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Rhabdo Virus.pptx

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Dr Sumitha Jagadibabu
Dr Sumitha Jagadibabu

Rhabdoviruses are enveloped viruses with bullet-shaped particles that contain single-stranded RNA. They replicate by entering host cells and using their RNA polymerase to transcribe and replicate their genome. New virus particles then bud from the host cell. Rhabdoviruses can infect many species and are transmitted by arthropods or bites. Rabies virus causes fatal neurological disease in humans and other mammals by traveling along nerves to the brain. It evades immunity and commonly causes fear of water, paralysis, and death from respiratory failure. Diagnosis involves clinical evaluation, exposure history, and fluorescent antibody or PCR testing of brain or saliva samples.

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Rhabdoviruses Dr Sumitha J
Morphology • Rhabdoviruses are enveloped viruses with a single-stranded, negative-sense RNA genome. • They have a distinctive bullet or rod-like shape, with a helical nucleocapsid enclosed by a lipid envelope. • The envelope contains viral glycoproteins that protrude from the surface, which are important for viral entry into host cells.
Replication The replication cycle of rhabdoviruses involves several steps: • Attachment and Entry: The virus attaches to specific host cell receptors using its glycoprotein spikes. It then enters the host cell by membrane fusion. • Transcription and Replication: Once inside the host cell, the viral RNA genome is transcribed into messenger RNA (mRNA) by the viral RNA-dependent RNA polymerase (RdRp). The mRNA is used to produce viral proteins, and the genome is replicated to generate more viral RNA.
Replication • Assembly: Viral components are assembled in the host cell's cytoplasm to form new virus particles. • Budding: New virus particles bud from the host cell's plasma membrane, acquiring their lipid envelope in the process. • Release: Mature virus particles are released from the host cell and can infect new cells, continuing the cycle.
Epidemiology • Rhabdoviruses can infect a wide range of hosts, including mammals, birds, fish, and insects. • Some rhabdoviruses are transmitted by arthropod vectors (e.g., mosquitoes) and cause diseases in animals (e.g., vesicular stomatitis virus) and plants. • Rabies virus, one of the most well-known rhabdoviruses, primarily infects mammals and is usually transmitted through the saliva of infected animals, often via bites.
Clinical Features • The clinical manifestations of rhabdovirus infections vary depending on the specific virus and the host species. • In humans, rabies is the most notorious rhabdovirus infection and is almost invariably fatal once clinical symptoms appear. • Rabies presents with symptoms such as fever, confusion, agitation, hallucinations, paralysis, and ultimately progresses to coma and death.
Pathogenicity • Rhabdoviruses can be highly pathogenic. • Their pathogenicity is often linked to their ability to infect the central nervous system (CNS), as is the case with rabies virus. • Once the virus reaches the CNS, it can cause severe neurological symptoms and death. • Other rhabdoviruses may cause diseases in different organs or tissues, depending on their tropism and the host species they infect.
Rabies • Rabies is a viral disease caused by the rabies virus, which is a member of the Rhabdoviridae family. It primarily affects mammals, including humans. Rabies is a highly pathogenic and almost invariably fatal disease once clinical symptoms appear. Here are the key aspects of the pathogenicity and clinical features of rabies
Pathogenicity • Neurotropism: The rabies virus has a strong affinity for neural tissue, particularly neurons. It gains entry into the central nervous system (CNS) by initially infecting peripheral nerves near the site of entry (usually a bite wound). From there, it travels along the peripheral nerves towards the CNS, where it causes severe neurological damage. • Anterograde and Retrograde Spread: The virus can spread both anterograde (from the site of entry towards the CNS) and retrograde (from the CNS towards peripheral nerves and other tissues). This allows the virus to reach various parts of the body. • Neglected Immune Response: The rabies virus is known for its ability to evade the host's immune system, partly due to its relatively slow replication rate and limited exposure of viral antigens. This allows the virus to establish infection in the CNS without triggering a robust immune response.
