By Raghda El-Sayed Farag Asisst prof. tropical medicine OPPORTUNISTIC INFECTIONS IN...
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Transcript of By Raghda El-Sayed Farag Asisst prof. tropical medicine OPPORTUNISTIC INFECTIONS IN...
By Raghda El-Sayed FaragAsisst prof. tropical medicine
OPPORTUNISTIC INFECTIONS
IN IMMUNOCOMPROMISED PATIENTS
objectives Know the immune system defense function Define opportunistic infections &
Immunocompromised person Discuss Common infection in
Immunocompromised person
Immune systeme &Defense Against Disease
If these barriers are penetrated,the body responds with
If the innate immune response is insufficient,the body responds with
Adaptive(specific) Immune Responsecell-mediated immunity, humoral immunity
Nonspecific External Barriersskin, mucous membranes
Innate Immune Responsephagocytic and natural killer cells,
inflammation, fever
First line of defense
Non-specific defenses are designed to prevent infections by viruses and bacteria. These include:
Intact skin Mucus and Cilia Phagocytes
Role of skin
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
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
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
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
The major players in the immune system include:
Macrophage T cells (helper, cytotoxic, memory) B cells (plasma, memory) Antibodies
Antigen recognition
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
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.
Clonal Selection
“Killer” T cells
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: 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:
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:
• 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
Genetic Physiology Acquired Chronic diseases Medications (Iatrogenic) Hematology
SOME EXAMPLES OF THE OPPORTUNISTIC INFECTIONS
FUNGAL INFECTIONSPneumocystis jiroveci
pneumonia (PCP) Candidiasis CryptococcosisAspergillosis
BACTERIAL INFECTIONSTuberculosis Mycobacterium avium
complex (MAC) infectionsMycosis Legionnaire’s disease
PARASITIC INFECTIONSToxoplasmosisCryptosporidiosisIsospridiamStrongyloides Stercolalis
VIRAL INFECTIONS Herpes simplex virus
infection (HSV) Cytomegalovirus virus CMVVaricella Zoster VirusAdenovirus
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
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 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 21Trisomy 21 and other
genetic disorders are linked to otitis media and upper respiratory infections, as well as to infections with Candida.
ACQUIRED
AIDS
AIDS (Acquired Immune Deficiency Syndrome) is caused by an infection by the HIV (Human Immunodeficiency Virus), which attacks and destroys T-helper cells.
Some drugs can slow down HIV reproduction, but no cure exists yet. Prevention is still the best “cure.”
Common infections associated AIDS
Bacterial: Mycobacterium avium-intracellulare 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
infections with Staphylococci sp., P aeruginosa, enteric organisms, fungi, H influenzae, mycobacteria, and viruses.
MEDICAL CONDITIONS
Hepatic complications (LCF): Enteric organisms, enterococci, streptococci, S aureus.
Metabolic complications (DM): S aureus infection, candidiasis, mucormycosis
Pregnancy complications:-- S agalactiae- Candida sp.- Listeria sp.- hep. E virus
Renal complications(CRF): - S aureus - S pneumoniae - E coli - enterococci- S viridans
HEMATOLOGY
B-CELL DEFECTSB-cell defects predispose patients
to:- 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
Predispose to infections with Candida, Mycobacterium avium-intracellulare complex, herpes viruses.
COMBINED B- AND T-CELL DEFECTS Patients often present with failure to thrive, thrush. Bacterial e.g. S pneumoniae, P aeruginosa, Legionella
pneumophila, L monocytogenes, Mycobacterium species Fungi
Virus e.g. VZV, HSV, CMV, Epstein-Barr virus (EBV)
PHAGOCYTE DEFICIENCY
predisposes patients to infections with:
S aureus, Nocardia sp., P aeruginosa, Serratia sp., streptococci, enteric organisms, and Candida, Aspergillus
COMPLEMENT DEFICIENCIES
Cryptosporidia, meningococcal infections, respiratory viruses, frequent respiratory tract infections in infancy and childhood.
invasive aspergillosis in immunocompromised patients.
bancroftian filariasis. neonatal gram-negative sepsis
Ficolin-3 (H-ficolin) deficiency : Recurrent infections, bronchiectasis, neonatal gram-positive sepsis
Deficiency C1q, C1r, C1rs, C4, C2, C3, or C5-9 : Recurrent sino-pulmonary infections, S pneumoniae, H influenzae, Neisseria sp.
Deficiency of factor D, factor P, factor I, factor H, or properdin : Meningococcal infections
IATROGENIC
ORGAN TRANSPLANT
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
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
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.