This powerpoint contains slides describing types of hepatitis viruses, pathogenesis, clinical course, laboratory diagnosis, treatment and prevention against hepatitis viruses. This presentation is intended to use by medical students, nurses, paramedics in the learning on virology. The slided could also be resource materials for the academicians.
This document discusses several types of hepatitis viruses. It covers hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus, and hepatitis E virus. For each virus, it describes key aspects such as transmission, pathogenesis, clinical manifestations, diagnosis, and prevention. Hepatitis viruses can cause liver inflammation and damage, and some may lead to chronic infection or liver cancer if not addressed. Vaccines exist to prevent hepatitis A and B.
This document discusses immunoprophylaxis and vaccination. It defines prophylaxis and vaccine preventable diseases. There are two types of immunization: active and passive. Active immunization involves inducing immunity through vaccination and works through humoral and cellular immunity. Vaccines can be live attenuated, killed/inactivated, toxoids, cellular fractions, subunit vaccines, or recombinant vaccines. Passive immunization provides immediate short-term protection through administration of antibodies or immunoglobulins. The document also discusses vaccination schedules and recent vaccination missions.
Cholera is a serious bacterial disease that usually
causes severe diarrhea and dehydration. The disease is typically spread through contaminated water.
Modern sewage and water treatment have effectively eliminated cholera in most countries. It’s still a problem in countries like Asia, America and Africa. Mostly in India.
Countries affected by war, poverty, and natural disasters have the greatest risk for a cholera outbreak.
Taxonomy:
class : Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: v.cholerae, v.parahaemolyticus,
v. vulnificus, v. alginolyticus
MORPHOLOGY:
Gram negative, actively motile, short, rigid curved bacilli
Resembling letter “V”
about 34 genus
most common in water
1.5µ X 0.2 -0.4 µ in size
polar flagellum , strongly aerobic
Smear – fish in stream appearance
PATHOGENESIS:
Source: Ingestion of contaminated water, food,
fruits and vegetables etc.,
Incubation periods: 1-5 days
Symptoms: Watery diarrhoea, vomiting, thirst, dehydration, muscle cramps
Complications: muscular pain, renal failure, pulmonary edema, cardiac arrhythrnias
DIAGNOSIS:
Specimen: stool sample, water sample(envt)
Microscopy: a) Hanging drop : +ve
b) Gram stain :-ve
Culture: Mac conkey Agar :colourless to light pink
TCBS : yellow colonies
Serology: serological tests are no diagnostic value
TREATMENT:
Adequate replacement of fluids and electrolytes.
Oral tetracycline reduces the period of vibrio excreation.
PREVENTION:
Drink and use bottled water
Frequent washing
Sanitary environment
Defecate in water
Cook food thoroughly
Poliovirus is an enterovirus that causes the acute infectious disease poliomyelitis. It is spherical and 27nm in diameter with an icosahedral capsid containing its single-stranded RNA genome. It infects and replicates in the intestinal tract and sometimes spreads to the central nervous system, destroying motor neurons and potentially causing flaccid paralysis. While most infections are asymptomatic, it can cause a range of illnesses from minor to paralytic. Diagnosis involves isolating the virus from specimens through cell culture and identification, and treatment involves vaccination to develop protective antibodies.
This document discusses various opportunistic fungal infections seen in immunocompromised patients. It describes the common causative fungi including Candida, Cryptococcus, Aspergillus, Penicillium marneffei, zygomycetes, and Pneumocystis. For each infection, it summarizes the clinical manifestations, laboratory diagnosis involving microscopy, culture, and other tests, as well as recommended treatment approaches. It also briefly mentions some other rare miscellaneous mycoses.
Vibrio cholerae is the bacteria that causes cholera. It is a facultative anaerobe that grows well between 37°C and pH 7.4-9.6. It can be cultured on ordinary media like nutrient agar as well as special transport and enrichment media. Pathogenesis involves ingesting contaminated food/water, with the bacteria multiplying in the intestines and producing cholera toxin which causes hypersecretion of fluids. Diagnosis involves microscopic examination of rice water stool samples and culturing in selective media. Treatment focuses on fluid replacement therapy and oral rehydration.
This document discusses several types of hepatitis viruses. It covers hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus, and hepatitis E virus. For each virus, it describes key aspects such as transmission, pathogenesis, clinical manifestations, diagnosis, and prevention. Hepatitis viruses can cause liver inflammation and damage, and some may lead to chronic infection or liver cancer if not addressed. Vaccines exist to prevent hepatitis A and B.
This document discusses immunoprophylaxis and vaccination. It defines prophylaxis and vaccine preventable diseases. There are two types of immunization: active and passive. Active immunization involves inducing immunity through vaccination and works through humoral and cellular immunity. Vaccines can be live attenuated, killed/inactivated, toxoids, cellular fractions, subunit vaccines, or recombinant vaccines. Passive immunization provides immediate short-term protection through administration of antibodies or immunoglobulins. The document also discusses vaccination schedules and recent vaccination missions.
Cholera is a serious bacterial disease that usually
causes severe diarrhea and dehydration. The disease is typically spread through contaminated water.
Modern sewage and water treatment have effectively eliminated cholera in most countries. It’s still a problem in countries like Asia, America and Africa. Mostly in India.
Countries affected by war, poverty, and natural disasters have the greatest risk for a cholera outbreak.
Taxonomy:
class : Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: v.cholerae, v.parahaemolyticus,
v. vulnificus, v. alginolyticus
MORPHOLOGY:
Gram negative, actively motile, short, rigid curved bacilli
Resembling letter “V”
about 34 genus
most common in water
1.5µ X 0.2 -0.4 µ in size
polar flagellum , strongly aerobic
Smear – fish in stream appearance
PATHOGENESIS:
Source: Ingestion of contaminated water, food,
fruits and vegetables etc.,
Incubation periods: 1-5 days
Symptoms: Watery diarrhoea, vomiting, thirst, dehydration, muscle cramps
Complications: muscular pain, renal failure, pulmonary edema, cardiac arrhythrnias
DIAGNOSIS:
Specimen: stool sample, water sample(envt)
Microscopy: a) Hanging drop : +ve
b) Gram stain :-ve
Culture: Mac conkey Agar :colourless to light pink
TCBS : yellow colonies
Serology: serological tests are no diagnostic value
TREATMENT:
Adequate replacement of fluids and electrolytes.
Oral tetracycline reduces the period of vibrio excreation.
PREVENTION:
Drink and use bottled water
Frequent washing
Sanitary environment
Defecate in water
Cook food thoroughly
Poliovirus is an enterovirus that causes the acute infectious disease poliomyelitis. It is spherical and 27nm in diameter with an icosahedral capsid containing its single-stranded RNA genome. It infects and replicates in the intestinal tract and sometimes spreads to the central nervous system, destroying motor neurons and potentially causing flaccid paralysis. While most infections are asymptomatic, it can cause a range of illnesses from minor to paralytic. Diagnosis involves isolating the virus from specimens through cell culture and identification, and treatment involves vaccination to develop protective antibodies.
