There are currently no studies detailing the long term outcome of chronic granulomatous disease with modern treatment. Without treatment, children often die in the first decade of life. The increased severity of X-linked CGD results in a decreased survival rate of patients, as 20% of X-linked patients die of CGD-related causes by the age of 10, whereas 20% of autosomal recessive patients die by the age of 35.

Recent experience from centers specializing in the care of patients with CGD suggests that the current mortality has fallen to under 3% and 1% respectively.

CGD was initially termed "fatal granulomatous disease of childhood" because patients rarely survived past their first decade in the time before routine use of prophylactic antimicrobial agents. The average patient now survives at least 40 years.

CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.

Chronic granulomatous disease affects all people of all races, however, there is limited information on prevalence outside of the United States. One survey in Sweden reported an incidence of 1 in 220,000 people, while a larger review of studies in Europe suggested a lower rate: 1 in 250,000 people.

A person's sex also seems to have some role in the development of autoimmunity; that is, most autoimmune diseases are "sex-related". Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases. According to the American Autoimmune Related Diseases Association (AARDA), autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women include: ankylosing spondylitis, type 1 diabetes mellitus, granulomatosis with polyangiitis, Crohn's disease, Primary sclerosing cholangitis and psoriasis.

The reasons for the sex role in autoimmunity vary. Women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. Involvement of sex steroids is indicated by that many autoimmune diseases tend to fluctuate in accordance with hormonal changes, for example: during pregnancy, in the menstrual cycle, or when using oral contraception. A history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. It has been suggested that the slight, direct exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female.

Another theory suggests the female high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. The X-inactivation skew theory, proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis. Other complex X-linked genetic susceptibility mechanisms are proposed and under investigation.

An allergy is an abnormal immune reaction to a harmless antigen.

- Seasonal allergy

- Mastocytosis

- Perennial allergy

- Anaphylaxis

- Food allergy

- Allergic rhinitis

- Atopic dermatitis

Primary immune deficiency diseases are those caused by inherited genetic mutations. Secondary or acquired immune deficiencies are caused by something outside the body such as a virus or immune suppressing drugs.

Primary immune diseases are at risk to an increased susceptibility to, and often recurrent ear infections, pneumonia, bronchitis, sinusitis or skin infections. Immunodeficient patients may less frequently develop abscesses of their internal organs, autoimmune or rheumatologic and gastrointestinal problems.

- Primary immune deficiencies

- Severe combined immunodeficiency (SCID)

- DiGeorge syndrome

- Hyperimmunoglobulin E syndrome (also known as Job’s Syndrome)

- Common variable immunodeficiency (CVID): B-cell levels are normal in circulation but with decreased production of IgG throughout the years, so it is the only primary immune disorder that presents onset in the late teens years.

- Chronic granulomatous disease (CGD): a deficiency in NADPH oxidase enzyme, which causes failure to generate oxygen radicals. Classical recurrent infection from catalase positive bacteria and fungi.

- Wiskott-Aldrich syndrome (WAS)

- Autoimmune lymphoproliferative syndrome (ALPS)

- Hyper IgM syndrome: X-linked disorder that causes a deficiency in the production of CD40 ligand on activated T-cells. This increases the production and release of IgM into circulation. The B-cell and T-cell numbers are within normal limits. Increased susceptibility to extracellular bacteria and opportunistic infections.

- Leukocyte adhesion deficiency (LAD)

- NF-κB Essential Modifier (NEMO) Mutations

- Selective immunoglobulin A deficiency: the most common defect of the humoral immunity, characterized by a deficiency of IgA. Produces repeating sino-pulmonary and gastrointestinal infections.

- X-linked agammaglobulinemia (XLA; also known as Bruton type agammaglobulinemia): characterized by a deficiency in tyrosine kinase enzyme that blocks B-cell maturation in the bone marrow. No B-cells are produced to circulation and thus, there are no immunoglobulin classes, although there tends to be a normal cell-mediated immunity.

- X-linked lymphoproliferative disease (XLP)

- Ataxia-telangiectasia

- Secondary immune deficiencies

- AIDS

The cause of immunodeficiency varies depending on the nature of the disorder. The cause can be either genetic or acquired by malnutrition and poor sanitary conditions. Only for some genetic causes, the exact genes are known. Although there is no true discrimination to who this disease affects, the genes are passed from mother to child, and on occasion from father to child. Women tend not to show symptoms due to their second X chromosome not having the mutation while man are symptomatic, due to having one X chromosome.

An interesting inverse relationship exists between infectious diseases and autoimmune diseases. In areas where multiple infectious diseases are endemic, autoimmune diseases are quite rarely seen. The reverse, to some extent, seems to hold true. The hygiene hypothesis attributes these correlations to the immune manipulating strategies of pathogens. While such an observation has been variously termed as spurious and ineffective, according to some studies, parasite infection is associated with reduced activity of autoimmune disease.

The putative mechanism is that the parasite attenuates the host immune response in order to protect itself. This may provide a serendipitous benefit to a host that also suffers from autoimmune disease. The details of parasite immune modulation are not yet known, but may include secretion of anti-inflammatory agents or interference with the host immune signaling.

