Infections in People With Immunodeficiencies

Slide 1 · Infections in People With

Immunodeficiencies

Pathogenesis • immune-defect patterns • clinicopathologic correlations

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Explain how loss of a defined defense changes infection susceptibility.

Link inherited defects to characteristic microbial vulnerabilities.

Analyze acquired immune deficits, reactivation, and nonimmune susceptibility.

Interpret clinical presentations using immune mechanism rather than organism lists.

Slide 3 · Why immunodeficiency changes infection risk

Loss of host defense

Impaired containment

Infection or reactivation

Impaired innate or adaptive immunity permits infections that effective host defenses usually control.

Defects may be inherited or acquired; The affected component determines the vulnerability.

Infection may represent a new exposure or reactivation of a previously contained organism.

Slide 4 · Defense is distributed across distinct layers

Barrier integrity

Phagocyte killing

Complement activity

T-cell / B-cell responses

Physical barriers reduce microbial access to tissues.

Phagocytes and complement provide rapid innate protection.

B-cell antibodies aid neutralization and opsonization; T cells coordinate cellular defense.

Slide 5 · An immune deficit predicts—but does not dictate—the pathogen

Host defect

Pathogen encounter

Observed syndrome

The clinical pattern reflects both the defect and the microbial exposure.

Innate defects favor infections requiring phagocytic or complement-mediated clearance.

Adaptive defects may compromise antibodies, cellular immunity, or both.

Nonimmune injuries can produce similar susceptibility without a primary immune defect.

Slide 6 · Primary versus secondary immunodeficiency

Primary / inborn

Secondary / acquired

Genetic defect in immune pathway

Disease, infection, treatment or malnutrition

Frequently recognized in early life

May arise at any age

Examples: CGD, SCID, BTK deficiency

Examples: HIV, leukemia, chemotherapy

Primary defects arise from inherited abnormalities of immune development or function.

Slide 7 · New infection versus reactivation

Prior containment

Declining immunity

Latent infection reactivates

New infection follows acquisition of an organism that breaches inadequate defenses.

Reactivation follows loss of control over organisms persisting after an earlier exposure.

Herpesviruses and Mycobacterium tuberculosis are textbook examples of reactivation.

Slide 8 · Pattern recognition begins with the impaired function

Predominant vulnerability

Immune component to consider

Pyogenic bacterial infections

Phagocytes, complement or antibodies

Viral and fungal infections

T-cell / combined immunity

Recurrent Neisseria

Terminal complement

Recurrent pyogenic infections suggest insufficient phagocyte, complement or antibody function.

Slide 9 · Age at recognition can help localize a defect

Recurrent infections

Age and exposures

Immune mechanism

Many inherited immune deficiencies become evident during infancy or childhood.

Some humoral defects appear after maternally acquired immunoglobulin declines.

Acquired causes should be sought when susceptibility develops in an appropriate clinical context.

Slide 10 · Leukocyte migration is essential for tissue protection

Leukocyte adhesion

Transendothelial migration

Tissue bacterial control

Neutrophils must adhere to endothelium and migrate into infected tissue.

Leukocyte adhesion deficiency disrupts this recruitment step.

The result is susceptibility to recurrent, sometimes life-threatening bacterial infections.

Slide 11 · Leukocyte adhesion deficiencies: Two distinct defects

LAD type 1

LAD type 2

β2 integrin chain defect

Fucosyltransferase-related defect

Defective stable adhesion

Defective selectin ligand production

Bacterial infection susceptibility

Bacterial infection susceptibility

Type 1 involves the β2 chain shared by LFA-1 and Mac-1 integrins.

Slide 12 · Chédiak–Higashi: Impaired vesicle trafficking

LYST defect

Abnormal granule trafficking

Impaired microbicidal function

Defective LYST-associated lysosomal trafficking disrupts phagolysosome function.

Neutropenia, abnormal degranulation and delayed microbial killing contribute to infection.

Giant leukocyte granules coexist with albinism, neurologic and bleeding manifestations.

Slide 13 · Chronic granulomatous disease: An oxidative burst defect

Phagocyte oxidase defect

Reduced superoxide

Delayed microbial killing

Inherited phagocyte oxidase defects prevent effective superoxide generation.

Neutrophils ingest organisms but have impaired oxygen-dependent killing.

