Chronic Granulomatous Disease

Updated: Jul 29, 2019
Author: Roman J Nowicki, MD, PhD; Chief Editor: Dirk M Elston, MD 


Practice Essentials

Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by defects in any of the five subunits of the NADPH oxidase complex responsible for the respiratory burst in phagocytic leukocytes. Patients with CGD are at increased risk of life-threatening infections with catalase-positive bacteria and fungi and inflammatory complications such as CGD colitis. The implementation of routine antimicrobial prophylaxis and the advent of azole antifungals has considerably improved overall survival. 


Chronic granulomatous disease (CGD) is a rare (∼1:250,000 births) disease caused by mutations in any one of the five components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in phagocytes. This enzyme generates superoxide and is essential for intracellular killing of pathogens by phagocytes.

CGD is a primary immunodeficiency that affects phagocytes of the innate immune system and leads to recurrent or persistent intracellular bacterial and fungal infections and to granuloma formation. In approximately two thirds of patients, the first symptoms of CGD appear during the first year of life in the form of infections, dermatitis (sometimes seen at birth), gastrointestinal complications (obstruction or intermittent bloody diarrhea due to colitis), and a failure to thrive. The clinical picture can be quite variable, with some infants having several of these complications and others appearing to be far less ill.[1] Cutaneous disease occurs in 60-70% of patients. Rasamsonia has been identified as an emerging pathogen in this population.[2]

Also see Pediatric Chronic Granulomatous Disease.


Chronic granulomatous disease (CGD) is a genetically heterogeneous immunodeficiency disorder resulting from the inability of phagocytes to kill microbes they have ingested. This impairment in killing is caused by any of several defects in the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme complex, which generates the microbicidal respiratory burst. In CGD, phagocytes ingest bacteria normally, but they cannot kill them.[3]

Patients with CGD are susceptible to severe and recurrent infections due to catalase-positive organisms and organisms resistant to nonoxidative killing. Catalase-negative bacteria, such as streptococci and pneumococci that have the capacity to generate hydrogen peroxide, are killed as they usually are. The intracellular survival of ingested bacteria leads to the development of granulomata in the lymph nodes, skin, lungs, liver, gastrointestinal tract, and/or bones.

CGD is usually inherited in an X-linked recessive fashion. Most patients (approximately 80%) are males, who have hemizygous mutations on the X-linked gene coding for gp91phox. The gene responsible for this form of the disease has been mapped to the p21.1 region of the X chromosome.[4] However, among chronic granulomatous disease subtypes, the autosomal recessive (AR) forms may be associated with milder disease. The extent to which environmental and secondary genetic factors influence phenotypic expression of disease is unknown. A wide variety of molecular defects have been described in the genes for the gp91phox component, the p22phox component,[5] and the p67phox component. These defects include frame shifts; deletions; and nonsense, missense, splice-region, and regulatory-region mutations.[6, 7, 8]

In contrast, a GT deletion at the beginning of exon 2 accounts for the defective genetic function in almost all patients with p47phox deficiency.[9] Another protein, p40phox, has been implicated in the regulation of the NADPH oxidase, but no individual with a mutation in the protein has been found to date. A new variant of CGD has been described; this form is caused by an inhibitory mutation in Rac2, which regulates activity of the neutrophil respiratory burst and actin assembly.[10]


The main defect in chronic granulomatous disease (CGD) is a failure of neutrophils, monocytes, macrophages, and eosinophils to mount a respiratory burst and, therefore, to generate superoxide anions and other reactive oxygen species derived from superoxide, such as hydrogen peroxide. This renders the patients susceptible to severe, recurrent bacterial and fungal infections. The intracellular survival of ingested bacteria leads to the development of granulomata in the lymph nodes, skin, lungs, liver, gastrointestinal tract, and/or bones.

Leukocytes ingest bacteria but do not kill them because of a defect in the production of the superoxide anion.

Most infections in CGD are caused by Staphylococcus aureus. Infections are also caused by unusual opportunistic organisms such as Chromobacterium violaceum; Serratia marcescens; and Nocardia, Legionella, and atypical Mycobacteria species.

BCG vaccination may cause CGD.