This document discusses various opportunistic fungal infections seen in immunocompromised patients. It describes the common causative fungi including Candida, Cryptococcus, Aspergillus, Penicillium marneffei, zygomycetes, and Pneumocystis. For each infection, it summarizes the clinical manifestations, laboratory diagnosis involving microscopy, culture, and other tests, as well as recommended treatment approaches. It also briefly mentions some other rare miscellaneous mycoses.
Vibrio cholerae is the bacteria that causes cholera. It is a facultative anaerobe that grows well between 37°C and pH 7.4-9.6. It can be cultured on ordinary media like nutrient agar as well as special transport and enrichment media. Pathogenesis involves ingesting contaminated food/water, with the bacteria multiplying in the intestines and producing cholera toxin which causes hypersecretion of fluids. Diagnosis involves microscopic examination of rice water stool samples and culturing in selective media. Treatment focuses on fluid replacement therapy and oral rehydration.
Salmonella typhi is a gram-negative enteric bacillus that causes typhoid fever in humans. It grows optimally at 37°C and pH 6-8, forming characteristic colonies on nutrient agar, blood agar, MacConkey agar, and selective media like XLD agar and Wilson-Blair bismuth sulfite agar. S. typhi causes typhoid fever through ingestion, incubating in the intestines before spreading to organs and causing systemic infection marked by fever, headache, and possible complications like intestinal perforation. Diagnosis involves blood, stool, and other cultures as well as serological tests. Treatment uses antibiotics like chloramphenicol and ampicillin.
This document provides an overview of rabies including its causative agent, transmission, pathogenesis, types, diagnosis, management, and prevention. Rabies is a fatal viral disease transmitted through animal bites that causes encephalitis. The rabies virus is in the Rhabdoviridae family and spreads from the site of a bite to the central nervous system. Post-exposure prophylaxis including wound cleaning and vaccination is highly effective in preventing death from rabies if administered promptly after exposure.
The document summarizes key information about HIV/AIDS, including:
1) HIV is a lentivirus that causes AIDS by progressively destroying the immune system, allowing other infections to thrive. Once infected, the body cannot rid itself of HIV.
2) Scientists believe HIV originated from chimpanzees in West Africa and was transmitted to humans through contact with their blood.
3) HIV is classified as a retrovirus and exists as two types, HIV-1 and HIV-2. HIV-1 is more widespread and virulent.
4) There is no cure for HIV, but treatment with antiretroviral drugs can control the virus and prevent transmission.
Poliovirus is an enterovirus in the Picornaviridae family that causes the disease poliomyelitis. It has a positive-sense RNA genome and protein capsid. There are three serotypes of poliovirus that share 36-52% genetic homology. Poliovirus is usually transmitted through the fecal-oral route or oral-oral contact with infected stool or respiratory secretions. It infects the gastrointestinal tract and in rare cases enters the central nervous system, where it can cause paralysis. Symptoms include fever, sore throat, headache, and muscle weakness. Treatment involves vaccination with the inactivated Salk vaccine or attenuated Sabin vaccine to prevent the spread of polio.
1. Mycobacterium is a genus of bacteria that includes M. tuberculosis and M. leprae, which are the causes of tuberculosis and leprosy, respectively.
2. These bacteria have an acid-fast staining pattern and lipid-rich cell walls that make them resistant to disinfectants and antibiotics.
3. M. tuberculosis spreads through the air and causes pneumonia and cavitary lesions in the lungs, while M. leprae spreads through skin lesions and can cause disfigurement if untreated.
The document describes three case studies of patients presenting with hepatitis. The first case involves a man who returned from Thailand with fatigue, nausea and abdominal discomfort. The second case is a pregnant woman who was a former heroin addict and had shared needles. The third case is a man who developed jaundice six months after coronary bypass surgery. The document then provides information about hepatitis A, B and C viruses, including their structures, modes of transmission, clinical presentations and approaches to diagnosis.
Hepatitis B virus is a double-stranded DNA virus that causes hepatitis B disease. It is able to establish chronic infections and has been shown to integrate into host DNA. The virus primarily infects liver cells and establishes lifelong infections in around 5% of adults and up to 90% of infants infected. While vaccination has been effective at reducing new infections, chronic hepatitis B remains an important global public health issue.
A picornavirus is a virus belonging to the family Picornaviridae, a family of viruses in the order Picornavirales. Vertebrates, including humans, serve as natural hosts. Picornaviruses are nonenveloped viruses that represent a large family of small, cytoplasmic, plus-strand RNA viruses with a 30-nm icosahedral capsid.
Streptococcus pyogenes is a Gram-positive bacterium that can cause a variety of infections in humans. It commonly colonizes the throat and skin. It produces toxins and enzymes that contribute to its virulence and ability to cause disease. S. pyogenes can cause suppurative infections like pharyngitis, impetigo, and necrotizing fasciitis. It can also cause non-suppurative sequelae after infection like acute rheumatic fever and glomerulonephritis. Diagnosis involves culturing samples on blood agar and testing for sensitivity to bacitracin. Treatment involves antibiotics like penicillin. Prevention focuses on proper treatment of streptococcal infections to reduce risk of
Shigella are Gram-negative bacilli that cause shigellosis (bacillary dysentery) in humans. There are four species (S. dysenteriae, S. flexneri, S. boydii, S. sonnei) which are differentiated based on antigen types. Shigellosis ranges from asymptomatic to severe diarrhea with blood/mucus and is typically transmitted through the fecal-oral route. The bacteria invade the colonic epithelium through attachment and enterotoxins can cause electrolyte/nutrient absorption issues leading to symptoms. Treatment focuses on rehydration while prevention emphasizes water/sewage sanitation and antibiotic treatment of carriers.
The Widal test is a serological test developed in 1896 by Farnand Widal to diagnose enteric fever. It detects antibodies against Salmonella typhi and paratyphi in patient serum. There are two types of Widal tests: the slide test which is rapid and qualitative, and the tube test which is quantitative. The tube test involves serially diluting patient serum and mixing it with antigens before incubating and examining for agglutination, allowing a titre value to be determined. Elevated or rising titres of certain antibodies can indicate active or past enteric fever infection.
Human Retroviruses are RNA viruses that contain the enzyme reverse transcriptase, allowing them to convert their RNA genome into DNA. The two major genera that affect humans are Lentiviruses, which include HIV-1 and HIV-2, and HTLV-BLV group, which includes HTLV-1 and HTLV-2. HIV binds host cells via gp120, enters via fusion, reverse transcribes into DNA then integrates into the host genome. It replicates using host cell machinery. Infection can lead to AIDS as CD4+ T cells are depleted. Opportunistic infections are treated with antiretrovirals that target reverse transcriptase and protease.
Streptococcus pyogenes is a Gram positive coccus that forms chains and causes beta hemolysis on blood agar. It is classified by Lancefield grouping based on cell wall carbohydrates and Griffith typing based on M proteins. S. pyogenes causes respiratory, skin, and genital infections and can lead to post-streptococcal sequelae like rheumatic fever and glomerulonephritis. Penicillin is usually the treatment of choice.
