Misc Viruses FINAL
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Clinical Causes Fifth Disease (Erythema Infectiosum) Miscellaneous viruses features Also causes aplastic anemia in pple with SSA, and fetal infections like hydrops fetalis 1st phase Important viruses from the Parvovirus family Viraemic phase B19 Virus Virus present in upper respiratory tract (site of shedding) Virology Virus Family Parvovirus Symptoms occur at the end of 1st week (constitutional symptoms) Very small virus (22 nm only) - Fever - Malaise Genotype - Myalgia Ss DNA - Chills Simplest DNA animal viruses. - Itching Negative strand DNA NO VIRION polymerase 2nd phase mediated by immune complexes Icosahedral capsid Rash in 1/3 of patients Envelope “Slapped cheek” appearance Small, naked particles (NON ENVELOPED) Rash appears particularly on the face This is the most characteristic appearance Replicate autonomously in rapidly dividing cells Differential diagnosis is child abuse Virus that lives only in human is Parvovirus B19 Rash can also appear on the trunk Only one serotype Has a reticulated lacy appearance Replicative After adsorption to host cell receptors, virion penetrates and moves to nucleus Pathogenesis cycle Replication occurs in nucleus Infects mainly 2 types of cells Single stranded genome DNA has hairpin loops at both ends providing double stranded areas for RBC precursors (erythroblasts) in the BONE MARROW aplastic anaemia cellular DNA polymerase to initiate synth of progeny genomes ENDOTHELIAL CELLS in blood vessels accounts in part for rash in erythema infectiosum Viral mRNA is synth by cellular RNA polymerase from Double stranded DNA intermediate Immune complexes composed of virus and IgM or IgG also contribute to pathogenesis of rash and to arthritis seen in some adults infected by B19 Progeny virons are assembled IN THE NUCLEUS Infection provides LIFELONG immunity against infection B19 only replicates when cell is in S phase. Which explains why it is only replicating in RBC precursors, BUT not in mature RBCs Hydrops fetallis manifests as massive edema of the fetus This is secondary to congestive heart failure ppt by SEVERE ANEMIA caused by death of parvovirus Epidemiology Transmission B19 infected ERYTHROBLASTS in FETUS Transmitted mainly by o Body fluids o Blood o Vertically from mother to fetus (transplacental also occurs) Mainly by respiratory route Symptoms usually appear within 4 days to 2 weeks after exposure Parvovirus infection is common in childhood Most infections are asymptomatic. B19 infection occurs worldwide About ½ the pple in US older than 18 have antibodies Humans are natural reservoir Animals not a source of human infection Printed with FinePrint - purchase at www.fineprint.com 4 main clinical presentations (5 if include chronic infection) Complications Special patients with B19 infection Disease Group affected Elaboration Erythema Children Mild disease primarily of childhood Because the B19 targets human erythroid progenitor cells infectiosum Char bright red rash most prominent on Cause lysis of cells leading to anaemia. cheeks Can also affect lymphocytes, granulocytes and platelets. Accompanied by Low grade fever Runny nose Hence must consider these patients Sore throat Especially in chronic anemia and pregnant women Lacy less intense erythematous rash appears on body Patient group Complications Patients with chronic Can cause Transient Aplastic Crisis Symptoms resolve in about 1 wk haemolytic anaemia (e.g. Aplastic anemia due to the aplasia of erythroid progenitors sickle cell disease or Other rashes thalassemia Can cause reticulocytosis (reticulocytes are one of the cells in Measles erythrocyte development) Rubella SSA is more common in Scarlet fever the Negroid races This is because Chronic haemolytic anemia requires a physiological Roseola response to produce more red blood cells from the bone marrow. Thalassemia is more However, B19 can cause lysis of cells thus aggravating chronic common in Asian haemolytic anemic condtions) Aplastic Children with chronic anemia due Transient but severe aplastic anemia (aplastic anemia to SSA, thalassemia, crisis) when infected populations, might confer spherocytosis some protection against malaria. Pple with normal RBC do not have clinically apparent anemia, but RBC precursors are still affected Immunocompromised Can cause severe aplastic anemia patients st nd Fetal infections Woman infected in 1 or 2 Virus crosses placenta and infects fetus trimester of pregnancy Pregnant patients (1st Can cause severe anaemia in fetus (non-immune hydrops fetalis) Infection in 1st trimester trimester > 2nd trimester) Fetal death Fetus can go into severe cardiac failure (chronic cardiac failure) This leads to generalized chronic edema Not an important cause of congenital Leading to hydrops fetalis