Fungal infections in CGD patients have been reported to account for approximately 20% of infections. The most common fungal infections in these patients are caused by Aspergillus species. The spectrum of infection caused by Aspergillus species varies from flulike pneumonia to life-threatening invasive aspergillosis. The most common form of aspergillosis in chronic granulomatous disease patients is Aspergillus pneumonia, which can be accompanied by dissemination to the ribs, chest wall, and soft tissues. Infections with Aspergillus species, particularly of the lungs or bones, are difficult to eradicate.

The most common infecting organisms, on the basis of the type and site of infection, include the following[11] :

  • Pneumonia -  Aspergillus species , Staphylococcus aureus, Nocardia, and Serratia species and Burkholderia cepacia (formerly Pseudomonas cepacia) [12]
  • Subcutaneous, liver, or perirectal abscess - Staphylococcus, Serratia, and Aspergillus species
  • Lung abscess - Aspergillus species
  • Brain abscess - Aspergillus species
  • Suppurative adenitis - Staphylococcus and Serratia species
  • Osteomyelitis - Can arise from hematogenous spread of organisms ( S aureus, Salmonella species, S marcescens) or contiguous invasion of bone, seen typically with non– Aspergillus fumigatus pneumonia, such as Aspergillus nidulans spreading to the ribs or vertebral bodies [1]
  • Bacteremia and/or fungemia -Salmonella and Candida species and B cepacia 
  • Other frequently encountered catalase-positive microbial agents -  Escherichia coli species, Listeria species, Klebsiella species, and  Nocardia.



United States

The exact incidence of chronic granulomatous disease (CGD) is unknown. CGD affects approximately 1 infant per 200,000-250,000 live births.


The prevalence of CGD varies among the populations investigated, with studies reporting variations from 1 case per 1 million individuals to 1 case per 160,000 individuals.[13, 14]


Chronic granulomatous disease affects persons of all races.


Approximately 80% of patients with CGD are male, because the main cause of the disease is a mutation in an X-chromosome–linked gene. However, defects in autosomal genes may also underlie the disease and cause CGD in both males and females.[1]


Symptom onset typically occurs at a young age, although the diagnosis has been at an older age in some patients.[15, 16, 17] Typically, patients with CGD have recurrent pyogenic infections that start in the first year of life. Occasionally, the onset may be delayed until the patient is aged 10-20 years.


The long-term survival of patients who develop symptoms after the end of the first year of life is significantly better than that of patients whose illness starts in infancy. Survival rates are variable but improving; approximately 50% of patients survive to age 30-40 years. Infections are less common in adults than in children, but the propensity for severe life-threatening bacterial infections persists throughout life.

Fungal infections remain a major determinant of survival in chronic granulomatous disease (CGD). Morbidity secondary to infection or granulomatous complications remains significant for many patients, particularly those with the X-linked form. X-linked patients generally have more severe disease, and this is generally in those with lower residual superoxide production. Survival in CGD has increased over the years, but infections are still major causes of morbidity and mortality.[18] Currently, the annual mortality rate is 1.5% per year for persons with autosomal recessive CGD and 5% for those with X-linked CGD.

Since the advent of prophylactic antibiotics, antifungals, and interferon-gamma (INF-gamma), the prognosis for patients with CGD has improved. Patients living to their 30s and 40s is now common.

Patients with CGD and modest residual production of reactive oxygen intermediates (ROIs) have significantly less severe illness and a greater likelihood of long-term survival than patients with little residual ROI production. The production of residual ROI is predicted by the specific NADPH oxidase mutation, regardless of the specific gene affected, and is a predictor of survival in patients with CGD.[19]

Patient Education

Good hygiene of the skin is an important element of treatment because the skin is a common portal of entry in serious infections. To prevent infections, chronic granulomatous disease (CGD) patients should receive lifelong antibiotics and antifungal prophylaxis.




Chronic granulomatous disease (CGD) becomes apparent during the first 2 years of life in most patients, but the onset is occasionally delayed into the second decade of life. The earliest manifestations often involve the skin. Recurrent pyodermas are common, and they often appear as perianal, axillary, or scalp abscesses.

Systemic findings include osteomyelitis, pulmonary abscesses and granulomas, spleen and/or liver abscesses, and hepatosplenomegaly. Pyrexia may be noted. Diarrhea may occur.

