6 курс / Кардиология / Kartikeyan_HIV and AIDS-Basic Elements and Properties
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Gregory C.D., Dive C., Henclerson S., et al., 1991, Activation of Epstein-Barr virus latent genes protects human B-cells from death by apoptosis. Nature 349: 712–614.
Hoffmann G.W., Kion T.A., and Grant M.D., 1991, An idiotypic network model of AIDS immunopathogenesis. Proc Nat Acad Sc USA 88: 3060–3064.
Koup R.A., Safrit J.T., Cao Y., et al., 1994, Temporal association of cellular immune responses with the initial control of viraemia in primary human immunodeficiency virus type-1 syndrome. Jour Virol 68: 4650–4662.
Lennette E.T., Blackbourn D.H., and Levy J.A., 1996, Antibodies to human herpes virus type 8 in the general population and in Kaposi’s sarcoma patients. Lancet 348: 858–861.
Levi J.A., 1993, Pathogenesis of human immunodeficiency virus infection. Micro Rev 57: 183–189. Livingstone W.J., Moore M., Innes D., et al., 1996, Frequent infection of peripheral blood CD8 pos-
itive T-lymphocytes with HIV-1. Lancet 348: 649–654.
Lunardi J., Skandor Y., Bryant J.L., et al., 1995, Tumorigenesis and metastasis of neoplastic Kaposi’s sarcoma cell line in immunodeficient mice blocked by human pregnancy hormone. Nature 357: 64–68.
Mackewicz C.E., Yang L.C., Lilson J.D., and Levy J.A., 1994, Non-cytolytic CD8 T-cell anti-HIV responses in primary HIV-1 infection. Lancet 344: 1671–1673.
Miles S.A., Martinez-Maza O., Razai A., et al., 1992, Oncostatin M as a potent mitogen for AIDS Kaposi’s sarcoma-derived cells. Science 255: 1430–1432.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 501. Candidiasis. University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 16 March.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 509. Herpes zoster (Shingles). University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 1 September.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 511. Kaposi’s Sarcoma. University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 23 May.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 512. Lymphoma. University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 19 July.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 513. Molluscum. University of New Mexico Health Sciences Center. www.aidsinfonet.org.Revised 23 May.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 515. Pneumocystis pneumonia (PCP). University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 15 February.
New Mexico AIDS Education and Training Center, 2006, Fact Sheet 537. Pentamidine. University of New Mexico Health Sciences Center. www.aidsinfonet.org. Revised 13 July.
Penn I., 1990, Cancers complicating organ transplantation. N Engl J Med 323: 1767–1769.
Petito C.K. and Cash K.S., 1992, Blood-brain abnormalities in acquired immunodeficiency syndrome: immunohistochemical localization of serum proteins in post-mortem brain. Ann Neurol 32: 658–665.
Petry K.U., Scheffel D., Bode U., et al., 1994, Cellular immunodeficiency enhances the progression of human papilloma virus-associated cervical lesions. Int J Cancer 57: 836–840.
Reynolds P., Saunders L.D., Layefsky M.E., and Lemp G.F., 1993, The spectrum of acquired immunodeficiency syndrome (AIDS)-associated malignancies in San Francisco 1980–1987. Am J Epid 137: 19–30.
Walker C.M., Moody D.J., Stiles D.P., and Levy J.A., 1986, CD8 + lymphocytes can control HIV infection in vitro by suppressing virus replication. Science 234: 1563–1566.
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CHAPTER 6
NATURAL HISTORY OF HIV INFECTION
Abstract
In the first stage of infection, individuals are highly infectious. Antibodies are not detectable by serological tests during the “window period”. The infection is clinically silent for 10 years or more. In about 70 per cent of cases, seroconversion illness is seen. The second stage lasts 3–5 years or longer. Antibodies are detectable by serological tests. The patient is less infective to others, as compared to stage 1, and is prone to small range of clinical problems and diseases. In stage 3, which lasts about 3–5 years, the patient becomes vulnerable to a select group of common infections as a result of immune suppression. The CD4 count is 200–500 cells per L. There may be common symptoms like chronic diarrhoea, loss of body weight, pyrexia of unknown origin, and manifestations of AIDS-related complex (ARC). The fourth or terminal stage is characterised by signs and symptoms of AIDS, including opportunistic infections; the CD4 count falls below 200 cells per L; and the patients are highly infectious. Wasting (or “slim disease”) and tuberculosis are mainly seen in this stage in developing countries.
