Presentation on theme: "OPPORTUNISTIC INFECTIONS IN IMMUNOCOMPROMISED PATIENTS"— Presentation transcript:
1 OPPORTUNISTIC INFECTIONS IN IMMUNOCOMPROMISED PATIENTS ByRaghda El-Sayed FaragAsisst prof. tropical medicine
2 objectives Know the immune system defense function Define opportunistic infections & Immunocompromised personDiscuss Common infection in Immunocompromised person
3 Immune systeme &Defense Against Disease Nonspecific External Barriersskin, mucous membranesIf these barriers are penetrated,the body responds withInnate Immune Responsephagocytic and natural killer cells,inflammation, feverIf the innate immune response is insufficient,the body responds withAdaptive(specific) Immune Responsecell-mediated immunity, humoral immunity
4 First line of defenseNon-specific defenses are designed to prevent infections by viruses and bacteria. These include:Intact skinMucus and CiliaPhagocytes
5 Role of skinIntact skin cells making it hard for invading bacteria to enter and colonize.Sweat and oils contain anti-microbial chemicals, including some antibiotics.
6 Role of mucus and ciliaMucus 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.
7 Role of phagocytesPhagocytes 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.
8 Specific defensesSpecific 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.
9 Major players The major players in the immune system include: MacrophageT cells (helper, cytotoxic, memory)B cells (plasma, memory)Antibodies
10 Antigen recognitionCells 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.
11 Helper T cellsHelper 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.
12 B cellsB-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.
14 “Killer” T cellsWhile 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.
17 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.
18 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.
19 CAUSES OF IMMUNODEFICIENCY GeneticPhysiologyAcquiredChronic diseasesMedications (Iatrogenic)Hematology
20 SOME EXAMPLES OF THE OPPORTUNISTIC INFECTIONS FUNGAL INFECTIONSPARASITIC INFECTIONSPneumocystis jiroveci pneumonia (PCP)ToxoplasmosisCryptosporidiosisCandidiasisIsospridiamCryptococcosisStrongyloides StercolalisAspergillosisVIRAL INFECTIONSBACTERIAL INFECTIONSHerpes simplex virus infection (HSV)TuberculosisMycobacterium avium complex (MAC) infectionsCytomegalovirus virus CMVVaricella Zoster VirusMycosisAdenovirusLegionnaire’s disease
25 FETAL AND NEONATALBacterial : E. coli, Chlamydia sp., M. pneumoniae, K. pneumoniae, Staphylococci sp., M. tuberculosis, streptococciVirus : Herpes simplex (HSV), HIV, CMV, and varicella zoster virus (VZV)Fungi : Candida albicans & Pneumocystis jiroveci
26 MALNUTRITIONInfectious diarrhea, pneumonia, TB, measles, malaria, salmonellosisMalnutrition is a significant immunocompromising condition worldwide. Those affected are less able than others to tolerate infection.
28 HEMOGLOBINOPATHYDef.: a kind of genetic defect that results in abnormal structure of one of the globin chains of the haemoglobin moleculeCommon infectious agents are encapsulated organisms, particularly Streptococcus pneumoniae. Others like Salmonella sp., E coli, H. influenzae, K pneumoniae, and Neisseria sp.
29 TRISOMY 21Trisomy 21 and other genetic disorders are linked to otitis media and upper respiratory infections, as well as to infections with Candida.
31 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.”AIDS
32 Common infections associated AIDS Bacterial: Mycobacterium avium-intracellulare complex ,S pneumoniae, S aureus, M.tuberculosis, SalmonellaViral: CMV, HCV, VZV, HSV, human papilloma virusFungal: Pneumocystis carnii, Cryptococcus neoformans, Candida speciesParasitic: Toxoplasma gondii, C parvum
38 B-CELL DEFECTS B-cell defects predispose patients to:- Frequent pulmonary and respiratory tract infectionsInfections 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
39 T-CELL DEFECTSPredispose to infections with Candida, Mycobacterium avium-intracellulare complex, herpes viruses.
40 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 speciesFungiVirus e.g. VZV, HSV, CMV, Epstein-Barr virus (EBV)
41 PHAGOCYTE DEFICIENCY predisposes patients to infections with: S aureus, Nocardia sp., P aeruginosa, Serratia sp., streptococci, enteric organisms, and Candida, Aspergillus
42 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
43 Ficolin-3 (H-ficolin) deficiency : Recurrent infections, bronchiectasis, neonatal gram-positive sepsisDeficiency 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
45 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)
46 STEM CELL TRANSPLANTAerobic gram-negative rods, staphylococci sp., streptococci, C difficileCandida, Aspergillus, Molds, T gondiiRespiratory and enteric viruses
47 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)
48 Drugs that decrease gastric acidity: Salmonella sp. , V. cholerae Inhibitors of TNF: TB, HSV encephalitis, histoplasmosis, Listeria infection, and severe falciparum malaria.
49 CONCLUSIONMost 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.