Physical Examination

Short stature is a prominent clinical feature in children and adults with chronic granulomatous disease (CGD). Patients with CGD usually present with recurrent bacterial and fungal infections in early childhood. The most common initial manifestations are as follows[20] :

  • Pneumonias [21]
  • Otitis
  • Adenitis
  • Skin infections
  • Septicemia
  • Diarrhea
  • Spleen and/or liver abscesses
  • Gingival abscesses
  • Suppurative lymphadenitis

Patients may have inflammatory and presumably noninfectious conditions such as granulomatous colitis and obstructive granulomas.

The earliest reports of CGD emphasize dermatitis as a characteristic and often presenting manifestation of the disease.[22, 23] The dermatitis was described as an eczematoid, seborrheic, or infectious eczematoid dermatitis that predominantly involved the eyelids and periorbital skin, nares, perioral skin, and ears. The skin lesions frequently became pustular. Similar eruptions were described on the scalp, neck, axillae, inguinal folds, retroauricular folds, and interdigital web spaces. Generalized maculopapular, pustular, and papulopustular eruptions of the newborn were also reported.

Cutaneous manifestations other than dermatitis can be present. Neonatal pustulosis is commonly the first sign of the disease. Recurrent pyodermas are common, and they appear as perianal or axillary abscesses. Eczema of the scalp and lesions of the periorbital, nasal, and postauricular regions are typical, and it is often complicated by infection with staphylococci or other bacteria. Minor abrasions frequently lead to furunculosis and subcutaneous abscesses. Abscesses characteristically heal slowly and leave prominent scars. Skin manifestations in older patients include healed scars of old lesions in the cervical or inguinal areas or scars secondary to multiple surgical procedures performed to drain abscesses.

Associated chronic blepharoconjunctivitis and serosanguineous nasal discharge is often described.

Intraoral ulcerations are described in many patients. These ulcerations resemble aphthous stomatitis, chronic gingivitis, perioral ulcers, scalp folliculitis, chronic suppurative paronychia, or seborrheic dermatitis. Recurrent ulcerative stomatitis is present at some time in almost all patients with CGD.

Systemic findings are pronounced and include the following:

  • Hepatosplenomegaly
  • Osteomyelitis (particularly that caused by Aspergillus species)
  • Recurrent pneumonia with lung abscesses and granulomas (Pneumonia occurs in almost all affected children and may lead to abscess formation, cavitation, and empyema.) 
  • Gastrointestinal manifestations (eg, malabsorption, perianal abscesses and fistulae, oral ulceration, characteristic obstructive lesions associated with granulomatous infiltration) [24]
  • Hepatic (and perihepatic) abscesses (Patients usually present with fever, malaise, and weight loss.)  
  • Perirectal abscesses (can persist for years despite aggressive antimicrobial therapy and fastidious local care)

Mothers of affected boys with the most commonly involved gene often have Jessner lymphocytic infiltrate or discoid lupus erythematosus. In rare instances, systemic lupus erythematosus is reported.


Invasive aspergillosis and candidiasis may occur in patients with chronic granulomatous disease (CGD). Patients with chronic granulomatous disease can be sensitized to Aspergillus species. Allergic bronchopulmonary aspergillosis can develop.

Gastrointestinal complications include the following:

  • Enteritis and/or colitis
  • Crohn disease
  • Gastric outlet obstruction
  • Chronic gastrointestinal inflammation

Rheumatologic disorders include the following:

  • Discoid lupus erythematosus
  • Systemic lupus erythematosus
  • Raynaud syndrome
  • Nodular vasculitis
  • Juvenile rheumatoid arthritis
  • Immune-mediated thrombocytopenia

Other complications include the following:

  • Chorioretinitis
  • Obstruction of the urinary tract
  • Severe aphthous stomatitis
  • Granulomatous cheilitis




Laboratory Studies

The nitroblue tetrazolium (NBT) dye test

Laboratory diagnosis of chronic granulomatous disease (CGD) can be made using the NBT test, stimulated with substances such as phorbol myristate acetate or Escherichia coli lipopolysaccharide, which promote an oxidative response in 90-100% of normal neutrophils.

Neutrophils in patients with chronic granulomatous disease are unable to reduce oxidized NBT to insoluble blue formazan; this principle forms the basis of the standard diagnostic screening test for chronic granulomatous disease.

This test is best used to identify gene carriers, and it has been used for the prenatal diagnosis of chronic granulomatous disease.

