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134 Cards in this Set
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Describe: Human Immune Deficiency Virus (HIV)
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LENTIVIRUS: retrovirus that uses enzyme reverse transcriptase. has two identical strands of RNA surrounded by a protein coat. envelope has glycoprotein spikes that enable the virus to attach to the CD4 receptors found on helper T cells that are abundant in lymph nodes. two strains of HIV: HIV-1 is the predominant form and has a worldwide distribution. HIV-2 is less common and is found mostly in West Africa.
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Disease: Human Immune Deficiency Virus (HIV)
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Acquired immune deficiency syndrome (AIDS)
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MOT / Pathology: Human Immune Deficiency Virus (HIV)
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blood and body fluids (sexual contact, placenta from mother to fetus, breast milk, blood-contaminated needles, organ transplants, and artificial insemination). The virus attaches to the host helper T cell, enters in and releases its RNA. The released RNA will be transcribed into DNA via the reverse transcriptase enzyme. The DNA of the virus will be integrated into chromosomal DNA of the host cell. During the initial active infection, the virus will replicate using the host cell as a source of its viral particles producing more viruses that will infect more helper T cells. In the later latent infection, few new viruses are formed, but the virus remains hidden in the host cell’s chromosome as a latent virus.
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2 Ways in which HIV evades the host immune system:
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1. Integration: the virus gene can become fully integrated into the host DNA which makes the virus difficult to detect by the immune system. 2. undergoes rapid antigenic shift. as many as 1 million variants in asymptomatic patients in the early stages of the disease and as high as 100 million in the end stage patients.
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Clinical Findings: Human Immune Deficiency Virus (HIV)
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2-4 weeks after: fever, sorethroat and generalized lymphadenopathy (swollen painful lymph nodes). A rash may also occur on the trunk, arms and legs. resolves spontaneously in about two weeks.Antibodies typically appear in the blood 3-4 weeks after the infection. After this initial stage the virus will continue to replicate in the host producing 10 billion new virions each day for years. The greater the viral load, the more likely the individual will progress to symptomatic AIDS. The late stage is clinical AIDS and is manifested by the decline of CD4 cells to below 200/mm³
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What is the result f resuced T cells from AIDS?
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repeated opportunistic infections by various organisms. (common examples are pneumonia by Pneumocystis carinii or CMV, oral thrush by Candida albicans, diarrhea caused by Cryptosporidium.)
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Diagnosis: Human Immune Deficiency Virus (HIV)
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RNA Test: Blood test to detect early infection. It detects the genetic material produced by the HIV virus and is therefore a measure of the plasma viral load (quantity of virus circulating in the blood). This test is also used to monitor the progress of the disease. ELISA (enzyme-linked immunosorbent assay) and Western blot tests are used to detect levels of antibodies against the HIV virus.
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Treatment: Human Immune Deficiency Virus (HIV)
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1. Antiretroviral treatment will slow the replication:a. Reverse transcriptase inhibitors which inhibit viral replication: AZT and Epivirb. Protease inhibitors inhibit the protein called protease which is essential for the final assembly and maturation of the virus: Norvir.c. Entry inhibitors prevent the virus from fusing with the host cell membrane, which enables its entry to new cells: FuzeonDue to the high incidence of drug resistance, combinations of several drugs are used at the same time.2. Treatment of opportunistic infections.
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Prevention: Human Immune Deficiency Virus (HIV)
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Blood and body fluid precautions
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Describe: Herpes Simplex Virus type 1 (HSV-1)
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HERPESVIRUSES
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Disease: Herpes Simplex Virus type 1 (HSV-1)
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Herpes simplex labialis (cold sores), kerato- conjunctivitis.
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MOT / Pathology: Herpes Simplex Virus type 1 (HSV-1)
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cold sores / kerato- conjunctivitis: human reservoir and transmission is through saliva. Roughly 80% of people in the United States have antibodies against HSV-1. Infection usually occurs during childhood. the virus replicates at the initial site of infection, then migrates up the neuron and becomes latent in the trigeminal nerve ganglia.During latency most- but not all- the viral DNA is in the cytoplasm of the neuron.During reactivation, it migrates to the nucleus and replicates.Reactivation in the host may be caused by sunlight, hormonal changes, stress, trauma, or fever.
