Medical Microbiology I - Virology Tutorial 8 - PDF

Microbiology & Pharmacognosy Department Medical Microbiology I 2025 (Tutorial 8)  Virology II (RNA Viruses) II RNA viruses Corona viruses (SARS, MERS, Covid 19). Paramyxovirus (e.g. Mumps, Measles, RS...

Microbiology & Pharmacognosy Department Medical Microbiology I 2025 (Tutorial 8)  Virology II (RNA Viruses) II RNA viruses Corona viruses (SARS, MERS, Covid 19). Paramyxovirus (e.g. Mumps, Measles, RSV). Orthomyxovirus (e.g. Infuenza virus, A, B & C). Togavirus (e.g. Rubella). Picorna virus (e.g. Poliomyelitis). Rhabdovirues (e.g. Rabies Virus). Retrovirus (e.g. HIV). Rota virus. Hepdavirus (e.g. Hepatitis A, C, D, E & G except B (DNA virus)  Poliovirus (Poliomyelitis) In the early years of the twentieth century, paralytic poliomyelitis was a feared and dreaded disease much like AIDS in today. After the introduction of a vaccine in 1955, the average number of cases of poliomyelitis in the 1980s was only 9. Now, the disease is eradicated in most countries all over the world. Clinical manifestations of Poliomyelitis 1-Early Symptoms (Prodromal Phase): At the onset of illness the patient has low grade fever, headache and stiffness in the neck. 2-Paralytic Phase (in ~1% of cases): In a small proportion of individuals (approximately 1%), the virus progresses to invade the central nervous system, leading to acute flaccid paralysis. Motor neurons that control voluntary muscles become non-functional, resulting in loss of motor function. This leads to muscle atrophy (wasting of muscles), as the nerves can no longer stimulate muscle activity. The paralysis is often asymmetric and may affect the legs, arms, or respiratory muscles, depending on the site of neural involvement.  Pathogenesis of Poliomyelitis Humans are the only host of poliovirus. Virus transmitted "fecal-oral route" through contaminated food, water, or milk and it passes through four phases: Alimentary phase: the virus replicates first at throat and intestinal mucosa. Lymphatic phase: the virus spreads from throat and intestine to tonsils, peyer s` paches of the ileum and cervical lymph nodes. This stage enables further viral multiplication and immune system evasion. Viremic phase: the virus is carried by bloodstream to various organs. Neurological phase: in rare cases (1%), the virus invades the brain and spinal cord through blood and thus affect the motor neurons leading to paralytic poliomyelitis (irreversible permanent disability ).  Diagnosis of poliomyelitis 1-Demonstration of the virus: The poliovirus can be recovered from fecal samples (most reliable) and throat swabs during the early stages of infection. Detection is done by: Polymerase Chain Reaction (PCR): for rapid and sensitive identification of viral RNA. Cytopathic Effects (CPE): observation of viral-induced damage in cultured cells, confirming the presence of active virus. 2-Serological Diagnosis (Detection of Antibodies): a) Neutralization Test: Detects neutralizing antibodies (neutralizing antibodies block the virus’s ability to enter and replicate in host cells) as early as the fourth day of infection. These antibodies provide lifelong immunity, indicating past or current infection or successful vaccination. b) Complement Fixation Test (CFT): Detects complement-fixing antibodies from around the tenth day of infection. Useful in confirming recent infections.  Rhabdoviruses ss enveloped RNA viruses that have unique bullet-shaped morphology under electron microscopy. The family Rhabdoviridae consists of more than one hundred virus. The most significant member of this family is rabies virus which causes a fatal neurological disease in humans and animals.  Rabies virus Pathogenesis: Infect most warm-blooded animals, including humans. Rabies is usually transmitted to people through the bite of infected animals (Zoonotic). IP long &variable (5 days to several years). The incubation period depends on the site of infection, the infectious dose of the virus, and the length of time required for the virus to migrate to the spinal cord or brain. Once the virus leaves the initial site of bite, it travels to the spinal cord and brain where it multiplies causing severe nerve cells damage. Pathogenesis of rabies  Clinical manifestations 1) Prodrome symptoms Pain at the site of the bite in addition to nonspecific symptoms as fever ,malaise ,headache and coryza. 2) Acute neurological symptoms Rabies presents in two clinical forms: Furious rabies (most common): marked by hyperactivity, agitation, confusion, hallucinations, and hydrophobia (fear and spasms triggered by water) Dumb/paralytic rabies: presents primarily with muscle weakness and progressive paralysis without hyperactivity 3) At the end of the acute neurological period: Irregular breathing, paralysis and coma occur which ends in death. Prevention : Human rabies is prevented by: 1. Avoid contact with animals. 