Recurrent bacterial infection and macrophage-rich granulomatous inflammation follow.

Slide 14 · CGD inheritance reflects oxidase subunits

Genetic example

Affected oxidase component

X-linked CGD

gp91phox, membrane component

Autosomal recessive CGD

p47phox, cytoplasmic

Autosomal recessive CGD

p67phox, cytoplasmic

The common X-linked form affects the membrane component gp91phox.

Slide 15 · Why granulomas form in CGD

Failed early killing

Persistent microbial stimulus

Granuloma formation

Failure of initial neutrophil killing permits persistent infection.

Macrophages accumulate and become activated in a later attempt at containment.

The resulting granulomas express chronic inflammation, not adequate bacterial eradication.

Slide 16 · Patterned innate sensing: TLR signaling

Innate sensing defect

Illustrative consequence

TLR3

Herpes simplex encephalitis

MyD88

Severe bacterial infection / pneumonia

TLR3 senses viral RNA; Defects are associated with recurrent herpes simplex encephalitis.

Slide 17 · Interleukin-12–interferon-γ axis

IL-12 signaling

Th1 / IFN-γ response

Control of mycobacteria

IL-12 promotes Th1 responses; IFN-γ activates antimicrobial defenses.

Inherited defects in IL-12 or IFN-γ receptors impair protection against intracellular microbes.

Environmental mycobacteria of low virulence can then cause disease.

Slide 18 · Type I interferons restrict viral infection

Viral recognition

Type I IFN response

Antiviral defense

Type I interferons participate in antiviral host defense.

Mutations affecting their function, or acquired antibodies against them, can increase viral susceptibility.

The source identifies severe COVID-19 among associated clinical infections.

Slide 19 · Complement contributes three forms of defense

Early pathways

C3-dependent functions

C5–C9 membrane attack

Early pathway proteins initiate complement activation.

C3 participates in shared central complement functions, including opsonization.

C5–C9 assemble the membrane attack complex that lyses susceptible organisms.

Slide 20 · C3 deficiency compromises multiple complement functions

Defective C3

Poor complement defense

Recurrent pyogenic infection

C3 acts downstream of both classical and alternative pathways.

Deficiency permits serious, recurrent pyogenic infections.

Immune complex–associated glomerulonephritis may also occur.

Slide 21 · Terminal complement deficiency favors Neisseria

C5–C9 deficiency

Impaired membrane attack

Neisseria susceptibility

Deficiency of any terminal component C5 through C9 impairs membrane attack complex formation.

Recurrent meningococcal or gonococcal infection is characteristic.

The organism pattern points toward a lytic complement defect.

Slide 22 · Different complement deficiencies give different clues

Affected segment

Reported infection association

Early classical (C2/C4)

Variable bacterial / viral infections

Alternative (properdin / factor D)

Recurrent pyogenic infections

Central C3

Serious recurrent pyogenic infections

Terminal C5–C9

Recurrent Neisseria

C2 or C4 deficiency may cause infection or immune dysregulation; Some carriers remain asymptomatic.

Slide 23 · A complement clue must be interpreted cautiously

A single episode of bacterial infection does not establish complement deficiency.

Several C2/C4-deficient individuals have no infectious phenotype.

The recurring organism, severity and clinical context matter more than any isolated association.

Slide 24 · Adaptive immune defects overlap in practice

B-cell / antibody arm

T-cell cellular arm

T-cell help for B cells

Combined immune deficiency

B lymphocytes mediate antibody production; T lymphocytes mediate cellular responses and provide B-cell help.

Severe T-cell deficits commonly diminish antibody responses as well.

Thus clinically ‘T-cell’ and ‘combined’ immunodeficiencies are not always separable by presentation.

Slide 25 · SCID is a failure of both adaptive arms

Developmental / signal defect

T-cell and antibody dysfunction

Severe broad infections

Severe combined immunodeficiency (SCID) includes several genetically distinct disorders.

The common phenotype is profound compromise of cellular and humoral immunity.

Infants are vulnerable to multiple unrelated pathogen groups.

Slide 26 · SCID: Early clinical pattern

Oral candidiasis (thrush) is a prominent early manifestation.

Extensive diaper rash, recurrent infection and failure to thrive may coexist.

A morbilliform neonatal rash can reflect maternal T-cell engraftment with graft-versus-host injury.