Flow cytometric reduction of dihydrorhodamine

This test can also be used to diagnose chronic granulomatous disease. The principles are the same as for the NBT dye test, but a different dye is used. Additionally, X-linked carrier status can also be detected.

Complete blood cell counts

Peripheral blood leukocytosis (>8.5 X 103/µL) is a characteristic finding that reflects increased numbers of circulating neutrophils. Most patients are anemic (hemoglobin < 12.5 g%), usually with a microcytic hypochromic picture.

Microbiologic studies

Culture and sensitivity studies may be helpful. Bacteria isolated from lesions in patients with chronic granulomatous disease are usually catalase positive.

Quantitative immunoglobulin tests

Levels of the three major classes of immunoglobulins, immunoglobulin G, immunoglobulin M, and immunoglobulin A, are increased. Immunoglobulin E levels are increased or in the reference range.

Imaging Studies

Radiography and CT imaging

Pulmonary disease is prominent, with recurrent pneumonia, empyema, and lung abscess formation.

Discrete areas of persistent consolidation may be observed on radiographs and are often called encapsulating pneumonia. This sign is highly distinctive of chronic granulomatous disease. Less specific reticulonodular shadowing and hilar lymphadenopathy are also commonly observed.

Other Tests

Other diagnostic tests include the following:

  • Chemiluminescence testing to detect the degree of light generated by activated phagocytic cells

  • Direct measurements of oxygen consumption

  • Direct measurements of superoxide anion production

Molecular diagnostics may include the following:

  • Polymerase chain reaction[25]

  • Sequencing

  • Allele-specific restriction enzyme analysis[26]


Skin biopsy is important in correctly diagnosing chronic granulomatous disease.

Histologic Findings

Chronic granulomatous disease (CGD) is histologically characterized by a mixed suppurative and granulomatous inflammation. A typical feature of visceral granulomas is the presence of golden-brown–pigmented histiocytes. Histochemical stains show that this material is composed of unsaturated fatty acids, phospholipids, and glycoproteins.

Periodic acid-Schiff (PAS) staining demonstrates the presence of carbohydrates, particularly polysaccharides such as mucoproteins. These substances stain reddish purple with the PAS reaction.

Electron microscopic findings suggest that the pigment represents lipofuscin bodies and appears to be derived from lysosomes. Granulomas consist of neutrophils and macrophages that contain yellow inclusions with areas of necrosis.

Aspergillus species is shown below.

Scanning electron micrograph of Aspergillus specie Scanning electron micrograph of Aspergillus species.


Medical Care

Early diagnosis and treatment can significantly improve the prognosis.[27] Modern therapy for chronic granulomatous disease (CGD) includes aggressive and prolonged administration of antibiotics and prednisone.[28] Treatment for inflammatory and autoimmune complications in patients with CGD is problematic because most agents are immune suppressive and immunity is already impaired in patients with CGD. Many patients respond well to corticosteroids, but they might require prolonged courses.

Sulfasalazine and azathioprine are useful steroid-sparing agents. Tumor necrosis factor-α (TNF-α) inhibitors such as infliximab are effective anti-inflammatory agents but might significantly increase the risk of severe and even fatal infections. The risk of infection needs to be weighed carefully against the risks of uncontrolled mucosal inflammation or surgery that might be further complicated by persistent inflammation, abscesses, and fistulae formation at surgical sites. If TNF-α inhibitors are used, augmented prophylaxis and enhanced vigilance regarding exposures are mandatory.

Methotrexate and hydroxychloroquine (Plaquenil) can be effective in those with arthritides or lupuslike problems.

Conventional treatment consists of lifelong anti-infectious prophylaxis with antibiotics such as trimethoprim-sulfamethoxazole (TMP-SMZ), antimycotics such as itraconazole, and/or interferon (INF)–gamma.