Key Words
Long-term non-progressors, Opportunistic infections, Oral hairy leukoplakia, Persistent generalised lymphadenopathy, Rapid progressors, Slim disease, Typical progressors, Window period.
6.1 – PROGRESSION OF HIV INFECTION
The range of incubation period is 1–14 years, with an average of 6 years. There are three patterns in the progression of HIV infection. Typical progressors comprise about 50–70 per cent of the HIV positive persons. The disease may progress over 8–10 years. Rapid progressors constitute about 5–10 per cent and may develop AIDS in 2–3 years. A small number of persons first infected with HIV 10 or more years ago have not developed symptoms of AIDS (NIAID, 2005). Such persons (called “long-term non-progressors”) have stable CD4 counts for long periods and comprise about 5 per cent of the HIV positive persons. In typical progressors, there are four stages in progression of the disease.
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6.2 – WHO CLINICAL STAGING CLASSIFICATION
Stage 1: Only a small number of infected persons have a clinically apparent illness. The symptoms of seroconversion illness are often mistaken for those of other viral infections. Most of the infected individuals are highly infectious to others in this stage and may not be aware that they have become infected. HIV is present in large quantities in their blood and genital secretions (NIAID, 2005). Antibodies are not detectable in the window period. The infection is clinically silent for 10 years or more. Though the CD4 count may be near normal (the normal CD4 cell count is 950–1700 cells per L) and the infection may be clinically silent or asymptomatic, and the HIV replication and CD4 cell reversal goes on. There is a selective damage to the immune system and the patient gets progressively immunocompromised (Panteleo et al., 1993).
Stage 2: This stage lasts 3–5 years or longer. The antibodies are detectable by serological tests. The CD4 cell count falls (but is more than 500 cells per L) and the viral load increases with simultaneous development of immune suppression. Usually, there are no symptoms, but persistent generalised lymphadenopathy (PGL) may be present (NACO, Training Manual for Doctors).
The patient is less infective to others, as compared to stage 1, and is prone to small range of clinical problems and diseases, that include weight loss, minor skin and oral problems, recurrent sinusitis, and herpes zoster (or “shingles”). These clinical manifestations do not affect the normal activities of an individual and require minimal clinical intervention (NACO, Training Manual for Doctors; Panteleo et al., 1993; WHO, 1990).
Stage 3: With further immune suppression, the patient becomes vulnerable to a select group of common and more virulent infections like bacterial pneumonia. These pathogens also cause diseases in individuals with normal and intact immune systems. But in case of HIV positive persons, they occur at much higher rates and with higher mortality. This stage lasts about 3–5 years. The CD4 count is 200–500 cells per L. This stage is characterised by common symptoms such as chronic diarrhoea, loss of body weight, and pyrexia of unknown origin. Patients may need hospitalisation, specific treatment, and extra follow-up visits to the health centre (NACO, Training Manual for Doctors; Panteleo et al., 1993; WHO, 1990). The signs and symptoms of immune deficiency, seen in ARC include opportunistic infections such as oral thrush, PGL, enlarged spleen, fatigue, acute weight loss (more than 10 per cent of body weight lost in one month), fever, night sweats, and malaise. Oral hairy leukoplakia seems to be unique to HIV-infected individuals. The margins of the tongue show white ridges of fronds on the epithelium. An association with EBV and papilloma viruses has been proposed (Simmonds & Peutherer, 2006).
Stage 4: With more profound immune suppression, the CD4 cell count falls below 200 cells per L and the individual becomes an easy victim for various opportunistic infections. The individual is considered to have advanced
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disease – AIDS. Patients are highly infectious in this stage. In the absence of specific therapy, AIDS patients present with multiple clinical problems and death may occur. This is the terminal stage, characterised by signs and symptoms of AIDS. In the developing countries, wasting due to HIV infection (also called “slim disease”), and tuberculosis are the most important health problems at the fourth stage of the disease. As a result of human exposure to environmental pathogens, the clinical spectrum of the disease that is seen in poor countries is different and diseases like tuberculosis, pneumonia, and salmonellosis are significantly more common as compared to other opportunistic infections seen in the developed world (Morgan et al., 1998).
