroids, and is therefore helpful as a reference agent for people taking other systemic corticosteroids. See Table. Prednisolone-equivalent dosing, duration of action and anti-inflammatory activity for various systemic corticosteroid preparations. 

Conventional immunosuppressive therapies act broadly to reduce the inflammatory responses associated with immune-mediated inflammatory disease. These include conventional non-biological medications used for treating rheumatic diseases (also known as disease-modifying anti-rheumatic drugs), autoimmune inflammatory diseases, cancer or organ rejections, such as:

• azathioprine
• calcineurin inhibitors (cyclophosphamide, tacrolimus, cyclosporin)
• hydroxychloroquine
• leflunomide
• methotrexate
• mercaptopurine
• mycophenolate
• sirolimus
• sulfasalazine

Each conventional immunosuppressive therapy has a unique mechanism of action in the inflammatory cascade and suppresses the immune system to varying degrees. See Table. Immunosuppressive potential of conventional (non-biological) immunosuppressive therapies.

Non-live vaccines

People taking conventional immunosuppressive therapy in the short or medium term can safely receive non-live vaccines. However, the immune response may be suboptimal. If non-live vaccines are received within 4 weeks of starting treatment or during treatment, these doses should be repeated after treatment and when immune competence is restored.

Live vaccines

Live vaccines can be safely administered to people receiving:

• hydroxychloroquine and sulfasalazine
• low-dose methotrexate (≤25 mg/week), azathioprine (≤3 mg/kg/day) or mercaptopurine (≤1.5 mg/kg/day)

People prescribed other conventional immunosuppressive therapy should receive live vaccines ≥4 weeks before starting, or ≥3 months after treatment ends.³⁰ Exceptions are people receiving mTOR (mammalian target of rapamycin) inhibitors (when used for treatment of rheumatic diseases, not for preventing organ rejection) and leflunomide who can receive live vaccines ≥4 weeks after treatment ends. See Table. Recommended timing of live vaccine administration for people receiving immunosuppressive therapies.

For people receiving leflunomide, there are minimal data on the safety of live vaccines.³¹ Leflunomide has a low risk of immunosuppression based on its mechanism of action. The use of live vaccines during therapy may also be considered after an individual risk–benefit assessment.

Biological therapies do not cause generalised immunosuppression like conventional immunosuppressive therapies (such as disease-modifying anti-rheumatic drugs and corticosteroids). However, biological therapies can affect the immune system, which may compromise host defences and increase the risk of serious infections.

Non-live vaccines

People receiving biological therapy in the short or medium term can safely receive non-live vaccines. However, the immune response may be suboptimal. If non-live vaccines are received within 4 weeks of starting treatment or during treatment, these doses should be repeated after treatment and when immune competence is restored.

Live vaccines

People taking complement inhibitors, anti-IL-5, anti-IgE, anti-RANK ligand or anti-CGRP therapies can receive live vaccines at any time before, during or after the treatment.

People taking other classes of biological therapies should receive recommended live vaccines ≥4 weeks before starting treatment, where possible.

After therapy, the length of time before live vaccines can be given varies by therapy. See:

• Table. Recommended timing of live vaccine administration for people receiving immunosuppressive therapies
• Table. Immunosuppressive potential of biological therapies

People receiving anti-B-cell antibodies directed against CD20 (such as rituximab) or CD52 (such as alemtuzumab) should not receive live vaccines until ≥6 months after therapy ends. This is because these agents cause substantial B-cell depletion that lasts for several months. This timing may also be affected by any blood products the person has received, including intravenous immunoglobulin (see Vaccination for people who have recently received normal human immunoglobulin and other blood products).

Infants exposed to TNF-alpha inhibitors in the 2nd or 3rd trimester in utero can receive live vaccines according to routine schedules.³² However, infants exposed to anti-CD20 B-cell antibodies (such as rituximab) should not receive live vaccines until >6 months of age (see Infants exposed to immunosuppressive therapy in utero or through breastmilk).³⁰

Combinations of immunosuppressive therapies may have a cumulative immunosuppressive effect. Providers should seek expert advice if they are uncertain about the severity of immunocompromise and whether it is safe for people receiving biological therapies to receive a vaccine.