Streptococcus pneumoniae, also known as pneumococcus, is a type of bacteria commonly found in the respiratory tract that can cause illnesses like pneumonia, ear infections, and sinus infections. It is a gram-positive, facultative anaerobic bacteria that is often found in pairs and does not form spores or exhibit motility. Pneumococcus bacteria are usually spread through respiratory droplets from coughing or sneezing of an infected person. Symptoms can include fever, chills, chest pain, cough, and confusion in the elderly. The infection is diagnosed by growing the bacteria from specimens and treated with antibiotics like penicillin, ampicillin, or ceftriaxone depending on the susceptibility of the strain.
Neisseria meningitidis, commonly known as meningococcus, is a Gram-negative bacterium that can cause meningitis and sepsis. It is a leading cause of bacterial meningitis, with highest incidence in children aged 1-5 years. The bacterium is usually carried harmlessly in the throat but can invade the bloodstream and brain. Symptoms of meningococcal disease include fever, headache, stiff neck and a rash. Timely treatment with antibiotics is crucial to recovery.
Rabies virus is a bullet-shaped RNA virus belonging to the family Rhabdoviridae. It causes rabies, a fatal disease transmitted through the bites of infected animals like dogs, foxes, and bats. The virus enters through wounds or bites and travels through nerves to the brain and spinal cord, causing encephalitis. There are two forms of rabies - furious rabies with symptoms like anxiety and hydrophobia, and dumb rabies characterized by paralysis. Diagnosis involves detecting the virus in samples or Negri bodies in tissue. Post-exposure prophylaxis includes wound cleaning, rabies immunoglobulin, and vaccination to prevent infection. Modern non-neural vaccines like cell culture vaccines are now used instead of
Herpesviruses are a leading cause of human viral diseases and include herpes simplex virus types 1 and 2, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, and human herpesvirus 8. They are capable of causing overt disease during primary infection or remaining latent in sensory ganglia or lymphocytes. Herpesviruses can be reactivated from latency to cause recurrent disease. Laboratory diagnosis involves virus isolation in cell culture, antigen or antibody detection, PCR, and histopathological examination of clinical samples. Treatment options include acyclovir, valacyclovir, and ganciclovir depending on the infecting virus.
Staphylococci are spherical bacteria that occur in grape-like clusters. Staphylococcus aureus is an important human pathogen that can cause a variety of infections, from minor skin infections to life-threatening conditions like toxic shock syndrome and endocarditis. S. aureus produces several virulence factors like toxins and enzymes that damage tissues and evade the immune system. Laboratory diagnosis involves culture, microscopy, and tests like coagulase to identify S. aureus. Antibiotics are used to treat infections, and prevention focuses on hygiene and safe food handling. Methicillin-resistant S. aureus is an antibiotic resistant form that is more difficult to treat.
Hepatitis B is caused by the hepatitis B virus (HBV) and is a serious infectious disease affecting the liver. It is transmitted through contact with infected blood or bodily fluids. The virus can cause both acute and chronic infections. Diagnosis involves testing for hepatitis B surface antigen and antibodies. There is no cure for chronic hepatitis B but vaccination provides effective prevention.
The hepatitis B virion (Dane particle):
outer lipid envelope with the surface antigen (HBsAg).
an electron-dense core (nucleocapsid): ds circular DNA and polymerase surrounded by the core antigen (HBcAg).
The HBsAg is produced in excess by the infected hepatocytes and is secreted in the form of spherical
and filamentous particles.
Salmonella typhi is a gram-negative enteric bacillus that causes typhoid fever in humans. It grows optimally at 37°C and pH 6-8, forming characteristic colonies on nutrient agar, blood agar, MacConkey agar, and selective media like XLD agar and Wilson-Blair bismuth sulfite agar. S. typhi causes typhoid fever through ingestion, incubating in the intestines before spreading to organs and causing systemic infection marked by fever, headache, and possible complications like intestinal perforation. Diagnosis involves blood, stool, and other cultures as well as serological tests. Treatment uses antibiotics like chloramphenicol and ampicillin.
This document provides an overview of rabies including its causative agent, transmission, pathogenesis, types, diagnosis, management, and prevention. Rabies is a fatal viral disease transmitted through animal bites that causes encephalitis. The rabies virus is in the Rhabdoviridae family and spreads from the site of a bite to the central nervous system. Post-exposure prophylaxis including wound cleaning and vaccination is highly effective in preventing death from rabies if administered promptly after exposure.
The document summarizes key information about HIV/AIDS, including:
1) HIV is a lentivirus that causes AIDS by progressively destroying the immune system, allowing other infections to thrive. Once infected, the body cannot rid itself of HIV.
2) Scientists believe HIV originated from chimpanzees in West Africa and was transmitted to humans through contact with their blood.
3) HIV is classified as a retrovirus and exists as two types, HIV-1 and HIV-2. HIV-1 is more widespread and virulent.
4) There is no cure for HIV, but treatment with antiretroviral drugs can control the virus and prevent transmission.
Poliovirus is an enterovirus in the Picornaviridae family that causes the disease poliomyelitis. It has a positive-sense RNA genome and protein capsid. There are three serotypes of poliovirus that share 36-52% genetic homology. Poliovirus is usually transmitted through the fecal-oral route or oral-oral contact with infected stool or respiratory secretions. It infects the gastrointestinal tract and in rare cases enters the central nervous system, where it can cause paralysis. Symptoms include fever, sore throat, headache, and muscle weakness. Treatment involves vaccination with the inactivated Salk vaccine or attenuated Sabin vaccine to prevent the spread of polio.
1. Mycobacterium is a genus of bacteria that includes M. tuberculosis and M. leprae, which are the causes of tuberculosis and leprosy, respectively.
2. These bacteria have an acid-fast staining pattern and lipid-rich cell walls that make them resistant to disinfectants and antibiotics.
3. M. tuberculosis spreads through the air and causes pneumonia and cavitary lesions in the lungs, while M. leprae spreads through skin lesions and can cause disfigurement if untreated.
The document describes three case studies of patients presenting with hepatitis. The first case involves a man who returned from Thailand with fatigue, nausea and abdominal discomfort. The second case is a pregnant woman who was a former heroin addict and had shared needles. The third case is a man who developed jaundice six months after coronary bypass surgery. The document then provides information about hepatitis A, B and C viruses, including their structures, modes of transmission, clinical presentations and approaches to diagnosis.
Hepatitis B virus is a double-stranded DNA virus that causes hepatitis B disease. It is able to establish chronic infections and has been shown to integrate into host DNA. The virus primarily infects liver cells and establishes lifelong infections in around 5% of adults and up to 90% of infants infected. While vaccination has been effective at reducing new infections, chronic hepatitis B remains an important global public health issue.
A picornavirus is a virus belonging to the family Picornaviridae, a family of viruses in the order Picornavirales. Vertebrates, including humans, serve as natural hosts. Picornaviruses are nonenveloped viruses that represent a large family of small, cytoplasmic, plus-strand RNA viruses with a 30-nm icosahedral capsid.
