Transcript OPPORTUNISTIC INFECTIONS

OPPORTUNISTIC INFECTIONS
IN IMMUNOCOMPROMISED PATIENTS
By
Raghda El-Sayed Farag
Asisst prof. tropical medicine
objectives
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Know the immune system defense function
Define opportunistic infections &
Immunocompromised person
Discuss Common infection in
Immunocompromised person
Immune systeme &Defense
Against Disease
Nonspecific External Barriers
skin, mucous membranes
If these barriers are penetrated,
the body responds with
Innate Immune Response
phagocytic and natural killer cells,
inflammation, fever
If the innate immune response is insufficient,
the body responds with
Adaptive(specific) Immune Response
cell-mediated immunity, humoral immunity
First line of defense
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Non-specific defenses are designed to
prevent infections by viruses and bacteria.
These include:
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Intact skin
Mucus and Cilia
Phagocytes
Role of skin
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Intact skin cells
making it hard for
invading bacteria to
enter and colonize.
Sweat and oils contain
anti-microbial
chemicals, including
some antibiotics.
Role of mucus and cilia
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Mucus contains
lysozymes, enzymes that
destroy bacterial cell walls.
The normal flow of mucus
washes bacteria and
viruses.
Cilia in the respiratory tract
move mucus out to keep
bacteria and viruses out.
Role of phagocytes
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Phagocytes are several
types of white blood cells
(including macrophages and
neutrophils) that seek and
destroy invaders.
Phagocytes are attracted by
an inflammatory response of
damaged cells.
Specific defenses
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Specific defenses are those that give us
immunity to certain diseases.
In specific defenses, the immune system
forms a chemical “memory” of the invading
microbe. If the microbe is encountered
again, the body reacts so quickly that few or
no symptoms are felt.
Major players
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The major players in the immune system
include:
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Macrophage
T cells (helper, cytotoxic, memory)
B cells (plasma, memory)
Antibodies
Antigen recognition
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Cells of the immune system are “trained” to
recognize “self” proteins vs. “not self”
proteins.
If an antigen (“not self”) protein is
encountered by a macrophage, it will bring
the protein to a helper T-cell for identification.
If the helper T-cell recognizes the protein as
“not self,” it will launch an immune response.
Helper T cells
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Helper T-cells have receptors for
recognizing antigens. If they are presented
with an antigen, they release cytokines to
stimulate B-cell division.
The helper T-cell is the key cell to signal an
immune response.
If helper T-cells are disabled, as they are in
people with AIDS, the immune system will
not respond.
B cells
B-cells differentiate into either plasma
cells or memory B-cells.
- Plasma cells rapidly produce antibodies.
- Memory cells retain the “memory” of the
invader and remain ready to divide rapidly
if an invasion occurs again.
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Clonal Selection
“Killer” T cells
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While B-cells divide and differentiate,
so do T-cells.
Some T-cells become cytotoxic, or
“killer” T-cells. These T-cells seek out
and destroy any antigens in the
system, and destroy microbes “tagged”
by antibodies.
Some cytotoxic T-cells can recognize
and destroy cancer cells.
DEFINITION:
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Immunocompromised :
Denoting an individual with deficient
immunologic mechanisms either because of
an immunodeficiency disorder or because
the system has been rendered so by
immunosuppressive agents.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
Opportunistic infection :
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An infection by a microorganism that normally does not
cause disease but becomes pathogenic when the body's
immune system is impaired and unable to fight off
infection, as in AIDS and certain other diseases.
Suspicion of immunodeficiency
disorder:
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Chronic or recurrent infections.
Infection caused by opportunistic or unusual pathogens.
Failure to respond as expected to standard treatment for infectious
process.
Unusual complications to a usual infection.
Family history of primary immunodeficiency.
CAUSES OF
IMMUNODEFICIENCY
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Genetic
Physiology
Acquired
Chronic diseases
Medications (Iatrogenic)
Hematology
SOME EXAMPLES OF
THE OPPORTUNISTIC INFECTIONS
FUNGAL INFECTIONS
 Pneumocystis jiroveci
pneumonia (PCP)
 Candidiasis
 Cryptococcosis
 Aspergillosis
BACTERIAL INFECTIONS
 Tuberculosis
 Mycobacterium avium
complex (MAC) infections
 Mycosis
 Legionnaire’s disease
PARASITIC INFECTIONS
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Toxoplasmosis
Cryptosporidiosis
Isospridiam
Strongyloides Stercolalis
VIRAL INFECTIONS
 Herpes simplex virus
infection (HSV)
 Cytomegalovirus virus CMV
 Varicella Zoster Virus
 Adenovirus
Oral
candidiasis
herpes simplex
virus infection
Varicella zoster
infection
Mycosis : ulcers on
leg
EXAMPLES OF OPPORTUNISTIC
INFECTIONS
ACCORDING TO
TYPES OF IMMUNOCOMPROMISED
INDIVIDUAL
PHYSIOLOGY
ASPECTS
FETAL AND NEONATAL
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Bacterial : E. coli, Chlamydia sp., M.
pneumoniae, K. pneumoniae,
Staphylococci sp., M. tuberculosis,
streptococci
Virus : Herpes simplex (HSV), HIV,
CMV, and varicella zoster virus (VZV)
Fungi : Candida albicans
& Pneumocystis jiroveci
MALNUTRITION
Infectious diarrhea, pneumonia,
TB, measles, malaria, salmonellosis
 Malnutrition is a significant
immunocompromising condition
worldwide. Those affected are less
able than others to tolerate infection.