2. Pre-exposure immunization for persons at high risk as veterinarians. This is done by giving rabies vaccine and immune serum. 3. Post exposure prophylaxis (PEP): wound cleansing (soap & water) rabies Ig: injected around the wound to provide immediate antibodies. rabies vaccine. Rabies vaccine 1)No safe attenuated strain of rabies virus has yet been developed for humans. The available vaccines are inactivated (killed) and designed to prevent rabies after exposure or for individuals at high risk of infection Vaccines in current use include: 1) The neurotissue vaccine: Preparation: The virus is grown in the spinal cords of rabbits, then inactivated. Drawbacks: This vaccine has been associated with a high incidence of neurological complications after administration, making it less favorable for use today. 2) A human diploid cell culture-derived vaccine: Preparation: The virus is cultured in human diploid cells, then inactivated. Advantages: This vaccine is much safer and has been in use since 1967. It is the most widely used vaccine today. 3) A recombinant vaccine called V-RG: Preparation: V-RG is a recombinant vaccine (genetically engineered), used in certain countries. Drawbacks: It is very expensive, limiting its widespread use. Post-Exposure Prophylaxis (PEP) After potential exposure to rabies (e.g., from a bite or scratch by a suspected rabid animal), the following treatment regimen is recommended: Human Rabies Immunoglobulin (HRIG) Dosage: One dose Administration: HRIG should be injected around the bite area. The remainder is injected deeply into the muscle at a site distant from the vaccine site. Rabies Vaccine Schedule: The individual should receive four doses of the rabies vaccine on days 1, 3, 7, and 14. This ensures the body’s immune system develops immunity to the rabies virus over the 14-day period. The combination of HRIG and the rabies vaccine is highly effective in preventing the onset of rabies after exposure to the virus.  HIV (Human Immunodeficiency Viruses) Human Retroviruses 2 serotypes: HIV-1 & HIV-2 Its 1ry target CD4+ TH cells. HIV 1 is the major cause of the AIDS (Acquired Immunodeficiency Syndrome) pandemic. More virulent and widespread. HIV 2 is of lower virulence and reduced transmissibility.Predominantly found in West Africa with limited global spread. Viral enzymes: Reverse transcriptase :Converts viral RNA into complementary DNA (cDNA) after entering the host cell. Integrase : Facilitates the integration of viral cDNA into the host genome. Protease: Processes viral polyproteins into functional viral proteins, essential for the maturation of new virions.  HIV transmission Infection is transmitted through: 1) Blood or blood product route ( blood transfusion, Sharing needles or syringes ). 2) Organ transplants. 3) Sexual intercourse (The majority of HIV infections). 4)Mother-to child route ( transplacental , at delivery ,breast-feeding)..  Clinical features 1-Primary infection :Occurs within 2 to 4 weeks after exposure. Patients develop a flu-like illness showing fever, night sweats and sore throat in the first 2 to 4 weeks. 2-Asymptomatic phase Of variable duration, from 2 to 10 years. Patients are clinically well, but infectious. 3- Prodromal phase These symptoms precede the progression to AIDS. Including: weight loss, Prolonged fever, persistent lymphadenopathy, oral candidiasis and Chronic diarrhea. These symptoms precede the progression to AIDS. Indicates immune system deterioration. 4-Acquired Immunodeficiency Syndrome (AIDS) syndrome with the following features: The final and most severe stage of HIV infection. ❖ Constitutional disease: Chronic fever, diarrhea, weight loss and skin rashes ❖ Neurological disease: dementia, myelopathy and peripheral neuropathy ❖ Immunodeficiency: Increased susceptibility to opportunistic infections ❖ Rare malignancies: Kaposi sarcoma(cancer that develops in the blood vessels or lymphatic vessels. It can manifest as skin lesions.it can also affect internal organs like the lungs, liver, and gastrointestinal tract) Skin lesion :Purple, red, or brown patches or nodules (often painless) that appear on the skin, most commonly on the legs, feet, arms, and face.  HIV Diagnosis 1. HIV-Ab-Ag reaction: screening (positive) 2. RT-PCR (HIV): Quantitative positive (confirm) :used to detect and measure the level of HIV RNA (viral load) in the blood. 4. CD4/CD8 ratio: monitor therapy (normal 1-4, if ratio