Streptococcus pyogenes is a Gram-positive bacterium that can cause a variety of infections in humans. It commonly colonizes the throat and skin. It produces toxins and enzymes that contribute to its virulence and ability to cause disease. S. pyogenes can cause suppurative infections like pharyngitis, impetigo, and necrotizing fasciitis. It can also cause non-suppurative sequelae after infection like acute rheumatic fever and glomerulonephritis. Diagnosis involves culturing samples on blood agar and testing for sensitivity to bacitracin. Treatment involves antibiotics like penicillin. Prevention focuses on proper treatment of streptococcal infections to reduce risk of
Shigella are Gram-negative bacilli that cause shigellosis (bacillary dysentery) in humans. There are four species (S. dysenteriae, S. flexneri, S. boydii, S. sonnei) which are differentiated based on antigen types. Shigellosis ranges from asymptomatic to severe diarrhea with blood/mucus and is typically transmitted through the fecal-oral route. The bacteria invade the colonic epithelium through attachment and enterotoxins can cause electrolyte/nutrient absorption issues leading to symptoms. Treatment focuses on rehydration while prevention emphasizes water/sewage sanitation and antibiotic treatment of carriers.
The Widal test is a serological test developed in 1896 by Farnand Widal to diagnose enteric fever. It detects antibodies against Salmonella typhi and paratyphi in patient serum. There are two types of Widal tests: the slide test which is rapid and qualitative, and the tube test which is quantitative. The tube test involves serially diluting patient serum and mixing it with antigens before incubating and examining for agglutination, allowing a titre value to be determined. Elevated or rising titres of certain antibodies can indicate active or past enteric fever infection.
Human Retroviruses are RNA viruses that contain the enzyme reverse transcriptase, allowing them to convert their RNA genome into DNA. The two major genera that affect humans are Lentiviruses, which include HIV-1 and HIV-2, and HTLV-BLV group, which includes HTLV-1 and HTLV-2. HIV binds host cells via gp120, enters via fusion, reverse transcribes into DNA then integrates into the host genome. It replicates using host cell machinery. Infection can lead to AIDS as CD4+ T cells are depleted. Opportunistic infections are treated with antiretrovirals that target reverse transcriptase and protease.
Streptococcus pyogenes is a Gram positive coccus that forms chains and causes beta hemolysis on blood agar. It is classified by Lancefield grouping based on cell wall carbohydrates and Griffith typing based on M proteins. S. pyogenes causes respiratory, skin, and genital infections and can lead to post-streptococcal sequelae like rheumatic fever and glomerulonephritis. Penicillin is usually the treatment of choice.
Streptococcus pneumoniae, also known as pneumococcus, is a type of bacteria commonly found in the respiratory tract that can cause illnesses like pneumonia, ear infections, and sinus infections. It is a gram-positive, facultative anaerobic bacteria that is often found in pairs and does not form spores or exhibit motility. Pneumococcus bacteria are usually spread through respiratory droplets from coughing or sneezing of an infected person. Symptoms can include fever, chills, chest pain, cough, and confusion in the elderly. The infection is diagnosed by growing the bacteria from specimens and treated with antibiotics like penicillin, ampicillin, or ceftriaxone depending on the susceptibility of the strain.
Neisseria meningitidis, commonly known as meningococcus, is a Gram-negative bacterium that can cause meningitis and sepsis. It is a leading cause of bacterial meningitis, with highest incidence in children aged 1-5 years. The bacterium is usually carried harmlessly in the throat but can invade the bloodstream and brain. Symptoms of meningococcal disease include fever, headache, stiff neck and a rash. Timely treatment with antibiotics is crucial to recovery.
Rabies virus is a bullet-shaped RNA virus belonging to the family Rhabdoviridae. It causes rabies, a fatal disease transmitted through the bites of infected animals like dogs, foxes, and bats. The virus enters through wounds or bites and travels through nerves to the brain and spinal cord, causing encephalitis. There are two forms of rabies - furious rabies with symptoms like anxiety and hydrophobia, and dumb rabies characterized by paralysis. Diagnosis involves detecting the virus in samples or Negri bodies in tissue. Post-exposure prophylaxis includes wound cleaning, rabies immunoglobulin, and vaccination to prevent infection. Modern non-neural vaccines like cell culture vaccines are now used instead of
Herpesviruses are a leading cause of human viral diseases and include herpes simplex virus types 1 and 2, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, and human herpesvirus 8. They are capable of causing overt disease during primary infection or remaining latent in sensory ganglia or lymphocytes. Herpesviruses can be reactivated from latency to cause recurrent disease. Laboratory diagnosis involves virus isolation in cell culture, antigen or antibody detection, PCR, and histopathological examination of clinical samples. Treatment options include acyclovir, valacyclovir, and ganciclovir depending on the infecting virus.
Staphylococci are spherical bacteria that occur in grape-like clusters. Staphylococcus aureus is an important human pathogen that can cause a variety of infections, from minor skin infections to life-threatening conditions like toxic shock syndrome and endocarditis. S. aureus produces several virulence factors like toxins and enzymes that damage tissues and evade the immune system. Laboratory diagnosis involves culture, microscopy, and tests like coagulase to identify S. aureus. Antibiotics are used to treat infections, and prevention focuses on hygiene and safe food handling. Methicillin-resistant S. aureus is an antibiotic resistant form that is more difficult to treat.
Hepatitis B is caused by the hepatitis B virus (HBV) and is a serious infectious disease affecting the liver. It is transmitted through contact with infected blood or bodily fluids. The virus can cause both acute and chronic infections. Diagnosis involves testing for hepatitis B surface antigen and antibodies. There is no cure for chronic hepatitis B but vaccination provides effective prevention.
The hepatitis B virion (Dane particle):
outer lipid envelope with the surface antigen (HBsAg).
an electron-dense core (nucleocapsid): ds circular DNA and polymerase surrounded by the core antigen (HBcAg).
The HBsAg is produced in excess by the infected hepatocytes and is secreted in the form of spherical
and filamentous particles.
There are 5 main hepatitis viruses (HAV, HBV, HCV, HDV, HEV) that cause inflammation of the liver. HAV and HEV are non-enveloped RNA viruses spread through the fecal-oral route, while HBV is a DNA virus and HCV and HDV are enveloped RNA viruses primarily spread through blood or sexual contact. These viruses are the most common causes of viral hepatitis in children and adults.
1. Hepatitis B is caused by the hepatitis B virus (HBV) and can lead to both acute and chronic liver infection or disease.
2. HBV is transmitted through contact with infectious blood or body fluids and can spread through sexual contact, sharing needles, or from infected mother to child during birth.
3. Diagnosis involves testing for hepatitis B surface antigen (HBsAg) and antibodies to HBV, while treatment focuses on antiviral medications to suppress viral replication and prevent progression to cirrhosis or liver cancer.
Advancement in treatment of viral hepatitisprabaldas16
The topic of my presentation is "Advancement in treatment of viral hepatitis" which aim to discuss the different types of viruses causing hepatitis, pathogenesis, their prevention, novel vaccines and current as well as newer modalities of treatment of viral hepatitis.
Hepatitis B virus was discovered in the 1980s through outbreak investigations. It is a DNA virus belonging to the Hepadnaviridae family. About 2 billion people have been infected worldwide, with 400 million having chronic infections. It is transmitted through bodily fluids and from mother to child.