The opportunistic infections in this stage are tuberculosis, herpes zoster, fungal, and parasitic infections. Kaposi’s sarcoma, non-Hodgkin’s lymphoma, and carcinoma of cervix are considered “AIDS-defining malignancies”. These diseases are disseminated throughout the body. AIDS encephalopathy and AIDS dementia are rare. AIDS dementia is probably due to direct action of HIV on the central nervous system, since HIV can cross the blood-brain barrier (NACO, Training Manual for Doctors; Panteleo et al., 1993; WHO, 1990).
6.3 – CDC CLASSIFICATION
6.3.1 – Group I: Acute HIV Infection
Seroconversion illness resembles glandular fever with lymphadenopathy and symptoms such as acute onset of fever, malaise, sore throat, myalgia, arthralgia, and skin rash. Only 5–10 per cent of individuals may experience this stage in its entirety though few individuals may experience few symptoms. Encephalitic presentations are rare (Simmonds & Peutherer, 2006). Peripheral blood shows lymphocytosis. Serological test for antibodies are usually negative at the onset of acute stage, but may become positive during its course. The virus itself, viral nucleic acid, or viral p24 antigen may be detected.
6.3.2 – Group II: Asymptomatic Infection
HIV-infected persons are symptomatic but test positive for HIV antibody tests and are infectious to others.
6.3.3 – Group III: Persistent Generalised Lymphadenopathy (PGL)
The lymph nodes are symmetrical, painless, and enlarged (Simmonds & Peutherer, 2006). They are more than 1 cm in size and present at two or more extra-genital sites for at least 3 months. Other causes of lymph node enlargement such as lymphomas need to be ruled out. PGL is present in 25–30 per cent of HIV-infected individuals, who may be otherwise asymptomatic (Simmonds & Peutherer, 2006).
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6.3.4 – Group IV: Symptomatic HIV Infection
SUB-GROUP A = Constitutional disease (ARC) SUB-GROUP B = Neurological disease SUB-GROUPS C1 & C2 = Secondary infectious diseases SUB-GROUP D = Secondary cancers
SUB-GROUP E = Other conditions
The infections are based on CD4 counts. When the CD4 count is less than 400 cells per mm3, signs and symptoms of immune deficiency are manifested. When the CD4 count drops below 200 cells per mm3, titre of virus increases markedly with an irreversible breakdown of immune mechanism. Most patients die of opportunistic infections and malignancies. AIDS is the terminal stage of HIV infection.
6.4 – DISEASE PROGRESSION
At the individual level, the progression of the disease and survival are both variable. Either the disease rapidly progresses over about 2 years or hardly progresses at all, for a longer period of 10 or 15 years (Morgan et al., 1997). Once the life-threatening severe diseases of clinical AIDS have developed, the life span of the patients is reduced due to scarcity of resources in the developing countries. The mean survival may be in the range of 6–7 years especially among patients belonging to the poorer communities (Morgan et al., 1998). The available data suggest that the progression of the disease is independent of race, ethnicity, or gender. Old age and low socio-economic status adversely affect the survival (Chaisson et al., 1995). Very few natural history studies have been conducted in developing countries. Individuals progress through various stages of HIV infection at a variable rate. In rich communities, deaths usually occur after clinical AIDS has developed. But, in poorer communities, HIV positive persons may die in early stages of the natural history of the disease due to higher exposure to virulent and opportunistic infections, and inadequate resources for clinical care at stages 1 and 2 (Morgan et al., 1997; Morgan et al., 1998; Chaisson et al., 1995; Gilks et al., 1996).