Long-term antibiotic therapy may be helpful. All infections should be treated with broad-spectrum systemic antibiotics. Aggressive treatment should be initiated at the first signs of infection. Every episode of fever must be treated promptly by an aggressive use of drugs able to cross the phagocyte cell membrane and accumulate within the phagocytic cells. Initial empirical therapy should include at least two antibiotics against gram-positive and gram-negative bacteria. In case of failure to respond within 48 hours, empirical changes in antibiotic coverage may be needed before definitive pathogen identification, including the administration of an antifungal drug, if not administered from the beginning. Treatment should be continued for weeks or months, even when there is significant improvement in the inflammatory index and the patient’s clinical condition in order to eradicate the infection completely.[23]

If a fungal invasive infection is identified or strongly suspected, intravenous voriconazole is recommended as initial treatment. Voriconazole serum concentrations present great variability, and drug monitoring is recommended to document bioavailability and efficient blood levels. Severe photosensitivity leading to squamous cell carcinoma and melanoma has been reported with long-term voriconazole treatment. Therefore, voriconazole should be used carefully for durations longer than 6-9 months, particularly among patients with risk factors for skin cancer. In patients requiring prolonged voriconazole, diligent skin examinations, avoidance of excess sunlight, and liberal use of ultraviolet protectants are advisable.[23] When infections are refractory to voriconazole or when there is intolerance, intravenous liposomal amphotericin B and caspofungin have been shown effective. Posaconazole, an orally well-tolerated broad-spectrum triazole antifungal agent, has proven efficacy as prevention of and salvage therapy for invasive fungal infection. When the fungal cause is uncertain, combined antifungal therapy can be considered. The most common combinations are voriconazole and caspofungin combination or caspofungin and liposomal amphotericin B. Amphotericin B should be added to the therapeutic regimen of CGD patients with established invasive aspergillosis. Aspergillus and other fungal infections of the lung typically require prolonged treatment (3-6 mo).[29]

In case of multidrug refractoriness, life-threatening infections (eg, aspergillosis), hematopoietic stem cell transplantation (HSCT) with reduced-intensity conditioning represents a valid curative option.[30]

Alternatively, a combination of sequential granulocyte transfusions (GTs), leading to a transitory beneficial effect on preexisting infections, and HSCT have been proposed.[23]

Gene editing is being studied.[31]

INF-gamma therapy subcutaneously appears to be a promising way of improving neutrophil and monocyte function and may prove to be of particular value in the prevention or treatment of deep fungal infections. INF-gamma is now recommended as life-long therapy for infection prophylaxis in persons with CGD.[32, 33]

HSCT may be considered as an early treatment option for CGD. Since the beginning of the 21st century, there have been many reports on HSCT in patients with CGD and the encouraging results obtained with regard to survival rate, engraftment, and graft versus host disease (GVHD). In particular, it is notable that HSCT can cure CGD and reverse organ dysfunction. There is continuing controversy about indications and optimum timing of HSCT in CGD. Patients with absent NADPH oxidase activity and poor prognosis have been recommended for early HSCT. Present HSCT indication criteria in children are as follows: (1) one or more life-threatening infection, (2) noncompliance with antimicrobial prophylaxis, or (3) steroid-dependent autoinflammation. Indication criteria in adolescents and young adults are more difficult to apply because organ dysfunction is frequent and transplant-related mortality after HSCT has been high.[23, 34]

Bone marrow transplantation (BMT), as a last resort, can be undertaken. This treatment has been partially successful. Transplantations with other than perfectly matched donors are presently discouraged.[35, 36]

Recurrent impetigo, frequently in the perinasal area and caused by S aureus, usually requires prolonged courses of oral and topical antibiotics to clear.

Noninfectious granulomas may resolve spontaneously, and they rarely require systemic corticosteroid therapy unless vital organs are compromised.

Gene therapy for CGD

Gene therapy for hematopoietic cells (GT-HSC) represents an attractive alternative to HSCT as therapy for CGD patients without a matched donor. The observation that XR-CGD carriers in whom 10% or greater of normal neutrophils were healthy suggested that a minor functional correction of neutrophils would be sufficient to restore a normal phenotype in GT-HSC–treated patients. Nevertheless, GT-CGD is difficult to perform because corrected HSCs do not have a selective growth advantage compared with deficient cells, and, at the same time, a large number of cells needs to be corrected to ensure a good restoration of neutrophil activity. Thus, myeloablative conditioning is necessary to ensure an efficient engraftment of progenitor cells.[23, 37, 38, 39, 40]

Surgical Care

In addition to systemic antifungal treatment, surgical debridement or excision of consolidated infection is advised when possible,[23] including surgical drainage of abscesses and resection (when possible) of granulomas.


Gastrointestinal manifestations include perineal abscesses; fistulae; and, characteristically, obstructive lesions associated with granulomatous infiltration; thus consultation with a surgeon may be necessary.