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Clinical Findings: Herpes Simplex Virus type 1 (HSV-1)
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cold sores / kerato- conjunctivitis: initial symptoms in children: fever, irritability and appearance of vesicular lesions in the mouth. resolve spontaneously in 2-3 weeks. Recurrent attacks: crops of vesicles commonly known as fever blisters or cold sores that appear around the lips and nose or eye. Blisters that affect the cornea will lead to scarring and blindness. blisters contain serous fluid and viral particles with cell debris. They are highly contagious.
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Treatment: Herpes Simplex Virus type 1 (HSV-1)
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cold sores / kerato- conjunctivitis: Antiviral: Acyclovir
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Prevention: Herpes Simplex Virus type 1 (HSV-1)
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cold sores / kerato- conjunctivitis: Avoid contact with vesicles or ulcers.
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Describe: Herpes Simplex Virus type 2 (HSV- 2)
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HERPESVIRUSES
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Disease: Herpes Simplex Virus type 2 (HSV- 2)
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Genital herpes
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MOT / Pathology: Herpes Simplex Virus type 2 (HSV- 2)
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Genital herpes: Human reservoir and transmission through sexual contact. virus replicates at the initial site of infection, then migrates up the neuron and becomes latent in the lumbar and sacral nerve ganglia. Reactivation also occurs as in type -1. Oral genital sexual practices can result in HSV-1 infection in the genitals and HSV-2 in themouth. This is the STD with the highest prevalence in the US. It is estimated that one out of five Americans is infected with the virus, and there are 45 million existing cases.
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Clinical Findings: Herpes Simplex Virus type 2 (HSV- 2)
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Genital herpes: Painful vesicular lesions of the male and female genitals and anal area. Asymptomatic infections may also occur in some individuals who become a source of infection to others.
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Treatment: Herpes Simplex Virus type 2 (HSV- 2)
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Genital herpes: Antiviral (Acyclovir) shortens the duration of the lesions and reduces the extent of shedding of the virus.
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Prevention: Herpes Simplex Virus type 2 (HSV- 2)
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Genital herpes: Avoid contact with vesicles or ulcers.
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Describe: Varicella Zoster Virus (VZV)
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HERPESVIRUSES
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Disease: Varicella Zoster Virus (VZV)
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Chicken pox (Varicella) – Shingles (Zoster)
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MOT / Pathology: Varicella Zoster Virus (VZV)
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Chicken pox (Varicella) – Shingles (Zoster): Humans are the natural reservoir and transmission is through respiratory droplets. It isa childhood disease. The virus spreads from the upper respiratory mucosa to the blood and causes the typical rash. The virus then becomes latent in nerve ganglia and if activated after several years, will present as shingles.
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Clinical Findings: Varicella Zoster Virus (VZV)
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Chicken pox (Varicella) – Shingles (Zoster): Chicken pox presents with fever and malaise followed by a generalized itchy vesicular rash. Varicella is usually mild in children and resolves within a few days. However serious complications such as pneumonia or encephalitis might occur. Shingles presents as a crop of vesicles along the course of a sensory nerve. It is usually associated with severe nerve pain that may remain even after the disappearance of the vesicles.
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Treatment: Varicella Zoster Virus (VZV)
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Chicken pox (Varicella) – Shingles (Zoster): No treatment other than symptomatic is necessary for chickenpox. Acyclovir is used to treat shingles together with pain medication.
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Prevention: Varicella Zoster Virus (VZV)
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Chickenpox vaccine is part of the routine childhood vaccination. Zostavax is a new vaccine that was licensed by the FDA in 2006 and is recommended for people 60 years and older to prevent against infection with shingles.
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Describe: Cytomegalovirus (CMV)
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HERPESVIRUSES
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Disease: Cytomegalovirus (CMV)
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Cytomegalic inclusion disease which is the most common cause of congenital abnormalities in the United States.
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MOT / Pathology: Cytomegalovirus (CMV)
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Cytomegalic inclusion disease: Humans are the natural hosts and transmission occurs by a variety of modes. It can be transmitted from the pregnant mother to her fetus via the placenta and is also secreted inbreast milk. In young children the most common MOT is the saliva. Later in life transmission is sexual and the virus is found in male seminal fluid and female cervical secretions. It can also be transmitted by blood transfusions and donated organs. CMV has a worldwide distribution and 80% of the adult population has antibodies against the virus.