Acute infection presents with non-specific symptoms like fatigue and jaundice. Chronic infection can lead to liver damage and cancer. Diagnosis involves detecting viral antigens and antibodies. While treatment cannot eliminate the virus, antivirals can suppress it. The WHO recommends treatment for those with significant liver disease or high risk of progression. Treatment aims to improve outcomes of this serious public health problem.
Hepatitis viruses include hepatitis A, B, C, D, and E. Hepatitis A virus is transmitted through the fecal-oral route while hepatitis B, C, and D are transmitted through blood and body fluids. Hepatitis B and C can cause chronic infections while hepatitis A usually does not. Diagnosis involves tests to detect viral antigens, antibodies, and nucleic acids. Treatment options depend on the hepatitis virus but may include antiviral drugs and vaccines to prevent transmission.
This document discusses chronic hepatitis B infection. It covers the epidemiology of chronic hepatitis B, including that approximately 400 million people are chronically infected worldwide. It also discusses the hepatitis B virus particle, noting it has a 3.2 kb DNA genome that encodes four overlapping genes. Regarding diagnosis, it emphasizes the importance of optimal HBV screening and diagnosis using markers such as HBsAg, HBeAg, anti-HBe and HBV DNA levels.
This document discusses viral hepatitis, summarizing the key points about hepatitis A-E viruses. It covers their virology, epidemiology, clinical features, pathogenesis, diagnosis and complications. The main points are:
1. Hepatitis A-E viruses are the primary causes of viral hepatitis. They produce similar illnesses but differ in modes of transmission, incubation periods and likelihood of chronic infection.
2. Hepatitis A and E are typically self-limited and do not usually lead to chronic liver disease. Hepatitis B and C have higher rates of chronic infection.
3. Acute viral hepatitis presents with non-specific symptoms but laboratory tests can identify the specific virus through detection of viral antigens or antibodies. Ful
This document provides information about hepatitis C virus (HCV) including its structure, genome, genotypes, epidemiology, transmission, pathogenesis, diagnosis, and management. It discusses:
- HCV has a single-stranded RNA genome within the Flaviviridae family. It exists as different genotypes that determine treatment response.
- HCV is a major cause of liver disease worldwide, with transmission primarily through blood exposure. Diagnosis involves antibody and RNA testing.
- Treatment aims to eradicate HCV and involves pegylated interferon and ribavirin combinations. Response is monitored via viral load decline. Adverse effects require monitoring and management. New direct-acting antivirals are improving treatment outcomes.
The document discusses hepatitis C virus (HCV), including its structure, genome, genotypes, epidemiology, pathogenesis, diagnosis, and management. Some key points:
- HCV is a single-stranded RNA virus of the Flaviviridae family with a genome encoding both structural and nonstructural proteins.
- It exists as different genotypes globally, with genotypes 1, 2, 3 being most common. Genotype helps determine treatment duration and response.
- HCV is a major cause of liver disease worldwide and is transmitted through blood exposure. Diagnosis involves HCV antibody and RNA testing.
- Treatment aims to eradicate the virus and involves use of pegylated interferon and ribavirin
This document summarizes chronic viral hepatitis caused by hepatitis B, C, and D viruses. It describes the modes of transmission, clinical manifestations, laboratory diagnosis, and morphology of each virus. Chronic hepatitis B and C can lead to cirrhosis and liver cancer over many years. Hepatitis B and D viruses can only replicate in hepatocytes infected with hepatitis B virus. Laboratory tests for hepatitis B, C, and D include detecting viral antigens, antibodies, RNA, and liver enzymes to determine infection and disease status.
Hepatitis C is caused by the hepatitis C virus (HCV), a single stranded RNA virus. It is transmitted through blood and infects liver cells, potentially causing cirrhosis or liver cancer. There is currently no vaccine but combination therapy with pegylated interferon and ribavirin can cure 50-80% of cases. Prevention focuses on avoiding sharing needles or personal items that may transmit infected blood.
Chronic hepatitis B and C are inflammatory conditions of the liver that persist for at least 6 months. Hepatitis B and C viruses are the most common causes. Chronic hepatitis B can progress to cirrhosis or liver cancer over many years if left untreated. Treatment aims to suppress viral replication and reduce liver inflammation. For hepatitis C, the goal is to eradicate the virus using direct-acting antiviral drugs, which now cure over 99% of patients. Both conditions require long-term management to prevent progressive liver disease.
HIV in Pregnancy
Dr. ARCHANA VERMA
1) HIV is a retrovirus that can be transmitted from mother to child during pregnancy, childbirth, or breastfeeding. Left untreated, the risk of mother-to-child transmission is 15-45%.
2) Treatment involves antiretroviral therapy for the mother during pregnancy and delivery, and for the newborn for 4-6 weeks to prevent transmission. Mode of delivery and avoiding breastfeeding can also reduce risk.
3) With treatment, the risk of mother-to-child HIV transmission can be reduced to less than 2%. Proper antenatal care, delivery management, and postpartum care and testing of
This document summarizes gene expression and the life cycle of hepatitis B virus (HBV). HBV is a DNA virus that can cause liver infection. It has a circular DNA genome organized into four open reading frames that encode the viral polymerase, envelope proteins, precore protein, and X protein. The virus attaches to hepatocytes and its DNA enters the nucleus to form covalently closed circular DNA, which is transcribed to produce viral RNA. This RNA is reverse transcribed back into DNA, which is packaged into viral capsids. The capsids acquire envelopes and are released from infected hepatocytes. HBV replication is regulated by histone modifications and interactions with host proteins. The host immune response is also important for viral
This document provides information on Hepatitis B virus (HBV) including its transmission, risks, diagnosis, and management. It describes how HBV causes liver inflammation and can lead to serious complications like cirrhosis and liver cancer if chronic infection develops. Diagnosis involves testing for hepatitis B surface antigen and other markers. Treatment may include antiviral drugs like lamivudine, while vaccination provides effective prevention. Standard precautions like hand hygiene and safe injection practices are important to control the spread of HBV.
Hepatitis B virus is a partially double-stranded DNA virus that can be transmitted both horizontally through infected blood or body fluids and vertically from mother to child. It has a 42nm enveloped virion structure containing DNA and antigen proteins. HBV replicates through reverse transcription and has 4 overlapping reading frames that encode the surface, core and polymerase proteins. HBV infection may be acute and self-limiting or develop into chronic lifelong infection. Diagnosis involves detecting hepatitis B antigens and antibodies. Current treatments include interferon which stimulates immunity, and nucleoside analogues like lamivudine and adefovir which inhibit viral replication but resistance can develop. Prevention is through vaccination and immunoglobulin administration to exposed newbor
This particular presentation includes slide on basic virology about rabies virus, pathogenesis of rabies and it's management specially emphasized on guide of pre and post exposure vaccination.
This presentation contains slides describing normal microbial flora of human body, significance of normal flora, distribution of normal flora, immune response to infection, source and transmission of infective agents, stages of infection
Contains slides describing essential elements for bacterial growth, bacterial growth curve, mechanism of energy production and metabolism, principle of in-vitro bacterial culture
This lecture presentation contains description of arbovirus particularly detailing Dengue virus infections. Lecture outlined general characteristics of Arbovirus, classification of Arboviruses, salient features of Dengue virus, dengue pathogenesis, clinical course, laboratory diagnosis, complications of secondary dengue and some recent aspect of dengue vaccine preparation.