GENETICALLY
HEMOGLOBINOPATHY
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Def.: a kind of genetic defect that results in abnormal
structure of one of the globin chains of
the haemoglobin molecule
Common infectious agents are encapsulated
organisms, particularly Streptococcus pneumoniae.
Others like Salmonella sp., E coli, H. influenzae, K
pneumoniae, and Neisseria sp.
TRISOMY 21
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Trisomy 21 and other
genetic disorders are
linked to otitis media
and upper respiratory
infections, as well as
to infections
with Candida.
ACQUIRED
AIDS
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AIDS (Acquired Immune Deficiency Syndrome) is
caused by an infection by the HIV (Human
Immunodeficiency Virus), which attacks and destroys Thelper cells.
Some drugs can slow down HIV reproduction, but no cure
exists yet. Prevention is still the best “cure.”
Common infections associated AIDS
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Bacterial: Mycobacterium aviumintracellulare complex ,S pneumoniae, S aureus,
M.tuberculosis, Salmonella
Viral: CMV, HCV, VZV, HSV, human papilloma virus
Fungal: Pneumocystis carnii, Cryptococcus
neoformans, Candida species
Parasitic: Toxoplasma gondii, C parvum
LEUKEMIA OR LYMPHOMA
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infections with Staphylococci sp., P aeruginosa, enteric
organisms, fungi, H influenzae, mycobacteria, and
viruses.
MEDICAL CONDITIONS
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Hepatic complications (LCF): Enteric organisms,
enterococci, streptococci, S aureus.
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Metabolic complications (DM): S aureus infection,
candidiasis, mucormycosis
Pregnancy complications:- S agalactiae
- Candida sp.
- Listeria sp.
- hep. E virus
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Renal complications(CRF):
- S aureus
- S pneumoniae
- E coli
- enterococci
- S viridans
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HEMATOLOGY
B-CELL DEFECTS
B-cell defects predispose patients
to:
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Frequent pulmonary and respiratory tract infections
Infections with non-enveloped viruses, parvovirus B19,
and rotavirus.
Also at risk for infections with S pneumoniae; S aureus;
Pseudomonas aeruginosa; M pneumoniae; Giardia
lamblia; Salmonella & Shigella
T-CELL DEFECTS
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Predispose to infections with Candida,
Mycobacterium avium-intracellulare complex,
herpes viruses.
COMBINED B- AND T-CELL DEFECTS
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Patients often present with failure to thrive, thrush.
Bacterial e.g. S pneumoniae, P aeruginosa, Legionella
pneumophila, L monocytogenes, Mycobacterium species
Fungi
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Virus e.g. VZV, HSV, CMV, Epstein-Barr virus (EBV)
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PHAGOCYTE DEFICIENCY
 predisposes
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patients
to infections
with:
S aureus, Nocardia sp., P aeruginosa,
Serratia sp., streptococci, enteric organisms,
and Candida, Aspergillus
COMPLEMENT DEFICIENCIES
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Cryptosporidia, meningococcal infections,
respiratory viruses, frequent respiratory tract
infections in infancy and childhood.
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invasive aspergillosis in immunocompromised
patients.
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bancroftian filariasis.
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neonatal gram-negative sepsis
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Ficolin-3 (H-ficolin) deficiency : Recurrent
infections, bronchiectasis, neonatal gram-positive
sepsis
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Deficiency C1q, C1r, C1rs, C4, C2, C3, or C5-9 :
Recurrent sino-pulmonary infections, S
pneumoniae, H influenzae, Neisseria sp.
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Deficiency of factor D, factor P, factor I, factor
H, or properdin : Meningococcal infections
IATROGENIC
ORGAN TRANSPLANT
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Toxoplasma sp. (heart or heart-lung
transplant)
Adenovirus (after renal transplant)
Candida (early post-transplantation
period), aspergillosis, cryptococcosis, other
molds, endemic fungi.
Nocardia, Listeria, mycobacteria, other
bacteria (early post-transplant)
STEM CELL TRANSPLANT
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Aerobic gram-negative rods,
staphylococci sp., streptococci, C difficile
Candida, Aspergillus, Molds, T gondii
Respiratory and enteric viruses
TREATMENTS AND MEDICATIONS MAY
INTERFERE DIRECTLY WITH IMMUNE FUNCTION
 Corticosteroid
therapy :
S aureus,
S pneumoniae, Legionella sp., Listeria sp.
 Inhaled
corticosteroid :
thrush
and community-acquired pneumonia (CAP)
 Drugs
that decrease gastric
acidity: Salmonella sp. , V. cholerae
 Inhibitors
of TNF: TB, HSV encephalitis,
histoplasmosis, Listeria infection, and severe
falciparum malaria.
CONCLUSION
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Most patients usually died from
infections rather than original disorder.
Managing opportunistic infections is the
MOST IMPORTANT part in the treatment
of immuno-deficient patients.
As a preventive measure, one must
prevent these patients from getting
exposed and getting the disease.