An internist consultation may be necessary because pyrexia should be carefully investigated to reveal the site of the causative infection and the responsible microorganism. Pulmonary disease (eg, recurrent pneumonia, empyema, lung abscess formation) should be treated.


Chronic granulomatous disease (CGD) in adults may be more common than previously assumed. Because timely treatment, infection prophylaxis, and genetic counseling for affected families are possible, CGD should be excluded in any patient with unexplained infections or granulomas. Patients with the disease should be counseled about prophylaxis for bacterial and fungal disease and avoidance of unnecessary exposure to mold and nonchlorinated water. Prophylactic therapy is based on daily doses of trimethoprim/sulfamethoxazole and itraconazole.

Long-Term Monitoring

Skin hygiene is an important element of further outpatient care for chronic granulomatous disease (CGD). The skin should be washed twice daily with a disinfectant soap. The fingernails should be cut short. The patient should be monitored for the results of antibacterial and antifungal prophylaxis.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Continuous antifungal therapy is effective in preventing infection by Aspergillus species.[41]


Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Trimethoprim and sulfamethoxazole (Bactrim, Septra)

Trimethoprim and sulfamethoxazole (TMP-SMZ) is current standard therapy. It inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Antifungal agents

Class Summary

These agents exert a fungicidal effect by altering the permeability of the fungal cell membrane. Their mechanism of action may also involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.

Itraconazole (Sporanox)

Continuous antifungal therapy is effective in preventing infection by Aspergillus species. Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Biologic response modifiers

Class Summary

These agents regulate the immune system by a variety of mechanisms including enhancing activity of macrophages and cytotoxic actions of T lymphocytes.

Interferon gamma - 1b (Actimmune)

Interferon (INF)–gamma 1b reduces the frequency and severity of serious infections associated with chronic granulomatous disease (CGD). Interferons are synthesized by eukaryotic cells in response to viruses and a variety of natural and synthetic stimuli. INF-gamma possesses antiviral, immunomodulatory, and antiproliferative activity. INF-gamma has potent phagocyte-activating effects not seen with other interferon preparations, including generation of toxic oxygen metabolites within phagocytes capable of mediating intracellular killing of microorganisms.


Questions & Answers


What is chronic granulomatous disease (CGD)?

How common is chronic granulomatous disease (CGD)?

What is the pathophysiology of chronic granulomatous disease (CGD)?

What causes chronic granulomatous disease (CGD)?

What is the US prevalence of chronic granulomatous disease (CGD)?

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What is the prognosis of chronic granulomatous disease (CGD)?

What is included in patient education about chronic granulomatous disease (CGD)?


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What are the possible complications of chronic granulomatous disease (CGD)?


What are the differential diagnoses for Chronic Granulomatous Disease?


How is chronic granulomatous disease (CGD)diagnosed?

What is the role of flow cytometry in the diagnosis of chronic granulomatous disease (CGD)?

What is the role of CBC counts in the workup of chronic granulomatous disease (CGD)?

What is the role of culture and sensitivity studies in the workup of chronic granulomatous disease (CGD)?

What is the role of immunologic testing in the workup of chronic granulomatous disease (CGD)?

What is the role of imaging studies in the workup of chronic granulomatous disease (CGD)?

Which tests are used to diagnose chronic granulomatous disease (CGD)?

What is the role of molecular testing in the diagnosis of chronic granulomatous disease (CGD)?

What is the role of skin biopsy in the diagnosis of chronic granulomatous disease (CGD)?

Which histologic findings are characteristic of chronic granulomatous disease (CGD)?


How is chronic granulomatous disease (CGD) treated?

What is the role of gene therapy in the treatment of chronic granulomatous disease (CGD)?

What is the role of surgery in the treatment of chronic granulomatous disease (CGD)?

Which specialist consultations are beneficial to patients with chronic granulomatous disease (CGD)?

What is the role of prophylactic therapy in the treatment of chronic granulomatous disease (CGD)?

What is included in the long-term monitoring of chronic granulomatous disease (CGD)?


What is the role of medications in the treatment of chronic granulomatous disease (CGD)?

Which medications in the drug class Biologic response modifiers are used in the treatment of Chronic Granulomatous Disease?

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Which medications in the drug class Antibiotics are used in the treatment of Chronic Granulomatous Disease?