This presentation contains 53 power point slides. These slides have description between virus and host cell interactions including concept of permissive and non-permissive infection, latent infection and host immune response to viral infection. Slides are designed for medical students, nurses, academicians who are teaching virology and microbiology in medical universities, schools or college.
This presentation contains 45 slides on general virology comprises of topics on viral classification, transmission, pathogenesis, viral cytopathic effect, stages of viral infections, antiviral drugs and viral vaccines. It also have a slide noting an outline of laboratory diagnosis of viral infection. This power point presentation was designed for medical students, nurses and academicians teaching virology and microbiology in medical universities, schools or colleges.
The document discusses the history of virology research from the late 19th century to present day. Some of the key events summarized include:
- In 1892, Iwanowski discovered an infectious agent that could pass through porcelain filters.
- In 1898, Loeffler and Frosch concluded that the foot-and-mouth disease agent was smaller than bacteria and must replicate.
- Advances in tissue culture and electron microscopy in the 1900s allowed visualization and growth of viruses outside of host cells.
- Discovery of plant, insect, bacterial, and oncogenic viruses followed. Twort and d'Herelle proved bacterial viruses.
- Methods of virus purification, structure determination, and growth in eggs and
This presentation is on basic virology on Enterovirus diseases. Viruses includes Coxsackie virus, entero virus 71, rota virus, polio virus. Slides are suitable for medical students and medical graduate.
This document describes the structures and components of bacterial cells. It discusses the essential structures like the cell wall, plasma membrane, ribosomes, and nucleoid as well as nonessential structures like capsules, flagella, and pili. The cell wall is composed of peptidoglycans, teichoic acids, and lipopolysaccharides. Gram-positive and gram-negative bacteria differ in their cell wall composition, affecting how they stain. Other structures like plasmids, capsules, and spores are described along with their functions. The roles of bacterial structure in laboratory identification through staining methods like gram and acid-fast staining are also summarized.
This document discusses the morphology and structures of bacterial cells. It begins by outlining the learning objectives which are to describe different bacterial shapes and arrangements, basic bacterial cell structures and their functions, staining characteristics based on structures, and how structure relates to laboratory identification. It then details the various bacterial cell components such as the cell wall, plasma membrane, ribosomes, and other internal structures. It explains how these structures determine staining properties and relates morphology to identification. The document uses diagrams to illustrate the different bacterial forms, components, and arrangements.
Contents of this presentation is targeted towards undergraduate medical students who have started their general Microbiology. Slides of this presentation shall also provide critical thinking to correlate basic Medical Microbiology with clinical aspect. Contents includes morphology of bacteria, cell wall structure of bacteria, accessory organs like flagellum, capsule, spore, plasmid etc. Also discuss the role of antibiotics over different structure of bacteria and staining characters of gram positive, gram negative or acid fast bacteria.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
1. Dr. Tarek Mahbub Khan
MBBS, M.Phil (virology)
Assistant Professor
2. Learning objectives
• Definition of hepatotropic virus and examples
• Outline of classification and characteristics of
hepatitis viruses
• Structure, epidemiology, pathogenesis, clinical
outcome and laboratory diagnosis of:outcome and laboratory diagnosis of:
– Hepatitis A virus
– Hepatitis B virus
– Hepatitis C virus
– Hepatitis D virus
– Hepatitis E virus
– Hepatitis G
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3. • Viral hepatitis is a systemic
disease caused by hepatitis
viruses that produce acute
inflammation of the liver
clinically characterized by
VIRAL HEPATITIS
clinically characterized by
fever, gastrointestinal
symptoms like nausea,
vomiting and jaundice.
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4. HEPATOTROPIC VIRUSES
• Viruses which infects hepatocytes are hepatotropic
• Two broad classification:
• Primary hepatotropic : Infects liver cell primarily:• Primary hepatotropic : Infects liver cell primarily:
– e.g., Hepatitis A, B, C, D, E and G viruses
• Secondary hepatotropic : Hepatitis occurs as a
consequences to infection of other organs:
– e.g., CMV, Yellow fever virus, HSV, Dengue viruses
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5. AN OVERVIEW OF HEPATITIS
VIRUSES
Viruses Genome On-set of
infection
Transmission Chronicity
HAV RNA Children Feco-oral No
HBV DNA Adult, Parenteral, YesHBV DNA Adult,
children
Parenteral,
Sexual, Vertical
Yes
HCV RNA Adult Parenteral, sexual Yes
HDV RNA Adult Parenteral, sexual Yes
HEV RNA Adult Feco-oral No
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6. HEPATITIS A VIRUS
(cause infectious hepatitis)
• Hepatitis A is non-envelop RNA virus
• ssRNA genome
• Possess seven genotypes (only one serotype)
• Virus family: Picornaviridae
• Genus: Hepatovirus
• Can be killed by autoclaving, boiling for 5 minutes,
heating food (1850 F for 1 minute), disinfection by
bleach (1:100 concentration)
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7. • Incubation periods: 10-50 days
• Children are asymptomatic (80-95%) in relation to adult
(10-25%)
• Viremia : Transient• Viremia : Transient
• Virus in stool: 2 weeks before and 2 week after jaundice
• Onset of infection is abrupt
• ALT level remains high up to 1-3 weeks
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8. Epidemiology of HAV infection
• Transmission is mainly fecal-oral route. Sexual and
intravenous route is not common
• Common in families, institutions, summer camp, day• Common in families, institutions, summer camp, day
care, over crowded and poor sanitary conditions
• Sources of infections: Raw oysters, undercooked foods,
frozen strawberries and non-human primates
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10. • Virus attaches with a glycoprotein receptor (HAV cell
receptor 1 glycoprotein-HAVCR1) on hepatocyte
• HAV itself is not cytopathic
• Cellular immunity particularly CD8+T cell , plays a key• Cellular immunity particularly CD8+T cell , plays a key
role in cell injury
• IgM appears in blood at the onset of symptoms
• IgG confers lifelong immunity against all strains
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12. Laboratory diagnosis
• SAMPLES: Blood, Stool, bile , liver
• COMON METHODS: ELISA, PCR, Hybridization
• SEROLOGICAL MARKERS (Anti-HAV):• SEROLOGICAL MARKERS (Anti-HAV):
• IgM: Acute infection, decline to non-detectable range by 3-6 months
• IgG: Indicates past infection, detected even after decades
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13. Management
• TREATMENT: Supportive
• PREVENTION:
• Improvement of personal hygiene and sanitation
• Treatment with 0.5% sodium hypochloride solution• Treatment with 0.5% sodium hypochloride solution
• Vaccination: Formalin inactivated vaccine
• HAV Ig can be given to person within 2 weeks of infection
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14. Because
– Most infected people are
contagious 10-14 days before
symptoms occurs
Why hepatitis A spread
readily in a community?
