1. OPPORTUNISTIC INFECTIONS IN IMMUNOCOMPROMISED PATIENTSBy
Raghda El-Sayed Farag
Asisst prof. tropical medicine

2. objectives Know the immune system defense function
Define opportunistic infections & Immunocompromised person
Discuss Common infection in Immunocompromised person

3. 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

4. First line of defense
Non-specific defenses are designed to prevent infections by viruses and bacteria. These include:
Intact skin
Mucus and Cilia
Phagocytes

5. 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.

6. 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.

7. 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.

8. 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.

9. Major players The major players in the immune system include:
Macrophage
T cells (helper, cytotoxic, memory)
B cells (plasma, memory)
Antibodies

10. 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.

11. 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.

12. 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.

13. Clonal Selection

14. “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.

16. 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

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
Genetic
Physiology
Acquired
Chronic diseases
Medications (Iatrogenic)
Hematology

20. SOME EXAMPLES OF THE OPPORTUNISTIC INFECTIONS
FUNGAL INFECTIONS
PARASITIC INFECTIONS
Pneumocystis jiroveci pneumonia (PCP)
Toxoplasmosis
Cryptosporidiosis
Candidiasis
Isospridiam
Cryptococcosis
Strongyloides Stercolalis
Aspergillosis
VIRAL INFECTIONS
BACTERIAL INFECTIONS
Herpes simplex virus infection (HSV)
Tuberculosis
Mycobacterium avium complex (MAC) infections
Cytomegalovirus virus CMV
Varicella Zoster Virus
Mycosis
Adenovirus
Legionnaire’s disease

21. herpes simplex virus infection
Oral
candidiasis
herpes simplex virus infection

22. Varicella zoster infection
Mycosis : ulcers on leg

23. EXAMPLES OF OPPORTUNISTIC INFECTIONS ACCORDING TO TYPES OF IMMUNOCOMPROMISED INDIVIDUAL

24. PHYSIOLOGY ASPECTS

25. 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

26. 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.

27. GENETICALLY

28. 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.

29. TRISOMY 21
Trisomy 21 and other genetic disorders are linked to otitis media and upper respiratory infections, as well as to infections with Candida.

30. ACQUIRED

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, Salmonella
Viral: CMV, HCV, VZV, HSV, human papilloma virus
Fungal: Pneumocystis carnii, Cryptococcus neoformans, Candida species
Parasitic: Toxoplasma gondii, C parvum

34. LEUKEMIA OR LYMPHOMA
infections with Staphylococci sp., P aeruginosa, enteric organisms, fungi, H influenzae, mycobacteria, and viruses.

35. MEDICAL CONDITIONS
Hepatic complications (LCF): Enteric organisms, enterococci, streptococci, S aureus.
Metabolic complications (DM): S aureus infection, candidiasis, mucormycosis

36. Pregnancy complications:-
- S agalactiae
- Candida sp.
- Listeria sp.
- hep. E virus
Renal complications(CRF):
- S aureus
- S pneumoniae
- E coli
- enterococci
- S viridans

37. HEMATOLOGY

38. B-CELL DEFECTS B-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 

39. T-CELL DEFECTS
Predispose 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 species
Fungi
Virus 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 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

44. IATROGENIC

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 TRANSPLANT
Aerobic gram-negative rods, staphylococci sp., streptococci, C difficile
Candida, Aspergillus, Molds, T gondii
Respiratory 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. 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.