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Ananthanaryan & Panicker's Textbook of Microbiology 12th Edition - Opportunistic infections.pptx
- 1. CHAPTER 31 OPPORTUNISTIC INFECTIONS Universities Press 3-6-747/1/A& 3-6-754/1, Himayatnagar Hyderabad 500 029 (A.P.), India Email: [email protected] [email protected] Phone: 040-2766 5446/5447 Part III Microbiology as Applied to Infectious Diseases
- 2. Dr Sonal Saxena,MD Director Professor and Head of the Department of Microbiology Maulana Azad Medical College, New Delhi and Dr Amala A Andrews, MD Maulana Azad Medical College, New Delhi UNIVERSITIES PRESS PVT LTD.
- 3. INTRODUCTION Immunocompromised individuals lackthe ability to defend themselves from microbial invasions because they lack of one or more defence mechanisms in their system Immunosuppression may be due to congenital or acquired immunodeficiencies May include humoral, cell-mediated or combined immunodeficiency An infection that arises due to immunosuppression is known as an opportunistic infection (OI) UNIVERSITIES PRESS PVT LTD.
- 4. FACTORS INFLUENCE THE DEVELOPMENTOF IMMUNOSUPPRESSION Malnutrition: Leads to impaired development of all body parameters including the immune system → compromised immunity → infection Ageing: Senescence of immunocompetent cells → suboptimal immune cell function → infection Leukopenia → Cytotoxic drugs (cyclophosphamide) → impaired first line of defence → infection Chronic immunodeficiency diseases: Agammaglobulinemia, SCID (severe combined immunodeficiency) → repeated bacterial infections Immunosuppressing agents: Prescribed for autoimmune disorders, transplant patients, chemotherapy → depletion of immunocompetent cells → infection Genetic predisposition: X-Linked agammaglobulinemia (XLA) → increased incidence of gram-positive infections Metabolic syndromes: Diabetes → increased incidence of infections UNIVERSITIES PRESS PVT LTD.
- 5. PHYSICAL FACTORS THATMAY RESULT IN DERANGED INNATE IMMUNITY UNIVERSITIES PRESS PVT LTD. Burns: Damage to the physical barrier and defects in polymorphonuclear (PMN) cellular function → leads to infection due to Pseudomonas, Staphylococcus, Streptococcus or fungi such as Fusarium, Zygomycetes Traumatic or surgical wound: Breach in the continuity of the skin → allows organisms to enter the body and for organisms that are part of the normal flora of the skin to establish infection Intravenous and prosthetic devices: The continued presence of foreign bodies in the form of cardiac pacemakers and valves, catheters and shunts predisposes the individual to infection by agents such as Candida, Staphylococcus aureus/S. epidermidis and other commensals of the skin Impaired clearance: Cystic fibrosis and chronic pulmonary obstructive disease predisposes the lung to infections by Pseudomonas.
- 6. UNIVERSITIES PRESS PVTLTD. INFECTIONS THAT CAUSE IMMUNOSUPPRESSION HIV CMV EBV Mumps Measles Tuberculosis
- 7. Table 31.1 Organismsassociated with opportunistic infections UNIVERSITIES PRESS PVT LTD.
- 8. OPPORTUNISTI C PATHOGENS Colonising opportunisticpathogens Commensals of the body (S. epidermidis, S. aureus, S. pneumoniae) become pathogens Generally low virulence (Pseudomonas, Acinetobacter, Burkholderia cepacia) They are found in air and soil (Aspergillus spores) UNIVERSITIES PRESS PVT LTD.
- 9. Formerly known assalivary gland viruses Largest viruses in the herpes virus family, 150–200 nm The virus exhibits strict host specificity and infection both in vivo and in vitro, i.e., it can be established only in homologous species Cytomegaloviruses have been identified in human beings, monkeys, guinea pigs and some other species CMV can be grown in human fibroblast cultures Epithelial cell cultures are not susceptible; however, they are affected in vivo Cultures have to be incubated for prolonged periods—up to 50 days—as the cytopathic effects are slow to appear CYTOMEGALOVIRUSES UNIVERSITIES PRESS PVT LTD.
- 10. EPIDEMIOLOGY UNIVERSITIES PRESS PVTLTD. CMV spreads slowly and probably requires close contact for transmission It may spread through salivary or other secretions or by sexual contact or by blood transfusion or organ transplants The virus has been detected in saliva, urine, cervical secretions, semen, blood and milk Congenitally infected infants have viruria for up to 4–5 years; they are highly infectious in early infancy About 1 per cent of neonates in the USA are infected with CMV; in developing countries, the rate may be much higher Up to 80 per cent of adults possess CMV antibodies, indicating the high prevalence of infection
- 11. UNIVERSITIES PRESS PVTLTD. CLINICAL FEATURES Congenital infections: Intrauterine infection—fetal death or cytomegalic inclusion disease of the newborn, which is often fatal; this is a generalised infection associated with hepatosplenomegaly, jaundice, thrombocytopenic purpura and hemolytic anemia Infection in infants: Seen almost exclusively in infants born to mothers who develop primary CMV infection during pregnancy Infection in children: Usually asymptomatic In the immunocompromised host: Severe and even fatal infections
- 12. LABORATORY DIAGNOSIS Specimen: Thevirus can be isolated from urine, saliva, semen and cervical secretions Isolation: By inoculating human fibroblast cultures; growth detected early by using shell vial cultures and by staining the cells with fluorescent- tagged antibody to early antigens of CMV; demonstration of cytomegalic cells in centrifuged deposits from urine or saliva in which ‘owl’s eye’ inclusion bodies are seen Serology: IgM useful in the diagnosis of primary infection but not in reactivation; serological techniques in use include CF, IHA, IF and ELISA; antibody detection may be necessary for screening blood or organ donors; IgM antibody detection helps in the diagnosis of congenital infections UNIVERSITIES PRESS PVT LTD.