Clinical Features • The clinical features of rabies typically progress through several stages: • Incubation Period: This is the period between the initial infection (e.g., a bite from an infected animal) and the onset of symptoms. The incubation period for rabies can vary but is often several weeks to months. During this phase, there are no noticeable clinical symptoms. • Prodromal Stage: This stage lasts for 2 to 10 days and is characterized by nonspecific symptoms such as fever, headache, malaise, and discomfort at the site of the bite (if applicable). The person may also experience anxiety, agitation, and nervousness.
Clinical Features Acute Neurological Stage: As the virus enters the CNS, severe neurologica symptoms begin to emerge. These may include: • Hydrophobia: An intense fear of water, as swallowing becomes difficult due to muscle spasms and the fear of choking. • Aerophobia: Fear of drafts of air or moving air. • Hallucinations: Patients may experience visual, auditory, or sensory hallucinations. • Agitation: Increased restlessness and aggression. • Paralysis: Muscles progressively become paralyzed, leading to difficulty in speaking, swallowing, and breathing.
Clinical Features • Coma and Death: The disease typically progresses to coma and death, usually within a few days to weeks from the onset of symptoms. Death results from respiratory failure as the muscles needed for breathing become paralyzed. • It's important to note that once clinical symptoms appear, rabies is almost universally fatal. Therefore, timely post-exposure prophylaxis (PEP) with rabies vaccines and rabies immune globulin (RIG) is crucial after a potential rabies exposure, such as a bite from a rabid animal. If administered promptly, PEP can prevent the progression of the disease.
Diagnosis • The diagnosis of rabies virus infection involves a combination of clinical evaluation, laboratory testing, and a detailed patient history, especially if there has been potential exposure to rabies.
Diagnosis Clinical Evaluation: • The clinical presentation of a patient with rabies may include neurological symptoms, hydrophobia, aerophobia, agitation, and paralysis. • A thorough physical examination, including assessment of neurological signs and symptoms, is important for clinical diagnosis. Patient History: • A detailed history is crucial, especially if there has been potential exposure to rabies. Information about animal bites or scratches, contact with potentially rabid animals, and travel history to areas where rabies is endemic should be obtained.
Diagnosis Laboratory Testing • Direct Fluorescent Antibody (DFA) Test: This is the most widely used and definitive diagnostic test for rabies. It involves examining brain tissue (typically from the brainstem) of a deceased or euthanized animal or a human suspected of having rabies. The test uses fluorescent antibodies to detect the presence of rabies virus antigens in nerve cells. It provides rapid results and is highly sensitive and specific. • Polymerase Chain Reaction (PCR): PCR can be used to detect viral RNA in clinical samples, including saliva, cerebrospinal fluid, or corneal samples. PCR is especially useful when examining non- neural tissues or in cases where the DFA test results are
Diagnosis Serology • Serological tests can detect the presence of antibodies against rabies virus in the patient's blood. However, these tests are not typically used for diagnostic purposes during acute rabies infection because the antibody response may not be detectable until later stages of the disease.
Histopathology • Post-mortem histopathological examination of brain tissue can reveal characteristic changes, including Negri bodies (eosinophilic, intracytoplasmic inclusions) in neurons. While these are suggestive of rabies, they are not always present and cannot be relied upon as the sole diagnostic criterion.