symptoms occurs
– 90% of the infected children
and 25%-50% of infected
adults have inapparent but
productive infections
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15. HEPATITIS B VIRUS
(serum hepatitis)
• DNA envelope virus
• Icosahedral capsid
• Family: HepadnaviridaeFamily: Hepadnaviridae
• dsDNA genome with incomplete positive strand
• Virus posses reverse transcriptase that acts in later part of
replication
• DNA integrates with host cell DNA by enzyme integrase
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16. HOSTS OF HEPATITIS B VIRUS
Woodchuck
Ground squirrel
Duck
Human
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17. Basic structure of hepatitis B virus
•Antibodies are formed against all types of viral antigens
•HBsAg is a part of the viral envelope
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20. STRUCTURE OF HEPATITIS B VIRUS
• DANE PARTICLE: A 42 nm complete virion of HBV
• VIRAL CORE:
– Contains a partially double stranded DNA of only 3.2 kbp
– Enzymes: Protein kinase and DNA polymerase having both
reverse transcriptase and ribonuclease H activityreverse transcriptase and ribonuclease H activity
– A P protein attached to its genome
– An icosahedral capsid formed by hepatitis B core antigen (HBcAg)
– HBeAg shares most of its protein sequence with HBcAg
• VIRAL SURFACE:
– An envelope containing three forms of glycoprotein hepatitis B surface
antigen (HBsAg)
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21. HEPATITIS B VIRUS GENOME
‘S’ gene: HBsAg
Four open reading frame (ORF)
‘P’’ gene: Polymerase Enzyme
‘X’ gene:
Transactivation of transcription
‘C’ genes: HBcAg, HBeAg
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22. HEPATITIS B SURFACE ANTIGEN
• HBsAg containing particles are released into the serum and
outnumber the actual virion.
• Originally termed as Australian Antigen
• This antigen is immunogenic
• HBsAg includes three glycoproteins (L, M and S)• HBsAg includes three glycoproteins (L, M and S)
• S glycoprotein is the major component of HBsAg particle
• The glycoproteins of HBsAg have group specific and type
specific determinants:
– Group specific determinants: ‘a’
– Type specific determinants: ‘d’ or ‘y’ and ‘w’ or ‘r’
• Combination of these antigens forms eight subtypes of HBV
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23. HBV REPLICATION
• HBV replication is unique because:
– Defined tropism for liver
– Small genome
– Replicates through an RNA intermediate– Replicates through an RNA intermediate
– Produce and releases antigenic decoy particles
(HBsAg)
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24. ATTACHMENT AND ENTRY
• ATTACHMENT to the hepatocytes is mediated by HBsAg
glycoprotein and several liver cell receptors:
– Transferrin receptor
– Asialoglycoprotein receptorAsialoglycoprotein receptor
– Human liver annexin V
• ENTRY: HBsAg binds to polymerized human serum albumin
and other serum proteins that may facilitate virus uptake by
the liver
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25. TRANSFER OF CORE TO THE NUCLEUS
• HBV core is transfer to the nucleus probably through microtubules.
• Capsid deliver the genome alongside with its own RNA polymerase
inside the nucleus.
• DNA REPAIR: incomplete positive strand is made complete with host
DNA polymerase and a cccDNA of HBV is formed.DNA polymerase and a cccDNA of HBV is formed.
• EARLY TRANSCRIPTION: This cccDNA is transcribed to several different
length mRNA (pre-genomic RNA) by virion RNA polymerase:
– 3500- base mRNA: encodes HBcAg, HBeAg, DNA polymerase and primer
– 2400-base mRNA : encodes large (L) HBsAg glycoprotein
– 2100-base mRNA : encodes medium (M) and small (S) glycoproteins
– 900-base mRNA : encodes the ‘X’ protein
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26. EXIT OF THE mRNA TO THE
CYTOPLASM
• mRNA exit to the cytoplasm through nuclear pore
• mRNA is read on host cell ribosome to translate different
proteins including DNA polymerase
• FUNCTIONS OF HBV DNA POLYMERASE:• FUNCTIONS OF HBV DNA POLYMERASE:
1. Priming: start synthesizing a negative DNA strand from the RNA
strand
2. Ribonuclease H activities: Cleaves the RNA strand that has been used
to synthesize DNA strand except a little RNA at the 3’ region of mRNA
3. Completion of genome synthesis
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27. FINAL STEPS IN REPLICATION
• ENCAPSIDATION:
– 3.5 kb-base RNA (pre-genomic RNA) is encapsidized by structural
protein (HBcAg)
• SYNTHESIS OF NEGATIVE STRAND:
– Use 3.5 kb RNA as template
– Catalyst by DNA polymerase with reverse transcriptase activity.– Catalyst by DNA polymerase with reverse transcriptase activity.
– RNAase H will cleave the initial RNA template except few nucleotides
• SYNTHESIS OF POSITIVE STRAND:
– The small RNA primer at the 5’ end of the newly synthesized negative
DNA strand will start synthesizing positive strand
• RELEASE:
– Provirus traveled through ER and Golgi body and acquire its envelope
and released by budding
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30. SPREAD OF HBV IN THE BODY
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31. PATHOGENESIS OF
HEPATITIS B INFECTION
• Transmission: Parenteral, Sexual ,Vertical
• Liver damage:
1. Virus reaches the hepatocytes and attached by receptor and
displayed on cell surfacedisplayed on cell surface
2. Cytotoxic T lymphocyte mediates an immune attack against
viral infected cells
3. Results in inflammation and cell necrosis –Hepatitis
4. Antigen-antibody complex can be deposited in different organs
and produce inflammation (eg. Arthritis,vasculitis)
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32. CLINICAL OUT COME OF
HEPATITIS B INFECTION
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33. OUTCOMES OF AGE OF
INFECTION
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34. CLINICAL FEATURES
• Two clinical types
1. Acute hepatitis
2. Chronic hepatitis
• Incubation period: 10-12 weeks• Incubation period: 10-12 weeks
• Many cases are asymptomatic
• Fever, anorexia, nausea, vomiting and jaundice
• Dark urine, pale feces, arthralgia, arthritis, rash
• Most chronic carriers are asymptomatic
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37. SIGNIFICANT OF HBV
SERO-MARKERS
Viral markers Significance
HBsAg Acute infection, if persists for more than six
months: chronic infection
Anti-HBs Protection: by natural infection or vaccination
Anti-HBcAg IgM: Acute infection
IgG: Past or chronic infection
HBeAg Active viral replication and high chance of
transmissibility
Anti-HBeAg Disease recovering
HBV-DNA Active viral replication and high chance of
transmissibility
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39. MANAGEMENT OF
HEPATITIS B INFECTION
A. Acute infection: Supportive treatment
B. Chronic hepatitis B infectionB. Chronic hepatitis B infection
– Alpha interferon, Lamivudin, Adefovir
TREATMENT
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40. C. Prevention strategy:
– Safe blood transfusion, safe sex, elective Caesarean
section
– Vaccines: Recombinant Hepatitis B vaccine contains
HBsAg antigens
PREVENTION
HBsAg antigens
– Prophylaxis: Hepatitis B immunoglobulin after accidental
exposure( eg. Needle stick injury)
– Newborn in infected mother: Both vaccine and HBIG
– Elective cesarean section
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41. COMPLICATION OF
HEPATITIS B INFECTION
• Cirrhosis of liver
• Hepatocellular carcinoma• Hepatocellular carcinoma
– FACTORS:
• Integration of HBV-DNA into host cell DNA
• Transactivation of transcription by X gene expression
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42. HEPATITIS C
• RNA envelope virus
• Family: Flaviviridae
• Genus: Hepacivirus
• Related to postranfusional NANB hepatitis
• Genome encodes:
– One core protein, two envelope glycoprotein and several NS
proteins
– Six major genotypes(Clades) and more than 100 subtypes
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43. GENOME OF HCV VIRUS
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44. SIGNIFICANCE OF GENOMIC
DIVERSITY
• Different genotypes(1-6) are prevalent in different parts of the world
• Virus undergoes sequence variation in chronic infection
• Treatment response depends on genotypes
• QUASI-SPECIES
a complex viral population presents in a single infected individual
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45. EPIDEMIOLOGY
• 3% of the world population has been infected (WHO, 1997)
• Mode of transmission: Parental, sexual, saliva , organ transplant
• HIGH RISK INDIVIDUALS:• HIGH RISK INDIVIDUALS:
– Intravenous drug users
– Hemophiliacs (Multiple blood transfusion)
– High risk sexual partners
– Health workers
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47. HCV INFECTION
• Incubation period: 6-7 weeks
• Antibody appears 8-9 weeks after exposure
• Antibodies are developed against core, envelope, NS3 and NS4
proteinsproteins
• 70-90% of infected individual develop chronic hepatitis
• 10-20% of chronic HCV infection leads to:
– Chronic active hepatitis
– Cirrhosis (20-50%)
– Hepatocellular carcinoma (5-25%)
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48. • Hepatitis C viral infection is more dangerous.