- 13. PREVENTION AND TREATMENT Prevention isindicated only in high-risk cases such as organ transplant patients, immunodeficient persons and premature infants Screening of blood and organ donors and administration of CMV immunoglobulins have been employed in prevention Prophylaxis: Acyclovir Treatment: Ganciclovir and foscarnet No vaccine is available UNIVERSITIES PRESS PVT LTD.
- 14. EPSTEIN– BARR (EB) VIRUS Infection withthe EB virus leads to latency, periodic reactivation and lifelong persistence EB virus is transmitted by intimate oral contact such as kissing appears to be the predominant mode of transmission, so much so that infectious mononucleosis is also called the ‘kissing disease’ Virus enters the pharyngeal epithelial cells through CR 2 (or CD 21) receptors, which are the same as for the C3d component of complement UNIVERSITIES PRESS PVT LTD.
- 15. UNIVERSITIES PRESS PVTLTD. PATHOGENICITY EB multiplies locally, invades the bloodstream and infects B lymphocytes, producing either of two: 1. Virus becomes latent inside the lymphocytes, which become transformed or ‘immortalised’; they are polyclonally activated to produce many kinds of immunoglobulins; the heterophile sheep erythrocyte agglutinin seen characteristically in infectious mononucleosis is an example of such polyclonal activation 2. Few infected B cells, develop lytic infection with cell death and release of mature progeny virions
- 16. UNIVERSITIES PRESS PVTLTD. PATHOGENESIS OF LYMPHOMA FORMATION Mononucleosis represents a polyclonal transformation of infected B lymphocytes EB virus antigens are expressed on the surface of infected B cells; the atypical T lymphocytes in blood smears undergo blast transformation in response to such neoantigens Intermittent reactivation of the latent EB virus leads to clonal proliferation of infected B cells In immunocompetent subjects, clonal proliferation is kept in check by activated T cells In the immunodeficient, B cell clones may replicate unchecked, resulting in lymphomas
- 17. CLINICAL FEATURES EB virus infectionmay lead to the following clinical conditions: •Infectious mononucleosis: Acute, self-limiting illness, usually seen in non- immune young adults •EBV-associated malignancies UNIVERSITIES PRESS PVT LTD. Fig. 31.2 Clinical and immunovirological events in Epstein–Barr virus infection
- 18. UNIVERSITIES PRESS PVTLTD. INFECTIOUS MONONUCLEOSIS Incubation period: 4–8 weeks Fever, sore throat and lymphadenopathy Abnormal lymphocytes are present in peripheral blood smears A mild transient rash may be present Often associated usually subclinical hepatitis Spontaneous resolution of the disease in 2-4 weeks Diagnosis is by atypical mononuclear cells in blood examination and serology
- 19. SEROLOGY Viral capsid antigen(VCA): Anti-VCA IgM appears early in EBV infection and usually disappears within four to six weeks Anti-VCA IgG: Appears in the acute phase, peaks at 2-4 weeks, declines slightly, then persists for the rest of the person’s life Early antigen (EA): Anti-EA IgG appears in the acute phase and falls to undetectable levels after 3-6 months EBV nuclear antigen (EBNA): Antibody to EBNA, is not seen in the acute phase but slowly appears 2-4 months after the onset of symptoms and persists for the rest of life Paul–Bunnell test: Heterophile antibodies are detected in infectious mononucleosis UNIVERSITIES PRESS PVT LTD.
- 20. UNIVERSITIES PRESS PVTLTD. FUNGAL AND PARASITIC INFECTIONS Opportunistic mycoses are caused by fungi that are of low virulence and found as contaminants in the environment (e.g., Mucor, Penicillium, Aspergillus) or as commensal flora of the body (e.g., Candida) Parasites associated with opportunistic infections include coccidian parasites and Strongyloides stercoralis, which causes hyperinfection
- 21. LABORATORY DIAGNOSIS OF OPPORTUNISTICINFECTIONS Immunocompromised status and type of immunodeficiency of the individual is established by hematological and immunological investigations Appropriate sample collection Direct microscopic examination: Demonstrate fungi or parasites in the sample. Isolation Antigen detection from tissue or blood Detection of specific microbial DNA or RNA by molecular methods UNIVERSITIES PRESS PVT LTD.