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Clinical Findings: Cytomegalovirus (CMV)
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Cytomegalic inclusion disease: Infection of a pregnant mother will result in cytomegalic inclusion disease in the fetus which is characterized by microcephaly (small size of skull), seizures, deafness, jaundiceand hepatosplenomegaly (enlarged liver and spleen). It is also one of the leading causes of mental retardation in the United States. Immunocompromized patients will experience fever, lethargy, pneumonitis or hepatitis. AIDS patients will suffer intractable diarrhea. Infection in healthy children and adults is asymptomatic.
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Treatment: Cytomegalovirus (CMV)
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Cytomegalic inclusion disease: Antiviral (Ganciclovir)
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Prevention: Cytomegalovirus (CMV)
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Cytomegalic inclusion disease: Screening blood transfusions and organ donors for the virus.
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Describe: Epstein-Barr Virus (EBV)
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HERPESVIRUSES
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Disease:Epstein-Barr Virus (EBV)
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Infectious mononucleosis
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MOT / Pathology: Epstein-Barr Virus (EBV)
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Infectious mononucleosis: Humans are the natural host and transmission is by exchange of saliva-hence called the kissing disease. The saliva of individuals who have an active infection, or who are undergoing reactivation from a latent state is contagious. More than 90% of adults in the United States have antibodies.After the initial infection, the virus remains latent in B lymphocytes with possible reactivation and reappearance of the symptoms.
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Clinical Findings: Epstein-Barr Virus (EBV)
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Infectious mononucleosis: Fever, sore throat, lymphadenopathy (enlargement of lymph nodes), anorexia, and lethargy are the main symptoms. Spontaneous recovery occurs in 2-3 weeks.
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Treatment: Epstein-Barr Virus (EBV)
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Infectious mononucleosis: Symptomatic.
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Prevention: Epstein-Barr Virus (EBV)
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Infectious mononucleosis: Avoid contact whenever possible.
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How long for HIV to become aids
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10 years avg
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Describe: Hepatitis A virus (HAV)
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Hepatitis Virus
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Disease: Hepatitis A virus (HAV)
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Hepatitis A: Gastroenteritis
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MOT / Pathology: Hepatitis A virus (HAV)
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Hepatitis A: Human reservoir / fecal-oral transmission /Childrenaremore susceptible / Outbreaks from contaminated source of food or water. (Raw Oysters) / About 50-75% adults in USA have antibodies
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Clinical Findings: Hepatitis A virus (HAV)
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Hepatitis A: Most infections asymptomaticfever, nausea, anorexia, vomiting and jaundice dark urine, pale feces / Most cases resolve spontaneously in 2-4 weeks. / no chronic hepatitis A, nochronic carrier state / HAV does not leave any permanent liver damage / doesnot predispose to liver cancer
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Treatment: Hepatitis A virus (HAV)
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Hepatitis A: Symptomatic
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Prevention: Hepatitis A virus (HAV)
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Hepatitis A: Hep A vaccinePersonal hygiene
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Describe: Hepatitis B virus (HBV)
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Hepatitis Virus
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Disease: Hepatitis B virus (HBV)
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Hepatitis B:
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MOT / Pathology: Hepatitis B virus (HBV)
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Hepatitis B: Humans reservoir for HBV / blood and body fluids and transmission very small amounts of blood are infective (needlestick)
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Clinical Findings: Hepatitis B virus (HBV)
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Hepatitis B: Signs and symptoms of hepatitis / liver functions such as transaminase levels (AST and ALT) will be elevated - liver cell inflammation and damage.5% of patients become chronic carriers for variable lengths of time. high rate of hepatocellular carcinoma (liver cancer) which occurs inchronic carriers.
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Treatment: Hepatitis B virus (HBV)
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Hepatitis B: Symptomatic treatment. Alpha interferon for chronic infections.
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Prevention: Hepatitis B virus (HBV)
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Hepatitis B: Blood and body fluid precautionsHepatitis B vaccine (choldhood / healthcare)
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Describe: Hepatitis C virus (HCV)
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Hepatitis Virus
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Disease: Hepatitis C virus (HCV)
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Hepatitis C:
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MOT / Pathology: Hepatitis C virus (HCV)
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Hepatitis C: Human reservoir / blood and body fluids transmission / Injection drug users account for most of the new cases in the USA.
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Clinical Findings: Hepatitis C virus (HCV)
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Hepatitis C: Signs and symptoms of hepatitis. 75% become chronically infected - continue to shed the virus for at least one year.Chronic carriers are much higher thanhepatitis B cases.It can also predispose to hepatocellular carcinoma.Some infections are asymptomatic and only detected by the presence of antibodies inthe blood.