Slide 27 · X-linked SCID: Cytokine receptor signaling fails

Common γ-chain defect

IL-7 / IL-15 signaling loss

T-cell ± NK-cell deficiency

Mutations affect the common γ-chain (γc) shared by several cytokine receptors.

Loss of IL-7 receptor signaling markedly impairs T-cell development.

IL-15 signaling deficiency also frequently reduces NK-cell development; B cells can persist but function poorly.

Slide 28 · ADA deficiency: Metabolic toxicity to lymphocytes

ADA deficiency

Toxic purine metabolites

Lymphocyte depletion

Autosomal recessive adenosine deaminase deficiency is an important form of SCID.

Accumulation of deoxyadenosine derivatives, including deoxy-ATP, is proposed to injure developing lymphocytes.

T-cell numbers may be reduced more profoundly than B-cell numbers.

Slide 29 · SCID may arise from receptor assembly or downstream signaling

Defect

Key functional consequence

RAG / receptor recombination

Failure of TCR and Ig gene rearrangement

JAK3

Loss of common γ-chain receptor signaling

TCR pathway components

Impaired T-cell activation / maturation

RAG-related defects prevent antigen-receptor gene rearrangements needed for T- and B-cell development.

Slide 30 · SCID-associated infections span multiple organism groups

Organism group

Examples described in SCID

Fungal / opportunistic

Candida; Pneumocystis

Viral

CMV; varicella

Bacterial

Pseudomonas and other bacteria

The Robbins examples include Candida albicans and Pneumocystis jirovecii.

Slide 31 · SCID morphology: Hypoplastic lymphoid organs

Small, lymphocyte-poor thymus

T-zone depletion

Variable B-zone depletion

Loss of normal lymphoid architecture

The thymus is small and lymphocyte-poor in common γc- and ADA-related SCID.

X-linked SCID may show immature-appearing thymic epithelial lobules.

Lymph nodes and other lymphoid tissue exhibit depletion of T-cell and sometimes B-cell zones.

Slide 32 · Thymic hypoplasia isolates a T-cell maturation problem

Thymic hypoplasia

Reduced mature T cells

Viral / fungal vulnerability

DiGeorge syndrome arises from abnormal developmental formation of thymic structures.

Reduced thymic T-cell maturation weakens defenses against some viral and fungal infections.

Loss of T-cell zones in nodes and spleen may be seen; Immunoglobulin levels vary with severity.

Slide 33 · MHC class II deficiency impairs CD4 T-cell development

Low MHC class II

CD4 T-cell dysfunction

Combined deficiency

Bare lymphocyte syndrome may follow defects in transcriptional control of MHC class II genes.

Without MHC class II, CD4 T-cell maturation and activation fail.

Defective T-cell help also impairs B-cell responses, producing combined deficiency.

Slide 34 · Antibody deficiency produces recognizable infection patterns

Opsonization

Viral neutralization

Mucosal IgA

B-cell help / class switching

Antibodies promote opsonization and phagocytic clearance of bacteria.

Neutralizing antibodies help prevent some viral infections and dissemination.

Secretory IgA is particularly important at mucosal surfaces.

Slide 35 · X-linked agammaglobulinemia: Blocked B-cell maturation

BTK signaling defect

B-cell maturation arrest

Low immunoglobulins

BTK mutations arrest development of pre-B cells into mature B cells.

Peripheral B cells and circulating immunoglobulins are profoundly reduced.

Recurrent infections typically become apparent as maternal Ig protection wanes.

Slide 36 · XLA: Bacterial and nonbacterial vulnerabilities

Organism / group

Why it matters

Encapsulated / pyogenic bacteria

Reduced antibody opsonization

Enteroviruses

Impaired neutralization

Giardia lamblia

Insufficient mucosal antibody defense

Typical respiratory pathogens include Haemophilus influenzae, Streptococcus pneumoniae and Staphylococcus aureus.

Slide 37 · XLA morphology mirrors the absent mature B-cell pool

Small germinal centers

Sparse or absent plasma cells

Low mature B cells

Relatively preserved T cells

Germinal centers in lymph nodes, Peyer patches and tonsils are underdeveloped.

Plasma cells are absent or markedly depleted across tissues.

T-cell–mediated responses are relatively normal.

