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Blood borne pathogens
Bloodborne pathogens like hepatitis B, hepatitis C, and HIV can be transmitted through contact with infected blood or bodily fluids. Workers who are exposed to bloodborne pathogens through injuries from needles, broken glass, or contact with mucous membranes or non-intact skin are at risk of serious infections. Prevention methods include vaccination, use of protective equipment, screening of blood and tissue donors, and modification of high-risk behaviors. Standard precautions should be followed to treat all bodily fluids as potentially infectious and avoid contact with blood or fluids.
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Blood borne pathogens
- 1. Bloodborne pathogens • Bloodbornepathogens are infectious microorganisms present in blood that can cause disease in humans. • These pathogens include HBV, HCV, HIV, but are not limited to these 3 only. • Workers exposed to bloodborne pathogens are at risk for serious or life-threatening infections or illnesses.
- 2. Source of infection-Potentially infectious body fluids. • Any body fluid that is visibly contaminated with blood. • Saliva (in dental procedures). • Semen • Vaginal secretions • Cerebrospinal fluid • Synovial fluid • Pleural fluid • Peritoneal fluid • Amniotic fluid
- 3. Transmission - HBVand HIV are most commonly transmitted through: • • • • Sexual Contact Sharing of hypodermic needles From mothers to their babies at/before birth Accidental puncture from contaminated needles, broken glass, or other sharps • Contact between broken or damaged skin and infected body fluids • Contact between mucous membranes and infected body fluids
- 4. Infected blood canenter HUMANS through: • • • • • Open sores Cuts Abrasions Acne Any sort of damaged or broken skin such as sunburn or blisters • Bloodborne pathogens may also be transmitted through the mucous membranes of the • Eyes • Nose • Mouth
- 5. HIV- Human Immunodeficiency Virus •Family Retroviridae, subgroup Lentivirus. • Enveloped spherical virus 90-120nm • Envelope – outer lipid membrane, inner glycoprotein, projecting knob like spikes • Nucleocapsid – outer icosahedral shell, inner cone shaped core covering RNP’s • Genome – diploid has 2 identical ss +ve sense RNA copies, in association with enzyme RT.
- 6. Viral genes andAntigens • Genome of HIV has 3 Structural genes(gag, pol env) Non structural and Regulatory genes. • The products of these act as antigens, sera of infected patients contains antibodies to them. • Envelope ags gp-120 (principal ag), gp41 (transmembrane pedicle protein) • Core ags – p24 principal core ag.
- 8. Antigenic Variation andDiversity of HIV • • • • • HIV highly mutable virus. Most common in envelope proteins. Error prone nature of Reverse Transcription. Based on this 2 types of HIV – type1, 2. HIV -Type 1 has 10 subtypes(based on gag and pol genes) • Frequent variations in antigens, nucleiotide sequences, cell tropism, growth characters and cytopathology.
- 9. Major differences betweenHIV 1 & 2 HIV 1 HIV 2 Present worldwide West Africa More virulent Less sever form of disease 2 genetic groups, M ??? Infection (Major) , O (Out-lier) prevent against M include 8 clades infection with HIV1 A,H
- 10. Pathogenesis • Primary pathogenicmechanism - CD4 cell damage Receptor - CD4(ag)cell or any cell bearing CD4 receptor • Specific binding through gp120 of HIV to CD4 • After fusion, uncoating, internalisation, RT mediates transcription of RNA into dsDNA, integrated into host cell genome, latent infection. • Reversal of cell ratio (CD4 & CD8) • Polyclonal B cell activation- Hypergammaglobulinaemia • Monocyte-Macrophage function affected
- 11. Clinical features ofHIV infecton • • • • • Acute HIV infection Asymptomatic or latent infection Persistent generalised lymphadenopathy AIDS related complex AIDS
- 12. Opportunistic infections • Bacterial– Mtb, MAC, Salmonella, Legionella, Actinomyes, Nocardia, Campylobacter • Viral- CMV, HHV 1,2. • Fungal – Candida, Cryptococcal, Aspergillosis • Parasitic – PCP, Toxoplasmosis, Isospora, Cryptospora, • Malignancies – Kaposi’s sarcoma, Lymphomas.