A paradoxical observation has been the strong association of certain microbial organisms with autoimmune diseases.

For example, "Klebsiella pneumoniae" and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1, respectively. This has been explained by the tendency of the infecting organism to produce super-antigens that are capable of polyclonal activation of B-lymphocytes, and production of large amounts of antibodies of varying specificities, some of which may be self-reactive (see below).

Certain chemical agents and drugs can also be associated with the genesis of autoimmune conditions, or conditions that simulate autoimmune diseases. The most striking of these is the drug-induced lupus erythematosus. Usually, withdrawal of the offending drug cures the symptoms in a patient.

Cigarette smoking is now established as a major risk factor for both incidence and severity of rheumatoid arthritis. This may relate to abnormal citrullination of proteins, since the effects of smoking correlate with the presence of antibodies to citrullinated peptides.

Secondary immunodeficiencies, also known as acquired immunodeficiencies, can result from various immunosuppressive agents, for example, malnutrition, aging, particular medications (e.g., chemotherapy, disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids) and environmental toxins like mercury and other heavy metals, pesticides and petrochemicals like styrene, dichlorobenzene, xylene, and ethylphenol. For medications, the term "immunosuppression" generally refers to both beneficial and potential adverse effects of decreasing the function of the immune system, while the term "immunodeficiency" generally refers solely to the adverse effect of increased risk for infection.

Many specific diseases directly or indirectly cause immunosuppression. This includes many types of cancer, particularly those of the bone marrow and blood cells (leukemia, lymphoma, multiple myeloma), and certain chronic infections. Immunodeficiency is also the hallmark of acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV). HIV directly infects a small number of T helper cells, and also impairs other immune system responses indirectly.

Various hormonal and metabolic disorders can also result in immune deficiency including anemia, hypothyroidism, diabetes and hypoglycemia.

Smoking, alcoholism and drug abuse also depress immune response.

G6PD-deficient individuals do not appear to acquire any illnesses more frequently than other people, and may have less risk than other people for acquiring ischemic heart disease and cerebrovascular disease.

Carriers of the underlying mutation do not show any symptoms unless their red blood cells are exposed to certain triggers, which can be of three main types:

- Foods (fava beans is the hallmark trigger for G6PD mutation carriers),

- Medicines and other chemicals such as those derived from quinine (see below), or

- Stress from a bacterial or viral infection.

In order to avoid the hemolytic anemia, G6PD carriers have to avoid a large number of drugs and foods. List of such "triggers" can be obtained from medical providers.

A contiguous gene syndrome (CGS), also known as a contiguous gene deletion syndrome is a clinical phenotype caused by a chromosomal abnormality, such as a deletion or duplication that removes several genes lying in close proximity to one another on the chromosome. The combined phenotype of the patient is a combination of what is seen when any individual has disease-causing mutations in any of the individual genes involved in the deletion. While it can be caused by deleted material on a chromosome, it is not, strictly speaking, the same entity as a segmental aneuploidy syndrome. A segmental aneuploidy syndrome is a subtype of CGS that regularly recur, usually due to non-allelic homologous recombination between low copy repeats in the region. Most CGS involve the X chromosome and affect male individuals.

One of the earliest and most famous examples of a CGS involves a male patient with Duchenne muscular dystrophy (DMD), chronic granulomatous disease (CGD), retinitis pigmentosa and intellectual disability. When it was discovered that an X chromosome deletion (specifically Xp21) was the underlying cause of all of these features, researchers were able to use this information to clone the genes responsible for DMD and CGD.

One of those more common CGS involves a deletion on the X chromosome (near Xp21) that encompasses "DMD" (causing Duchenne muscular dystrophy), "NROB1" (causing X-linked adrenal hypoplasia congenita) and "GK" (causing glycerol kinase deficiency). These patients will have all the common features of each individual disease, resulting in a very complex phenotype. Deletions near the distal tip of the p arm of the X chromosome are also a frequent cause of CGS. In addition to the previously described CGS that occur on the X chromosome, two other common syndromes are Langer-Giedion syndrome (caused by deletions of "TRPS1" and "EXT1" on 8q24 and WAGR syndrome (caused by deletions on 11q13 encompassing "PAX6" and "WT1".)

CGD is an atypical grief response, occurring only in a minority of the bereaved population. It is considered more common in those experiencing disasters, violence or the loss of a child.

It has also been found in family members (or friends) of:

- Patients with life-threatening illnesses

- Suicides and homicides

CGD is found to be prevalent cross-culturally in Europe, the Middle East, Africa, and Asia.

Although more research is needed to determine the multiple pathways to complicated grief disorder, preexisting conditions (such as major depression, PTSD, and sleep disorders) are thought to exacerbate the interruption of the natural healing process.

There are some known predictive characteristics for CGD. An individual is at increased risk for CGD if they are:

- Female

- Pessimistic

- Previously diagnosed with a mood disorder

- Low self-reported social support

- An insecure attachment

- High stress

- A positive caregiving experience and dependency on the deceased

- Have had a early pregnancy loss (miscarriage)