Slide 38 · CVID: B cells may be present but ineffective

B-cell / helper dysfunction

Poor plasma-cell output

Low effective antibodies

Common variable immunodeficiency has heterogeneous mechanisms and hypogammaglobulinemia.

Circulating B-cell numbers are often preserved, but plasma-cell differentiation is impaired.

Recurrent sinopulmonary pyogenic infections and Giardia-related diarrhea are typical.

Slide 39 · XLA and CVID differ in B-cell maturation stage

Feature

XLA

CVID

B-cell count

Markedly reduced

Often near normal

Principal block

Early maturation

Plasma-cell differentiation / function

Germinal centers

Underdeveloped

May be hyperplastic

Infection pattern

Sinopulmonary; enterovirus; Giardia

Sinopulmonary; Giardia; some viral

XLA is an early, BTK-related arrest with few mature B cells.

Slide 40 · Selective IgA deficiency exposes mucosal surfaces

Low secretory IgA

Weakened mucosal defense

Local recurrent infections

Failure to generate IgA-producing plasma cells lowers serum and secretory IgA.

Most affected individuals have no symptoms.

Symptomatic patients may develop recurrent respiratory, gastrointestinal and urogenital infection.

Slide 41 · Hyper-IgM syndrome: Class switching is defective

Defective CD40L / CD40 / AID

Failed class switching

Restricted antibody repertoire

IgM is present, whereas IgG, IgA and IgE are deficient.

CD40L deficiency in helper T cells is a common X-linked mechanism.

Other cases involve CD40 or activation-induced cytidine deaminase (AID).

Slide 42 · CD40–CD40L also links antibody and macrophage defense

CD4 T-cell CD40L

B-cell CD40 engagement

Class-switched antibodies

CD40L on activated CD4 T cells engages CD40 on B cells and antigen-presenting cells.

This interaction supports antibody class switching and affinity maturation.

It also enhances microbicidal activity of macrophages: Loss can therefore impair more than antibodies.

Slide 43 · X-linked lymphoproliferative disease: EBV is a clue

SAP signaling defect

Ineffective EBV control

Severe EBV disease

SAP-associated signaling defects impair NK/T-cell responses to Epstein–Barr virus.

Affected patients may develop fulminant mononucleosis and B-cell lymphoproliferation.

This illustrates a narrowly patterned pathogen association despite broader immune signaling changes.

Slide 44 · Th17 response defects affect mucosal and skin defense

Defective Th17 responses

Weakened mucocutaneous defense

Candida / skin infection

Inherited defects of Th17 responses are associated with chronic mucocutaneous candidiasis.

Bacterial skin infections may also recur.

The infection phenotype directs attention to local barrier-associated lymphocyte responses.

Slide 45 · Wiskott–Aldrich: Combined clinical clues

Thrombocytopenia

Eczema

Infections

WASP-related immune defect

The core phenotype includes thrombocytopenia, eczema and recurrent infection.

WASP defects alter cytoskeleton-linked immune signaling and cellular responses.

Peripheral T-cell depletion and poor antibody responses contribute to infection susceptibility.

Slide 46 · Ataxia–telangiectasia: DNA repair and immune function

ATM DNA-repair defect

Abnormal antibody development

Respiratory bacterial infection

ATM deficiency causes impaired DNA-damage responses and disordered immune development.

Isotype-switched antibody deficiencies, especially IgA and IgG2, may occur.

Bacterial upper and lower respiratory infections are prominent among manifestations.

Slide 47 · Immune dysregulation and infection may coexist

Altered immune regulation

Autoimmunity + poor defense

Infection vulnerability

Some primary immune regulatory disorders cause autoimmunity, infection susceptibility and lymphoproliferation.

Defects may change cytokine signaling or regulatory T-cell function.

Clinical autoimmunity should not automatically be interpreted as intact antimicrobial immunity.

Slide 48 · Secondary deficits arise through several mechanisms

Marrow impairment

Drug suppression

Infection-associated loss

Nutritional / age effects

Bone marrow infiltration or injury reduces generation of immune cells.

Immunosuppressive drugs interfere with lymphocyte and other immune responses.

Infection, malnutrition, aging or systemic disease can also reduce host defense.

Slide 49 · Leukemia can suppress hematopoietic defense

Marrow infiltration

Reduced normal leukocyte production

Susceptibility to infection

Infiltration of bone marrow by malignant cells can impair normal blood-cell production.