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Treatment: Hepatitis C virus (HCV)
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Hepatitis C: Alpha interferon reduces viral replication.
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Prevention: Hepatitis C virus (HCV)
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Hepatitis C: No vaccine. Blood and body fluid precautions. Donated blood containing HCVantibodies must be discarded.
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Describe: Human Papillomavirus (HPV)
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Hepatitis Virus
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Disease: Human Papillomavirus (HPV)
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Skin, plantar, genital warts: Genital warts predispose to cancer of thecervix in females.
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MOT / Pathology: Human Papillomavirus (HPV)
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Skin, plantar, genital warts: Skin warts are transmitted by skin contact. HPV is the STD with the highestincidence in the US. There are an estimated 6.2 million reported new cases every year.
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Clinical Findings: Human Papillomavirus (HPV)
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Skin, plantar, genital warts: Skin warts Genital warts seen on the female vulva or cervix, male penis and anal area. In the female cervix the wart may grow into a large cauliflower-like mass that easily bleeds on contact e.g. afterintercourse. Masses like these may be precancerous and are treated very seriously.
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Treatment: Human Papillomavirus (HPV)
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Skin, plantar, genital warts: Liquid nitrogen is commonly used to remove skin warts. Genital warts can also bechemically removed, or surgically if large. Interferon is used to prevent recurrence.
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Prevention: Human Papillomavirus (HPV)
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Skin, plantar, genital warts: Avoid contact.Gardasil vaccine available in 2007 and recommended for femalesbetween 9-26 years old
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Describe: Influenza Virus
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Hepatitis Virus
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Disease: Influenza Virus
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Influenza:
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MOT / Pathology: Influenza Virus
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Influenza: Droplet. Influenza A virus causes worldwide epidemics and pandemicsInfluenza B causes major outbreaks. enveloped virus with 2 types of protein spikes in its membrane:heamagglutinin (HA)by which it attaches to the host cellneuroaminidase (NA) enzyme that breaks down the host cell toallow virions to be released.The influenza virus is constantly changing its antigenicity by reassortment of HA andNA, a phenomenon called antigenic shift. This is the reason why a new vaccine isprepared every year.In the 1918 influenza epidemic, more Americansdied than in WW1, WW2, Korean War, and Vietnam War combined.
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Clinical Findings: Influenza Virus
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Influenza: After 24-48 hours, fever, myalgias (muscle pains), sorethroat, headache, and cough occur. Symptoms subside within a week. Pneumonia is uncommon but may be life threatening to the elderly or those with chronic illnesses of the heart and lungs.
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Treatment: Influenza Virus
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Influenza: Several medications may be used to shorten the duration but the emphasis is onprevention.
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Prevention: Influenza Virus
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Influenza: Flu vaccine which is reformulated annually to contain the current antigenic strains.
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Describe: Measles Virus
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PARAMYXOVIRUSES
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Disease: Measles Virus
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Measles (Rubeola):
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MOT / Pathology: Measles Virus
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Measles (Rubeola): Humans are natural host transmission is by respiratory droplets from patientsduring the early prodromal stage.Lifelong immunity occurs in individuals who had the disease.
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Clinical Findings: Measles Virus
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Measles (Rubeola): Clinical FindingsAfter a two-week incubation period, prodromal symptoms such as fever, malaise, runny nose, cough, and conjunctivitis (causing photophobia) During this stage, Koplik’s spots which are bright red lesions with a white central spot are seen on thebuccal mucosa. This is a diagnostic sign.This is followed by the appearance of a maculopapular rash that appears on the face and then extends to the rest of the body, including palms and soles. Symptoms subsidespontaneously in a few days.Uncommon severe complications such as encephalitis may occur.
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Treatment: Measles Virus
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Measles (Rubeola): Symptomatic
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Prevention: Measles Virus
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Measles (Rubeola): MMR vaccine
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Describe: Mumps virus
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PARAMYXOVIRUSES
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Disease: Mumps virus
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Mumps:
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MOT / Pathology: Mumps virus
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Mumps: Humans are the natural host and transmission is by respiratory droplets.The virus spreads through the blood to infect the parotid glands, testes, ovaries, and sometimes the meninges.Lifelong immunity occurs in individuals who had the disease.