6.5 – LONG-TERM NON-PROGRESSORS
Since the onset of the HIV/AIDS epidemic, it has been observed that some HIVinfected individuals (called long-term non-progressors) took a long time to progress to AIDS, while some individuals did not get infected at all, in spite of repeated exposures to HIV. These individuals have very low levels of detectable virus in their blood or in the peripheral blood mononuclear cells. On the other hand, they have high levels of active HIV-specific cytotoxic T-cells and CAF, the antiviral factor produced by CD8 T-cells (Barker et al., 1995). It is not known how some HIV-affected individuals have remained asymptomatic for long periods of time. Factors responsible for their non-progression to AIDS could include
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particular features of their immune system or possible past infection with a less virulent strain of the virus. It is possible that these individuals have received a low dose of infection (equivalent to low-dose vaccination) leading to protective immunity. This has been seen in primates infected with SIV. National Institute for Allergy and Infectious Diseases (NIAID) supported researchers continue to trace how the disease progresses in different people (NIAID, 2005). Genetic factors may have a role since the presence of human leukocyte antigen (HLA) types B-8 and DR-3 are associated with faster progression of HIV infection. If a blood donor has slowly progressing HIV infection, then the recipient also gets the same type of infection (Learmont et al., 1992; Ashton et al., 1994).
REFERENCES
Ashton L.J., Learmont J., Luo K., et al., 1994, HIV infection in recipients of blood transfusion from donors with known duration of infection. Lancet 344: 718–720.
Barker E., Mackewicz C.E., and Levy J.A., 1995, Effect of TH1 and TH2 cytokines on CD8 + T-cell response against human immuno deficiency virus: implications for long-term survival. Proc Natl Acad Sci USA 92: 11135–11139.
Chaisson R.E., Keruly J.C., and Moore R.D., 1995, Race, sex, drug use and progression of HIV disease. N Engl J Med 333: 751–756.
Gilks C.F., et al., 1996, Invasive pneumococcal disease in a cohort of predominantly HIV-1 infected female sex workers in Nairobi, Kenya. Lancet 547: 718–724.
Learmont J., Tindall H., Evans L., et al., 1992, Long-term symptomless HIV-1 infection in recipients of blood products from a single donor. Lancet 340: 863–867.
Morgan D., et al., 1998, Early manifestations (pre-AIDS) of HIV-1 infection in Uganda. AIDS 12: 591–596.
Morgan D., et al., 1997, HIV-1 disease progression and AIDS defining disorders in a rural Ugandan cohort. Lancet 550: 245–250.
NACO. Training manual for doctors. New Delhi: Government of India.
National Institute of Allergy and Infectious Diseases (NIAID), 2005, HIV infection and AIDS: an overview. NIAID Fact Sheet. Bethesda: National Institutes of Health. www.niaid.nih.gov/. March.
Panteleo G., Graziosi C., and Fauci A.S., 1993, The immuno-pathogenesis of HIV. N Engl J Med 528: 327–333.
Simmonds P. and Peutherer J.F., 2006, Retroviruses. In: Medical microbiology (D. Greenwood, R.C.B. Slack, and J.F. Peutherer, eds.), 16th edn. New Delhi: Elsevier, pp 527–538.
WHO, 1990, AIDS – Interim proposal for WHO staging system for HIV infection and disease. Wkly Epidemiol Rec 65: 221–228.
CHAPTER 7
INFECTION CONTROL METHODS
Abstract
Infection control involves good housekeeping (sanitation and dust control), hand washing, using personal protective equipment (PPE) such as gloves, and using natural, physical, or chemical methods to make the environmental conditions detrimental for pathogens. The type of likely pathogens should be considered while choosing the type of disinfection. Nearly all the chemical disinfectants are toxic or harmful to the eyes, skin, and lungs. Sterilisation is recommended for critical items that are directly introduced into the blood stream or into the normally sterile areas of the body. Semicritical items come in contact with mucous membranes, do not ordinarily penetrate body surfaces, and require high level chemical disinfection. Non-critical items that do not come in contact with the patients or touch their intact skin only, require general housekeeping measures like washing with detergents and water. The basic principle of universal biosafety precautions is that blood and body fluids from all patients ought to be considered as potentially infected, irrespective of their serological status. These precautions should be followed during patient care and handling of dead bodies in health care settings.