Reduced functional leukocyte output diminishes protection against infection.

This is acquired immunodeficiency arising from another disease process.

Slide 50 · Cancer therapy may diminish host immunity

Anticancer treatment

Immune-cell injury / depletion

Infection risk

Chemotherapy and radiation therapy can injure hematopoietic and immune compartments.

Some cancer treatments produce lymphocyte depletion or suppress immune activity.

The timing and degree of immunosuppression influence infection vulnerability.

Slide 51 · Drug immunosuppression is an intended effect with a cost

Immunosuppressive therapy

Reduced immune reactivity

Infection susceptibility

Autoimmune disease treatments suppress harmful immune activity but may weaken antimicrobial defense.

Solid-organ transplant recipients often require immunosuppressive drugs to prevent graft rejection.

Suppressing immunity against host or graft antigens can simultaneously expose patients to infections.

Slide 52 · Hematopoietic stem cell transplantation changes defense

HSC transplantation

Impaired immune defense

Infection vulnerability

The source includes hematopoietic stem cell transplantation among contexts of acquired immunodeficiency.

The immune compartment may be quantitatively or functionally impaired in the transplantation setting.

The transplantation context must be considered when interpreting a new infection.

Slide 53 · HIV-related immune suppression is a central example

HIV infection

Progressive immunosuppression

Opportunistic infections

HIV infection causes acquired immunodeficiency syndrome (AIDS).

AIDS features profound immunosuppression and susceptibility to opportunistic infections.

Tumors and neurologic manifestations also contribute to the pathologic spectrum of AIDS.

Slide 54 · Different acquired causes can converge on one phenotype

Context

Major immune disturbance

HIV/AIDS

Virus-associated immunosuppression

Leukemia

Bone marrow infiltration / reduced output

Cancer therapy

Marrow / immune injury

Transplant treatment

Drug-mediated immune suppression

HIV-related immunodeficiency follows an infectious cause.

Slide 55 · Why suppressed immunity reactivates latent pathogens

Persistent organism

Lost immune containment

Reactivation

Some microbes persist after primary infection despite apparent clinical recovery.

Effective immunity prevents their renewed proliferation.

Reduced surveillance can release this containment, producing reactivated infection.

Slide 56 · Herpesviruses and tuberculosis illustrate latency

Latent example

Event when control declines

Herpesviruses

Viral reactivation

Mycobacterium tuberculosis

Reactivated mycobacterial infection

Herpesviruses are among the latent infections capable of reactivation.

Slide 57 · Immunosenescence contributes to acquired susceptibility

Aging

Decline in immune responsiveness

Higher infection vulnerability

Host immune responses decline with aging.

The source links this age-related decline to increased infections in older adults.

Chronologic age is contextual information rather than a pathogen-specific diagnosis.

Slide 58 · Malnutrition impairs antimicrobial defense

Malnutrition

Impaired host defense

Infection susceptibility

Inadequate nutrition can compromise immune defenses.

Malnutrition is included among causes of secondary immunodeficiency.

Nutritional and disease-related vulnerabilities may coexist and compound infection susceptibility.

Slide 59 · Not all infection susceptibility is immune-cell failure

Mucociliary / epithelial function

Splenic clearance

Skin barrier

Immune-cell function

An intact immune system still depends on barriers, clearance mechanisms and organ function.

Cystic fibrosis, sickle cell disease and burns are examples of nonimmune settings associated with infection.

Identifying the damaged host function explains the organism association.

Slide 60 · Cystic fibrosis: Altered airway host defense

CFTR dysfunction

Disordered airway defense

Pseudomonas / Burkholderia

A defective CF transmembrane conductance regulator underlies cystic fibrosis.

The source identifies Pseudomonas aeruginosa and Burkholderia cepacia as notable infections.

This exemplifies infection risk from abnormal organ function, not necessarily intrinsic leukocyte failure.

Slide 61 · Sickle cell disease: Loss of splenic protection

Sickle cell disease

Loss of splenic function

Pneumococcal infection

Loss of functional splenic activity impairs protective host clearance.

Streptococcus pneumoniae is a highlighted infection in sickle cell disease.

A disease of erythrocytes can therefore present a major infectious vulnerability.