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Clinical Findings: Mumps virus
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Mumps: Prodromal symptoms of fever, malaise and anorexia are followed by tender swelling of the parotid gland either unilateral or bilateral. It resolves spontaneously in one week.If orchitis (inflammation in testis) occurs in older boys, it may lead to sterility.
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Treatment: Mumps virus
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Mumps: Symptomatic
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Prevention: Mumps virus
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Mumps: MMR vaccine
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Describe: Respiratory Syncytial Virus (RSV)
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PARAMYXOVIRUSES
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Disease: Respiratory Syncytial Virus (RSV)
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Pneumonia / bronchiolitis in infants:
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MOT / Pathology: Respiratory Syncytial Virus (RSV)
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Pneumonia / bronchiolitis in infants: Respiratory droplets and hand-to nose or hand-to mouth. RSV causes outbreaks ofrespiratory infections every winter in infants especially hospitalized ones.
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Clinical Findings: Respiratory Syncytial Virus (RSV)
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Pneumonia / bronchiolitis in infants: Bronchiolitis which manifests with cough, difficulty breathing and wheezing. It alsogives rise to symptoms of pneumonia.
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Treatment: Respiratory Syncytial Virus (RSV)
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Pneumonia / bronchiolitis in infants: Symptomatic and with aerosols to open the bronchi.
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Prevention: Respiratory Syncytial Virus (RSV)
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Pneumonia / bronchiolitis in infants: Hand washing and use of disposable gloves in hospital settings.
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Describe: Rubella Virus
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TOGAVIRUS
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Disease: Rubella Virus
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Rubella (German measles):
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MOT / Pathology: Rubella Virus
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Rubella (German measles): Respiratory droplets and transplacental. Humans are the natural host. The virusinitially replicates in the nasopharynx and local lymph nodes. From there it spreads to the blood and internal organs and skin.
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Clinical Findings: Rubella Virus
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Rubella (German measles): A brief period of fever and malaise is followed by maculopapular rash that starts onthe face and extends to the extremities. Posterior auricular lymphadenopathy ischaracteristic. The virus also has a teratogenic effect. If a non-immune pregnant woman is infectedin the first trimester, significant congenital malformations can occur to her fetus.
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Treatment: Rubella Virus
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Rubella (German measles): Symptomatic
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Prevention: Rubella Virus
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Rubella (German measles): MMR vaccine
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Describe: Variola
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TOGAVIRUS
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Disease: Variola
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Small pox: the only disease that has been successfully eradicated from the face of the earth by global vaccination. The last case was reported in Somalia in 1977.
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MOT / Pathology: Variola
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Small pox: Respiratory droplets. The virus reaches the blood and spreads to the skin.
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Clinical Findings: Variola
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Small pox: Fever, malaise and rash that evolves through the stages of macules, papules, vesicles, pustules, and finally a crust. When the scab falls, it leaves a disfiguring scar.
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Prevention: Variola
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Small pox: The disease has been eradicated by vaccine which is no longer needed for the general public. It is given to military personnel because the virus might be used as an agent of bioterrorism.
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Describe: Rabies Virus
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TOGAVIRUS: Bullet-shaped virus.
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Disease: Rabies Virus
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Rabies:
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MOT / Pathology: Rabies Virus
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Rabies: Transmission is through the bite of a rabid animal such as dog,cat, raccoon, skunk, or bat. The virus multiplies locally at the bite site and then travels through the nerve axons to the CNS. In the CNS it causes encephalitis which results in death of neurons leading to the appearance of a characteristic cytoplasmic inclusion called Negri body. This is a diagnostic finding when examining brain tissue of infected animals or humans. The virus then travels down to the salivary glands (and other organs) and is secreted in saliva.
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Clinical Findings: Rabies Virus
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Rabies: Fever and anorexia (loss of appetite) for a few days after the bite. followed by confusion, lethargy (weakness or tiredness), and painful spasm in the throat muscles with swallowing which causes patients to avoid drinking. This aversion from water has beentermed hydrophobia. If not treated, patients may die.Rabid animals will manifest aggressive behavior due to the encephalitis withexcessive salivation later.
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Treatment: Rabies Virus
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Rabies: Postexposure rabies vaccine and rabies immune globulin are given. Immediate wound cleaning.
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Prevention: Rabies Virus
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Rabies: Rabies vaccine is routinely given to domesticated animals and individuals at risk such as veterinarians and zookeepers. It is also given to individuals bitten by rabid animals.