Key Words
Antisepsis, Barrier nursing, Biomedical waste management, Cohort nursing, D value, Decontamination of spills, Disinfection, Hand washing, Handling dead bodies, Infection control, Needle stick injuries, Personal protective equipment, Sterilisation, Survivor curve, Task nursing, Universal biosafety precautions
7.1 – DEFINITIONS
1.Sterilisation (Latin: sterilis = barren): This is a “process by which, an article, surface, or medium is freed of all living entities (including vegetative microorganisms and spores)”. An article may be regarded as sterile if it can be demonstrated that the probability of viable microorganisms on it is less than one in a million as per pharmacopoeia definition (Simpson & Slack, 2006).
2.Antisepsis (Greek: anti = against; sèpsis = putrefaction): This is a “process by which, living tissues are freed of pathogens”. This is usually done by destruction of pathogens or by growth inhibition.
3.Disinfection (Latin: dis = reversal of): It is defined as a “process by which, inanimate objects, or surfaces are freed of all pathogens”. Usually, disinfection does
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not affect spores. A disinfectant in higher dilution can act as an antiseptic. But, the reverse is not always true. Prophylactic disinfection is defined as “measures applied before the onset of disease” and includes chlorination of drinking water, pasteurisation of milk, and washing of hands before clinical procedures. Concurrent disinfection refers to “measures applied during illness, to prevent further spread of the disease” and includes disinfection of patient’s excretions, secretions, linen, and materials used in treating the patient. Terminal disinfection is defined as “measures applied after the patient has ceased to be a source of infection after cure, discharge, or death”. This technique is obsolete. Terminal disinfection is now replaced by terminal cleaning of rooms, including ventilation. Rarely, bedding is fumigated (Ananthanarayan
& Paniker, 2000; Collins & Grange, 1990; Sathe & Sathe, 1991).
4.Incineration (Latin: cineris = ashes): Incineration is “total combustion of all living and organic matter, by dry heat at not less than 800°C”
5.Decontamination (Latin: dis- or de- = reversal of; contamunätum = pollutant): This is a general term that indicates procedures put into practice to make equipment safe to handle. The word “contamination” may refer to chemical, microbiological or radioactive contamination (Simpson & Slack, 2006).
6.Sanitation (Latin: sanitas = health): This refers to reduction in the number of pathogens (Ananthanarayan & Paniker, 2000). Sanitation includes cleaning, wet mopping, dust control, environmental hygiene, and safe disposal of waste.
7.2 – KINETICS OF STERILISATION AND DISINFECTION
7.2.1 – Survivor Curve
When microorganisms are subjected to a lethal process, the number of viable survivors decreases exponentially in relation to the extent of exposure to the lethal process. If a logarithm (to the base 10) of the number of surviving organisms is plotted against the lethal dose received such as duration of exposure to a particular temperature, the resulting curve is called the “survivor curve”. This survivor curve is independent of the original population of microorganisms. Ideally, the survival curve should be linear. Extrapolation on the survivor curve helps in determining the lethal dose required to give 10−6 survivors to meet the pharmacopoeia definition of “sterile” (Simpson & Slack, 2006).
7.2.2 – D Value
While manufacturing sterile products, a figure known as “D value” is used. It is the abbreviation for “death rate value” (Collins & Grange, 1990) and is also called “decimal reduction value” (Simpson & Slack, 2006). The “D value” is the time and dose of exposure, as determined in the laboratory, to reduce the viable count by one log, i.e. one order of magnitude = 1/10 (Collins & Grange, 1990). “D value” is the time and dose of exposure required to inactivate 90 per cent of
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organisms in the initial population (Simpson & Slack, 2006). The D value remains constant over the full range of the survivor curve. This means that the time and dose required to reduce the population of organisms from 106 to 105 is the same as that required to reduce the population of organisms from 105 to 104 (Simpson & Slack, 2006). In order to ensure effectiveness of sterilisation, the magnitude of exposures used is many times more than the “D value”, which is calculated according to the known “bio-burden” (Collins & Grange, 1990).
7.2.3 – Components of Infection Control
Infection control involves: (a) good housekeeping (cleaning, wet mopping, and dust control), (b) using PPE (gloves, masks, etc.), and (c) using physical or chemical methods to make the environmental conditions detrimental for pathogens. Many physical methods act by chemical mechanisms. For example, heat kills the pathogens by denaturing cellular proteins (Sathe & Sathe, 1991). The process of disinfection should be technically correct. Many commonly used methods of disinfection are mentioned below, but the type of likely pathogens should be considered while choosing the type of disinfection.