- 13. Diagnosis • • • • • ELISA for detectingAbs and as a screening test Antigen Detection – p24 Western blot test for confirmation PCR Supportive evidence… – CD4 cell count.
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- 16. HBV : Structure Mostabundant form 2nd most abundant 3rd most abundant
- 17. HBV • Hepadnaviridae family-Circular partially dsDNA virus • Enveloped virus, inner core covering genome and polymerase. • 3 antigens of HBV are - HBs Ag surface Ag from envelope - HBc Ag nucleocapsid Ags from core - Hbe Ag • Genome – DNA 2 linear strands, one is incomplete, DNA polymerase, has both DNA dependent DNA polymerase n RNA dependent Reverse Transcriptase.
- 18. • Virion isalso referred to as Dane particle • Exists in 3 different forms 22nm spherical and filamentous forms - no DNA in these forms so they are not infectious (composed of surface antigen only) - these forms outnumber the actual virions 42nm enveloped virus – complete virus, most infectious.
- 19. • Replicates withinhepatocytes • Replication involves a reverse transcriptase. • Does not grow in any conventional culture system. • HBV proteins have been cloned in bacteria and yeasts.
- 20. Epidemiology • Endemic inthe human population and hyper endemic in many parts of the world. • Natural infection seen only in humans. • Rich and poor countries differ in the age and modes of infection. • Carriers –healthy, asymptomatic, subclinical. - Play major role in transmission of HBV. • Transmission - Parenteral, Perinatal, Sexual
- 21. Concentration of HepatitisB Virus in Various Body Fluids High Moderate blood semen serum vaginal fluid wound exudates saliva Low/Not Detectable urine feces sweat tears breastmilk
- 22. Pathogenesis of HBV- Immunemediated
- 23. Clinical features- Spectrumof Chronic Hepatitis B Diseases • Acute to chronic course • I P = 1-6 months, insidious in onset. • Acute stage Mild flu-like symptoms - Fatigue ‰ ‰ -Loss of appetite -Nausea -Jaundice ‰ -Darkened urine ‰
- 24. Clinical features- Spectrumof Chronic Hepatitis B Diseases • 90-95% of infected recover in 1-2 months of onset, eliminate virus from body within 6 months • Chronic Persistent Hepatitis – asymptomatic (80-90%) • Chronic Active Hepatitis - symptomatic exacerbations of hepatitis (10-20%) • Cirrhosis of Liver (<10%) • Hepatocellular Carcinoma (<1%)
- 25. Diagnosis • Clinical –jaundice, fever, yellow urine. • Lab – serological markers HBs Ag, HBe Ag, anti-HBc( core ag never appears in serum) • HBe ag – acute infection, highly infectious
- 26. Prevention • Vaccination -highly effective recombinant vaccines are now available. Vaccine can be given to those who are at increased risk of HBV infection such as health care workers. It is also given routinely to neonates as universal vaccination in many countries. • Hepatitis B Immunoglobulin - HBIG may be used to protect persons who are exposed to hepatitis B. It is particular efficacious within 48 hours of the incident. It may also be given to neonates who are at increased risk of contracting hepatitis B i.e. whose mothers are HBsAg and HBeAg positive. • Other measures - screening of blood donors, blood and body fluid precautions.
- 27. HCV • Flaviridae family,Hepacivirus genus • Enveloped RNA virus (50-60nm) • Shows considerable genetic and antigenic diversity. 6 different genotypes and many subtypes. • Transmission- blood transfusion, blood products • C/F – 5-80% chronic hepatitis, some cirrhosis and hepato-cellular carcinoma. • Diagnosis –ELISA( standard method), immunoblotting, PCR. • Treatment- interferon alpha, Ribavirin. • Prevention – No vaccine, standard precautions
- 28. Risk Factors Associatedwith Transmission of HCV Transfusion or transplant from infected donor Injecting drug use Hemodialysis (yrs on treatment) Accidental injuries with needles/sharps Sexual/household exposure to anti-HCVpositive contact Multiple sex partners Birth to HCV-infected mother
- 29. Laboratory Diagnosis • HCVantibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. • HCV-RNA - various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. • HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out.
- 30. Prevention of bloodborne pathogens Practice Standard precautions Treat all fluids, specimens, tissues as potential infectous Screening of blood, organ, tissue donors High-risk behavior modification Blood and body fluid precautions
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