• REASONS:
– 70-90% of HCV infections progress to chronic hepatitis
HCV OR HBV ?
WHICH ONE IS MORE DANGEROUS?
– 70-90% of HCV infections progress to chronic hepatitis
– Inapparent infection is more in HCV than HBV
– Delay in development of antibody even in low titer
– No vaccine is available due to antigenic diversity of HCV
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49. LABORATORY DIAGNOSIS
• SAPMLE: Blood (Serum, Plasma)
• METHODS OF TEST: ELISA, ICT, RIBA, RT-PCR
• SEROLOGY (Anti-HCV):
– In 50-70% cases antibody appears with symptoms
– In other cases antibody appears in 3-6 weeks time
– Can not be distinguish between acute, chronic or resolved infection
• RT-PCR:
– Detects viral RNA
– Useful in prognosis after antiviral drug
– Used to detect genotypes to guide anti-viral therapy
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50. ALGORITHAMS OF HCV INFECTION
DIAGNOSIS
Anti-HCV (Screening)
POSITIVE NEGATIVE
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NEGATIVE
HCV-RNA/anti-HCV core Ab
Repeat after 3 months
POSITIVE
51. RECOMBINANT IMMUNOBLOT
ASSAY (RIBA)
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RIBA detects more specific HCV antibodies. Test is
interpreted as positive (2 or more antigens) indeterminate(1
antigen) , negative (0 antigen). More specific than ELISA.
HCV-RNA has now replace the importance of RIBA.
52. LIMITATIONS OF THE
SEROLOGICAL TEST
• Limitations of the serological test:
– Long delay (even >6 months) in development of anti-HCV
antibodyantibody
– Reactive screening test does not distinguish between
current and past infection
– False reactive test result
– Cannot provide information about treatment response
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53. MANAGEMENT
• TREATMENT
– Alpha interferon or pegilated interferon
– Lamivudine
– Relapse is common
• PREVENTION
– No vaccine developed
– Practicing safe sex, blood transfusion, prohibiting IV addiction,
safe organ donation may protect
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54. HEPATITIS D VIRUS
• RNA envelop (HBsAg) virus
• Virus contains a single stranded negative sense RNA genome
• Is a defective virus: Needs HBsAg for effective infection• Is a defective virus: Needs HBsAg for effective infection
• One serotype
• RNA genome encode one core protein: Delta antigen
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56. Co-infection and super
infection with HBV
• Simultaneous infection of HBV and HDV results in co-infection
• HDV infects in preexisting HBV infection results in super infection
• Fulminant hepatitis is associated with super-infection
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57. • In co-infection
– HDAg, HDV-RNA and anti-HDV IgM
– All markers of HDV replication disappear in convalescence
stage, even anti-HDV antibody disappear within months
LABORATORY DIAGNOSIS
• In super-infection
– Persistence of high level of anti-HDV IgM and IgG, HDAg,
HDV-RNA
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58. HEPATITIS E VIRUS
• Non enveloped positive sense ssRNA virus
• FAMILY: Hepeviridiae
• GENUS: Hepevirus
• Most common cause of water borne epidemic in Asia, Africa, Mexico
• 20% of pregnant women develops fulminant hepatitis
• Detection of anti-HEV antibody in blood helps diagnosis
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59. HEPATITIS G VIRUS
• Belongs to Flaviviridae family
• RNA envelope virus
• HGV is also known as GB virus C
• Transmitted through parenteral and sexual route
• Have strong significance in HIV co-infection (35% cases)• Have strong significance in HIV co-infection (35% cases)
• HGV interfere HIV virus replication lower mortality rate
• Laboratory detection:
– GBV-C RNA detection
– Anti-GBV-C antibody
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61. Histology of Chronic hepatitis
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Right: Granular cytoplasm, ground-glass hepatocytes
Left: Immunoperoxidase test for HBsAg (HBsAg particles in
cytoplasm of hepatocytes
62. 1. HAV is a picornavirus
2. HAV can be detected in the blood 2 weeks prior to jaundice
3. Anti-HBcAg IgM is an useful viral marker in acute HB
infection
4. Viral cytopathic effect is the main pathogenesis in liver4. Viral cytopathic effect is the main pathogenesis in liver
damage by HBV
5. Reverse transcription occurs in the initial stage of HBV
replication
6. 70-80% of HCV infection leads to chronic hepatitis
7. Quasi-species is observed in HEV infection
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63. 8. HDAg is detected in co-infection only
9. HDV genome is a ssRNA with positive polarity
10. HEV commonly infects adults
11. HEV is a flavivirus
12. Fulminant hepatic failure is frequently observed in pregnant12. Fulminant hepatic failure is frequently observed in pregnant
women with HEV infection
13. HGV is a DNA virus
14. HGV interfere with HIV replication
15. Anti-HBsAg is not detectable in chronic HBV infection
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64. Reference
• Review of Medical Microbiology and Immunology. Warren Levinson,
12th May 2012. Mc Graw-Hill (Lange)
• Jawetz, Melnick and Adelberg’s Medical Microbiology
George F. Brooks, Karen C. Carroll, Janet S. Butel,
25th Mar 2010. Mc Graw-Hill (Lange)
• Bailey and Scott’s Diagnostic Microbiology.Betty A.Forbes,
Daniel F. Sahm, Alice S. Weissfeld,12th 2007. Mosby Elsevier
• Lippincott’s illustrated review Microbiology. Richard A Harvey,
Pamella C. Champe, Bruce D. Fisher, 2007. Lippincott William &
Wilkins
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