Slide 62 · Burns: Disruption of the physical barrier

Burn injury

Barrier disruption

Pseudomonas infection

Severe burn injury disrupts the skin barrier that normally blocks microbial entry.

Pseudomonas aeruginosa is an example highlighted by Robbins.

The proximate defect is barrier failure rather than a defining inherited immunodeficiency.

Slide 63 · The same organism can accompany different host defects

Clinical setting

Primary vulnerability

Cystic fibrosis

Disease-associated airway defense defect

Burn injury

Disrupted epithelial barrier

SCID

Severe combined immune deficit

Pseudomonas appears in the source examples for burns, cystic fibrosis and SCID.

Slide 64 · From infection phenotype back to mechanism

Observed infection

Likely failed defense

Relevant clinical context

Define whether infections are recurrent, severe, persistent or reactivated.

Localize the defense component suggested by pathogen group and involved organ.

Review inherited conditions, treatments, malignant disease, nutrition and barrier injuries.

Slide 65 · An infection association is not a diagnosis

Observed clue

Mechanistic possibilities

Recurrent bacterial respiratory infection

Antibody, phagocyte or other defenses

Severe herpes simplex encephalitis

TLR3-linked signaling defects

Recurrent Neisseria

Terminal complement deficiency

Candida + broad severe infections in infancy

SCID / combined defect

Complement, phagocyte and antibody defects can all present with bacterial infection.

Slide 66 · Lymphoid morphology can localize developmental failure

Condition

Source-described morphologic pattern

SCID

Hypoplastic thymus / T-cell zones

X-linked agammaglobulinemia

Poorly formed germinal centers; few plasma cells

CVID

Potentially hyperplastic germinal centers

SCID can produce a small, lymphocyte-poor thymus and depleted lymphoid zones.

Slide 67 · Application: Severe multisystem infection in infancy

CLINICAL CLUE

Infant with thrush, rash, poor growth and recurrent severe infections

MECHANISM TO RECOGNIZE

Consider SCID: Both cellular immunity and antibody responses are compromised.

Illustrative case: An infant has thrush, extensive diaper rash and failure to thrive.

Several organism groups cause recurrent, severe infections.

The pattern is more consistent with combined than isolated humoral deficiency.

Slide 68 · Application: Recurrent bacterial infection with granulomas

CLINICAL CLUE

Recurrent infection accompanied by macrophage-rich granulomas

MECHANISM TO RECOGNIZE

CGD: Phagocyte oxidase deficiency → inadequate oxidative microbial killing.

Illustrative case: Recurrent bacterial infections occur in a child with granulomatous inflammation.

A phagocyte oxidative burst disorder can explain failed early killing.

Macrophage-rich granulomas develop during persistent microbial stimulation.

Slide 69 · Application: Recurrent Neisseria infection

CLINICAL CLUE

Repeated episodes involving Neisseria species

MECHANISM TO RECOGNIZE

Terminal components C5–C9, required for the membrane attack complex.

Illustrative case: Recurrent Neisseria meningitidis infections suggest a selective defect in serum bacterial lysis.

Terminal complement activity is important in membrane attack complex formation.

The association supports assessment of complement function rather than presuming an antibody defect.

Slide 70 · Application: Pneumococcal infection in sickle cell disease

CLINICAL CLUE

Sickle cell disease with Streptococcus pneumoniae infection

MECHANISM TO RECOGNIZE

Functional asplenia / loss of splenic protection.

Illustrative case: A patient with sickle cell disease develops invasive pneumococcal infection.

The source associates this with loss of splenic function.

This is a functional organ-defense problem, not necessarily a primary lymphocyte defect.

Slide 71 · Synthesis: Four questions organize the topic

Defense function

Type of defect

New vs latent

Clinical context

What defense normally prevents the organism from causing disease?

Is that defense genetically defective, secondarily suppressed, or mechanically impaired?

Is the event a new infection or reactivation of a latent organism?

Which features of timing, pathogen and tissue response support the proposed mechanism?

Slide 72 · Principal source and contextual sections

Robbins, Cotran & Kumar. Pathologic Basis of Disease, 11th ed. (2026).

Chapter 8, Infectious Diseases: Infections in People With Immunodeficiencies (p. 308).

Chapter 6, Diseases of the Immune System: Immunodeficiency Diseases (pp. 213–219).

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