Immune checkpoint inhibitors are immunomodulatory antibodies that block checkpoint proteins from binding with their partner proteins. This stimulates the immune system to attack cancer cells. These drugs include:

• CTLA-4 inhibitors such as ipilimumab and tremelimumab
• PD-1 and PD-L1 inhibitors such as nivolumab, pembrolizumab and atezolizumab

Immune checkpoint inhibitors are a comparatively recent drug class with limited available evidence so far. The risk of immunosuppression appears to be low when they are used as monotherapy.³³

Non-live vaccines

People who are being treated with a single immune checkpoint inhibitor can receive non-live vaccines.

Some studies suggest that people receiving multiple immune checkpoint inhibitors may have a higher risk of adverse events following immunisation with influenza vaccine^34,35 than those on a single checkpoint inhibitor.³⁶

Live vaccines

There are no conclusive data on the safety or administering live vaccines to people receiving immune checkpoint inhibitors as a treatment for cancer. Although these therapies are not immunosuppressive given their directed mechanism of action when used as a treatment for cancer, there is a theoretical concern about a potential risk of immune-related adverse events.⁴

Complement inhibitors (including eculizumab and ravulizumab) may be prescribed to treat atypical haemolytic uraemic syndrome, paroxysmal nocturnal haemoglobinuria and myasthenia gravis. These agents target the membrane attack complex of the complement cascade, without affecting any other immune system cells.

People receiving complement inhibitors can receive all recommended live and non-live vaccines according to routine schedules.

During therapy, people receiving complement inhibitors are at high risk of infection with Neisseria meningitidis and other Neisseria species, as well as other encapsulated bacteria. This means that:

• At least 2 weeks before starting complement inhibitor therapy, people should have received a full primary course of MenACWY (meningococcal ACWY) and MenB (meningococcal B) vaccines, and routinely recommended primary courses of pneumococcal and Hib (Haemophilus influenzae type b) vaccines,37,38 if possible.
• During therapy, people should receive booster doses of MenACWY and MenB vaccines. The number of doses for primary vaccine courses and booster timing depends on the vaccine brand and age. See recommendations for MenACWY and MenB vaccines for people at risk of invasive meningococcal disease.
• Even if they are fully vaccinated, people receiving complement inhibitor therapy remain at higher risk of infections, especially invasive meningococcal disease.39 Providers should advise patients of the ongoing risk of infection and consider antibiotic prophylaxis, especially if treatment starts before vaccination schedules are complete.

Small molecule targeted therapies target intracellular pathways to decrease the signalling of several cytokine and growth factor receptors. They are usually prescribed as oral medications and have a short half-life. Small molecule targeted therapies are generally associated with a moderate risk of infections.³³

Non-live vaccines

People receiving small molecule targeted therapies can safely receive non-live vaccines. However, the immune response may be suboptimal due to blunted humoral and cell-mediated responses.

Live vaccines

Live vaccines are often contraindicated in people receiving small molecule targeted therapies because the underlying disease in these people is usually a malignancy. But there are some exceptions:

• JAK inhibitors are often prescribed to treat autoimmune disorders. People receiving JAK inhibitors should receive any live vaccines ≥4 week before starting therapy or ≥4 weeks after therapy ends. If therapy is likely to be long-term, doses may be withheld to enable live vaccines to be safely administered.³⁰
• Children on BCR-ABL inhibitors have safely received live vaccines. The vaccines were well tolerated but seroconversion did not always occur.⁴⁰
• ALK inhibitors and other tyrosine kinase inhibitors target neoplastic cells in non-small cell lung cancer. Live vaccines may be considered for people receiving ALK inhibitors, as no safety concerns have been reported. Consult with the treating oncologist for an individual risk–benefit assessment. 

See Table. Recommended timing of live vaccine administration for people receiving immunosuppressive therapies for more details.

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