abnormalities because fetus dies when Leads eventually to spontaneous abortion infected early in preg Cancer patients This is because the bone marrow cells are trying to replicate to 2nd trimester replace the stuff that is destroyed by chemotherapy Hydrops fetalis 3rd trimester Not result in important clinical findings Arthritis B19 infection in adults esp women Causes arthritis Involving small joints of hands and feet BILATERALLY Resembles rheumatoid arthrititis Other infections that cause immune complex related arth 1. hep B 2. rubella CHRONIC B19 Pple with immunodeficiencies esp • Chronic anemia infections • HIV infection • Leukopaenia • Chemotherapy • Thrombocytopaenia due to chronic • Tpt patients infection S Printed with FinePrint - purchase at www.fineprint.com Lab diagnosis Viral culture and isolation is NOT possible Virus is difficult to grow. Can be isolated from throat swabs BUT not usually done Serology Hence diagnosis depends on serology Usually dx by detecting IgM abs IgM appears 4 - 7 days IgG appears 7 - 10 days later and persists for years (unsure if this gives long-term protection) In the case of Pregnancy: Tests for mother Mother’s Serology IgM and IgG (rising titres) PCR - detect B19 DNA in maternal serum Tests for fetus Ultrasound screening for non-immune hydrops. Percutaneous umbilical blood sampling (PUBS) – this is a more invasive procedure Molecular methods PCR In immunocompromised, abs may not be detectable Hence can detect viral DNA in blood by PCR methods Fetal infection can also be det by PCR analysis of amniotic fluid Management Treatment and Control No known specific treatment (not needed in most cases) Pooled immune globulins may have beneficial effect in chronic infection with immunodeficient patients. No chemoprophylaxis either Blood transfusion for transient aplastic crisis In the case of Fetal infection 1.Watchful waiting (conservative management) 2.High-dose IgG therapy 3.Intrauterine fetal transfusion Vaccine Not available yet PREVENTION IS THE SAFEST Avoid exposure during pregnancy Printed with FinePrint - purchase at www.fineprint.com Pox virus induced diseases Genus Virus Primary host Disease Orthopoxvirus Variola Smallpox Humans Vaccinia Smallpox vaccination Humans This was very useful for vaccination against small pox Monkey pox Monkey Human infections rare, localized lesions Cowpox Cows Parapoxvirus Orf Sheep Human infections rare Localized lesions Milker’s node Cows More important for Australia and New Zealand Unclassified Molluscum Many benign skin nodules contagiousm Humans Tanapox Monkeys Human infections rare Localized lesions Yabapox Monkeys Printed with FinePrint - purchase at www.fineprint.com Transmission Transmission Important Poxviruses Infection transmitted by respiratory route from Spread by direct contact or fomites (towels, lesions in respiratory tract swimming pools) Variola Virus (smallpox virus) Molluscum contagiosum Respiratory aerosols Virology Virus family May be transmitted from Poxviruses OR BY DIRECT contat with virus either in skin - Skin to skin Brick shaped particles containing double stranded DNA, a disk shaped core within a DOUBLE lesions or on fomites such as bedding - After sexual intercourse (sexually transmitted) membrane and a lipoprotein envelope - Tends to occur in children Features of the virus Tm by close personal contact Large virus: 250 - 300 nm (the largest and most complex viruses known) Pathogenesis Small pox begins when virus infects upper Have been known about for centuries respiratory tract and local LN Viral genome Then enters the blood (10 viraemia) Double-stranded DNA virus Has a DNA dependent RNA polymerase Internal organs are infected Replicates in the cytoplasm and does not have access to cellular RNA polymerase which is located in the nucleus Virus then REENTERS the blood and spreads to the skin Smallpox has a single stable serotype which was key to the success of the vaccine These EVENTS OCCUR DURING THE Easy to grow in the lab INCUBATION PERIOD. WHEN PATIENT IS STILL WELL. Poxviruses have their specific animal hosts Rash is a result of the viral replication in skin Characteristics of pox infection followed by damage by cytotoxic T cells attacking Infections mostly characterised by a rash virus infected cells Important Antigen features Immunity following small pox is lifelong Antigenically, poxviruses are very complex, inducing both specific and cross-reacting antibodies Immunity following vaccination is 10 years Epidemiology Smallpox has now been eradicated - the last Human disease of worldwide distribution Clinical Incubation period Incubation period: naturally occurring outbreak of smallpox was in This will be commonly seen in GP practice features During 12-day incubation, virus distributed to 1 week to 6 months Somalia on 26th October 1977. internal