7.2.4 – Classification of Medical Equipment
Medical equipment or items can be divided into three categories (Chitnis, 1997; Simpson & Slack, 2006).
1.Critical Items: All equipment or items that are directly introduced into the blood stream or into the normally sterile areas of the body, e.g. surgical instruments, cardiac catheters, needles, arthroscopes, parenteral fluids, and implants. These articles have to be sterile at the time of use.
2.Semi-Critical Items: Articles that come in contact with mucous membranes and do not ordinarily penetrate body surfaces, e.g. non-invasive flexible and rigid fibrooptic endoscopes, endobronchial tubes and ventilation equipment, cystoscopes, aspirators, and gastroscopes. High-level chemical disinfection is sufficient for items belonging to this category.
3.Non-Critical Items: Items that do not touch the patients or touch the intact skin only, e.g. blood pressure cuffs, crutches, bed pans, urine pots, and furniture. General housekeeping measures like washing with detergents and water are adequate.
7.2.5 – Prior Cleansing
Before subjecting any article or equipment to sterilisation or disinfection, it is essential that the lowest possible bioburden is present at the start of the process. Any used article or instrument is to be soaked in a chemical disinfectant, cleaned with a detergent, followed by thorough rinsing (Mitchell et al., 1997). This is necessary before subjecting the material or equipment to the sterilising
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process. Cleaning, per se, is also a valuable method of low-level disinfection. Ultrasonic baths are useful in removing dried debris on instruments that are ordinarily difficult to clean. This partially reduces the bioburden. Detergents have surface tension reducing property – they wash away many organisms. The dilution effect of thorough rinsing further reduces the burden and thus increases the probability of successful sterilisation (Simpson & Slack, 2006). Lipid membrane envelope of HIV is highly susceptible to surface tension reducing action of detergents. Hence clothes and utensils may be decontaminated by washing with detergents.
7.2.6 – Factors Affecting Sterilisation and Disinfection
1.Species or Strain of Microorganism: In general, vegetative organisms are
more vulnerable, while spores are resistant to action of sterilising and disinfecting agents. There is an interspecies variation in the D value at 60°C –
Escherichia coli (few minutes) to Salmonella enterica subtype Senftenberg (one hour); D value at 70°C – Staph aureus (less than 1 minute) and Staph
epidermidis (3 minutes). Prions (organisms that cause scrapie, bovine spongiform encephalopathy, and Creutzfeldt-Jakob disease) are killed at 134°C for 18 minutes. Hence it is desirable to use gamma-sterilised disposable instruments for operating on nervous tissue including retina because risk of exposure to prions is high (Simpson & Slack, 2006).
2.Growth Conditions: Organisms that grow under nutrient-rich conditions are more resistant to sterilising and disinfecting agents. Resistance usually increases through the late logarithmic phase of microbial growth and declines erratically during the stationary phase.
3.Spore Formation: Bacterial spores are more resistant, as compared to fungal spores. In general, disinfection processes have little or no action against bacterial spores.
4.Micro-Environment: The presence of organic matter (blood, body fluids, pus, faeces, urine) reduces the effectiveness of chlorine-releasing agents (Simpson & Slack, 2006). Presence of salt reduces effectiveness of ethylene oxide (Simpson & Slack, 2006). Chemical disinfectants will inactivate at least 105 viruses within few minutes. With the exception of phenols, many chemical disinfectants are inactivated in the presence of organic matter. Hence thorough cleaning is necessary before disinfection (Simpson & Slack, 2006).
5.Bioburden: Higher the initial bioburden (number of microorganisms) the lethal process must be more stringent and extensive to achieve high quality of sterility.
6.Time Factor: All microorganisms do not get killed instantly when exposed to physical agents or to chemical disinfectants because in any population of microorganisms, some will be more resistant than others (Collins & Grange, 1990). Higher the bioburden, longer will be the time taken to destroy all of them (Simpson & Slack, 2006).