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Rhabdo Virus.pptx

  • 2. Morphology • Rhabdoviruses are enveloped viruses with a single-stranded, negative-sense RNA genome. • They have a distinctive bullet or rod-like shape, with a helical nucleocapsid enclosed by a lipid envelope. • The envelope contains viral glycoproteins that protrude from the surface, which are important for viral entry into host cells.
  • 3. Replication The replication cycle of rhabdoviruses involves several steps: • Attachment and Entry: The virus attaches to specific host cell receptors using its glycoprotein spikes. It then enters the host cell by membrane fusion. • Transcription and Replication: Once inside the host cell, the viral RNA genome is transcribed into messenger RNA (mRNA) by the viral RNA-dependent RNA polymerase (RdRp). The mRNA is used to produce viral proteins, and the genome is replicated to generate more viral RNA.
  • 4. Replication • Assembly: Viral components are assembled in the host cell's cytoplasm to form new virus particles. • Budding: New virus particles bud from the host cell's plasma membrane, acquiring their lipid envelope in the process. • Release: Mature virus particles are released from the host cell and can infect new cells, continuing the cycle.
  • 5. Epidemiology • Rhabdoviruses can infect a wide range of hosts, including mammals, birds, fish, and insects. • Some rhabdoviruses are transmitted by arthropod vectors (e.g., mosquitoes) and cause diseases in animals (e.g., vesicular stomatitis virus) and plants. • Rabies virus, one of the most well-known rhabdoviruses, primarily infects mammals and is usually transmitted through the saliva of infected animals, often via bites.
  • 6. Clinical Features • The clinical manifestations of rhabdovirus infections vary depending on the specific virus and the host species. • In humans, rabies is the most notorious rhabdovirus infection and is almost invariably fatal once clinical symptoms appear. • Rabies presents with symptoms such as fever, confusion, agitation, hallucinations, paralysis, and ultimately progresses to coma and death.
  • 7. Pathogenicity • Rhabdoviruses can be highly pathogenic. • Their pathogenicity is often linked to their ability to infect the central nervous system (CNS), as is the case with rabies virus. • Once the virus reaches the CNS, it can cause severe neurological symptoms and death. • Other rhabdoviruses may cause diseases in different organs or tissues, depending on their tropism and the host species they infect.
  • 8. Rabies • Rabies is a viral disease caused by the rabies virus, which is a member of the Rhabdoviridae family. It primarily affects mammals, including humans. Rabies is a highly pathogenic and almost invariably fatal disease once clinical symptoms appear. Here are the key aspects of the pathogenicity and clinical features of rabies
  • 9. Pathogenicity • Neurotropism: The rabies virus has a strong affinity for neural tissue, particularly neurons. It gains entry into the central nervous system (CNS) by initially infecting peripheral nerves near the site of entry (usually a bite wound). From there, it travels along the peripheral nerves towards the CNS, where it causes severe neurological damage. • Anterograde and Retrograde Spread: The virus can spread both anterograde (from the site of entry towards the CNS) and retrograde (from the CNS towards peripheral nerves and other tissues). This allows the virus to reach various parts of the body. • Neglected Immune Response: The rabies virus is known for its ability to evade the host's immune system, partly due to its relatively slow replication rate and limited exposure of viral antigens. This allows the virus to establish infection in the CNS without triggering a robust immune response.
  • 10. Clinical Features • The clinical features of rabies typically progress through several stages: • Incubation Period: This is the period between the initial infection (e.g., a bite from an infected animal) and the onset of symptoms. The incubation period for rabies can vary but is often several weeks to months. During this phase, there are no noticeable clinical symptoms. • Prodromal Stage: This stage lasts for 2 to 10 days and is characterized by nonspecific symptoms such as fever, headache, malaise, and discomfort at the site of the bite (if applicable). The person may also experience anxiety, agitation, and nervousness.
  • 11. Clinical Features Acute Neurological Stage: As the virus enters the CNS, severe neurologica symptoms begin to emerge. These may include: • Hydrophobia: An intense fear of water, as swallowing becomes difficult due to muscle spasms and the fear of choking. • Aerophobia: Fear of drafts of air or moving air. • Hallucinations: Patients may experience visual, auditory, or sensory hallucinations. • Agitation: Increased restlessness and aggression. • Paralysis: Muscles progressively become paralyzed, leading to difficulty in speaking, swallowing, and breathing.
  • 12. Clinical Features • Coma and Death: The disease typically progresses to coma and death, usually within a few days to weeks from the onset of symptoms. Death results from respiratory failure as the muscles needed for breathing become paralyzed. • It's important to note that once clinical symptoms appear, rabies is almost universally fatal. Therefore, timely post-exposure prophylaxis (PEP) with rabies vaccines and rabies immune globulin (RIG) is crucial after a potential rabies exposure, such as a bite from a rabid animal. If administered promptly, PEP can prevent the progression of the disease.
  • 13. Diagnosis • The diagnosis of rabies virus infection involves a combination of clinical evaluation, laboratory testing, and a detailed patient history, especially if there has been potential exposure to rabies.
  • 14. Diagnosis Clinical Evaluation: • The clinical presentation of a patient with rabies may include neurological symptoms, hydrophobia, aerophobia, agitation, and paralysis. • A thorough physical examination, including assessment of neurological signs and symptoms, is important for clinical diagnosis. Patient History: • A detailed history is crucial, especially if there has been potential exposure to rabies. Information about animal bites or scratches, contact with potentially rabid animals, and travel history to areas where rabies is endemic should be obtained.
  • 15. Diagnosis Laboratory Testing • Direct Fluorescent Antibody (DFA) Test: This is the most widely used and definitive diagnostic test for rabies. It involves examining brain tissue (typically from the brainstem) of a deceased or euthanized animal or a human suspected of having rabies. The test uses fluorescent antibodies to detect the presence of rabies virus antigens in nerve cells. It provides rapid results and is highly sensitive and specific. • Polymerase Chain Reaction (PCR): PCR can be used to detect viral RNA in clinical samples, including saliva, cerebrospinal fluid, or corneal samples. PCR is especially useful when examining non- neural tissues or in cases where the DFA test results are
  • 16. Diagnosis Serology • Serological tests can detect the presence of antibodies against rabies virus in the patient's blood. However, these tests are not typically used for diagnostic purposes during acute rabies infection because the antibody response may not be detectable until later stages of the disease.
  • 17. Histopathology • Post-mortem histopathological examination of brain tissue can reveal characteristic changes, including Negri bodies (eosinophilic, intracytoplasmic inclusions) in neurons. While these are suggestive of rabies, they are not always present and cannot be relied upon as the sole diagnostic criterion.