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Describe: Poliovirus
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ENTEROVIRUSES
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Disease: Poliovirus
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Poliomyelitis:
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MOT / Pathology: Poliovirus
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Poliomyelitis: Fecal-oral route, humans are the natural reservoir. The organism replicates in the intestine and spreads through the blood to the CNS. It destroy motor neurons in the brain which leads to muscle paralysis, and may travel to the brain stem and lead to respiratory paralysis and death.
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Clinical Findings: Poliovirus
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Poliomyelitis: Flaccid asymmetrical paralysis in certain groups of muscles, mainly in lower limbs / accompanied by muscle wasting
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Treatment: Poliovirus
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Poliomyelitis: None
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Prevention: Poliovirus
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Poliomyelitis: Two types of vaccines are available: IPV (inactivated polio vaccine) is the currently preferred vaccine in the USA. A live attenuated vaccine (Sabin) is available in other countries.
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Describe: Rotavirus
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ENTEROVIRUSES:
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Disease: Rotavirus
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Gastroenteritis: the most common cause of gastroenteritis in youngchildren
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MOT / Pathology: Rotavirus
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Gastroenteritis: Fecal oral. It is very widespread and most children are immune by the age of 6 years.
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Clinical Findings: Rotavirus
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Gastroenteritis: Nausea, vomiting and watery diarrhea which may be severe leading to dehydration and electrolyte imbalance.
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Treatment: Rotavirus
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Gastroenteritis: Fluid and electrolyte replacement.
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Prevention: Rotavirus
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Gastroenteritis: Personal hygiene FDA approved a live oral vaccine in 2006 called Rota Teq to be added to the routine childhood immunizations.
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Describe: Adenovirus, Coronavirus, and Rhinovirus
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ENTEROVIRUSES
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Disease: Adenovirus, Coronavirus, and Rhinovirus
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Common cold:
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MOT / Pathology: Adenovirus, Coronavirus, and Rhinovirus
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Common cold: Droplet aerosols but also finger-to-nose transmission. In the latter, droplets deposited on hands or on a surface can be picked up by fingers and introduced to the nose.
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Clinical Findings: Adenovirus, Coronavirus, and Rhinovirus
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Common cold: Mild upper respiratory symptoms such as sore throat, runny nose, cough and headache.
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Treatment: Adenovirus, Coronavirus, and Rhinovirus
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Common cold: None needed, the disease is self-limiting.
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Prevention: Adenovirus, Coronavirus, and Rhinovirus
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Common cold: Prevention against exposure to aerosols from infected patients and hand washing.
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Disease: ARBOVIRUSES
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Eastern Equine Encephalitis (EEE) – common in FloridaWestern Equine Encephalitis (WEE)St. Louis Encephalitis (SLE)
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Describe: ARBOVIRUSES
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Arthropod-borne viruses are transmitted by arthropods, mainly mosquitoes. The wild birds harbor the virus, and mosquitoes are the vector between the birds and humans. Forthe lifecycle of the arbovirus to be completed, it must multiply both in the human and in the mosquito.
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MOT / Pathology: ARBOVIRUSES
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EEE, WEE, SLE:The mosquito draws the virus from wild birds during its blood meal. The virusreplicates in the mosquito for about 1-2 weeks and reaches its salivary glands. The infected mosquito inoculates the virus into horses or humans during its next blood meal.
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Clinical Findings: ARBOVIRUSES
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EEE, WEE, SLE: Encephalitis characterized by fever, headache, nausea, vomiting, and changes inmental status such as confusion, stupor, which may progress to coma. Mortality rate is high in EEE.
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Treatment: ARBOVIRUSES
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EEE, WEE, SLE: Symptomatic
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Prevention: ARBOVIRUSES
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EEE, WEE, SLE: Personal protection against mosquitoes. Mosquito control by spraying, draining standing water…
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Disease: Norwalk Virus
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Gastroenteritis: the most common cause of gastroenteritis in young children
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MOT / Pathology: Norwalk Virus
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Gastroenteritis: Transmission is fecal-oral Norwalk virus causes outbreaks of gastroenteritis in schools, camps, and on cruise ships. It was named after Norwalk, Ohio where an outbreak in a school occurred in 1969.
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Clinical Findings: Norwalk Virus
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Gastroenteritis: Nausea, vomiting and diarrhea that spontaneously resolve in 12-24 hours
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Treatment: Norwalk Virus
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Gastroenteritis: Supportive
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Prevention: Norwalk Virus
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Gastroenteritis: Hygiene.
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