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Hepatitis and Herpes Viruses - tpida.org Flipbook PDF
Hepatitis and Herpes Viruses These two virus groups are very diverse, but cause much human morbidity and mortality
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Hepatitis and Herpes Viruses These two virus groups are very diverse, but cause much human morbidity and mortality
Liver Functions
• Performs 3 major functions:
– Regulation: of blood composition • glucose levels, pyruvate levels, protein & fat concentrations
– Metabolism: processes nutrients adsorbed from intestine • converts them into useful components, stores Vitamins (especially A), and minerals, (especially iron), manufactures, serum albumin, cholesterol, clotting factors, etc.
– Detoxifies: removing drugs, alcohol, & potentially harmful chemicals, excreting them in urine or feces • Removes bilirubin--jaundice and icterus
Hepatitis • Cholestatic
• Any of 5 hepatotropic viruses • Acute – abrupt, malaise, fatigue, elevated liver enzymes, dark urine, light stools, icterus
• Anicteric – mild, some enzyme elevation, no icterus
• Fulminant – severe hepatitis, liver failure, high serum enzymes, fatal without liver transplant
– acute obstructive hepatitis, deep jaundice, pruritus,slow recovery
• Chronic – persistent hepatic injury, elevated serum enzymes, often asymptomatic
• Cirrhosis – end-stage liver disease, loss of liver function, fatal
• Primary liver cancer – due to chronic/cirrhosis
Hepatitis A • Extremely infectious – highly stable virus – oral/fecal/fomite • food, minimal contamination needed • poor sanitation
• From GI to liver – virus in feces – also in blood
• Asymptomatic in children • Serious hepatitis in adults – over 50 years may be fulminant
• World wide
– due to immune response
– American adults are immuno-naïve – Greatly at risk visiting underdeveloped countries
• Acute hepatitis
• New vaccine available
• liver necrosis
– 70% jaundice
Hepatitis B • Replication in liver • Major antigen stored in cells--HBsAG – immune avoidance?
• Parental transmission – “serum hepatitis” – blood, I.V. drug use – needle sticks
• Virus in semen, vaginal secretions, – sexual transmission • especially homosexual
– neonatal infections
• 10 weeks incubation • pathology due to immune response – 70% mild disease – 30% acute disease – 10% no effective immunity--chronic • chronic is silent • >50% cirrhosis • final stage=cancer
• type III hypersensitiv. – glomerulonephritis – polyarthritis
• High in China, Africa
Hepatitis B, continued
• Liver infections seed blood @ 107 viruses per mL!!
– Infectious dose is very low—transmission is high • Razors, tooth brushes, tattoos, etc.
• Hepatocellular carcinoma – one of most common • 1 million deaths/annum
– nearly always fatal – China, Africa, SE Asia, – Chronic > Cirrhosis > Cancer
– Coinfection with HCV is greater risk
HBV from tattooing needle virus is highly infectious
• “Non A, Non B” • rapid mutations impede immunity • Parental exposure
Hepatitis C
– sexual less important
• Anicteric hepatitis – rarely acute – fatigue & malaise – some autoimmune disorders – 20% lead to cirrhosis, cancer • Liver transplants common
– >20% i.v. drug users
urobilin
Hepatitis D • “Delta agent” – a defective virus – Needs HBV “helper” – RNA surrounded by delta protein and shell of HBsAG – Must be co-infected • high risk to fulminant • rapid progress to cirrhosis • no higher risk for cancer
– Distribution not same as HBV • S. America, Middle East, Africa
Scleral icterus
Hepatitis E • Unrelated to others • Similar to HAV • oral/fecal – See in developing countries – Strangely fatal in 1525% pregnant women – Acute and epidemic
Jaundice
Herpes Viruses Herpo means to “creep”, known since ancient times. Nearly all humans have at least one herpes infection
Herpes Diseases • • • •
All display latency DNA viruses, most form proviruses most often integrate in neural cells lytic state induced by stress, malnutrition, changes in immune status, etc. • most infections are asymptomatic, but may cause serious diseases, even cancer.
Cytomegalovirus, CMV • Large spectrum – asymptomatic to fatal – immunosuppressed • transplant patients • AIDS patients
• Enlarges cells • Congenital, perinatal and post natal – 40% Europe, 100% Africa – 30% homosexual males have in semen • sexually transmitted especially in homosexuals
Fatal neonatal disseminated CMV
CMV continued • Most asymptomatic – symptoms look like IM – Congenital are most serious • encephalitis, mental retardation, liver damage,, chorioretinitis, may be fatal, depends on maternal immunity
– AIDS • fevers, pneumonitis, hepatitis, encephalitis • serious complication of AIDS
– Transplant patients • increasing problems
Congenital Cytomegalovirus infection with numerous birth defects
Epstein-Barr Virus & Diseases • Virus originally isolated from Burkitt’s lymphoma--but IM was first recognized dis. • Ubiquitous B lymphotropic herpes virus • World wide seroconversion = 80-90% • As with others, both lytic and latent phases • Latency in immortalized B-lymphocytes • Numerous EBV neoplasms noted – Burkitt’s and other lymphomas, nasopharyngeal carcinoma, etc.
• Range of diseases not yet defined
Biology of Epstein-Barr Virus • DNA virus, with adult seroconversion = 90%+ • Primary infection in children is asymptomatic, in adults it is IM • Saliva transmission • Mucosal cells introduce to blood, to B-cells – polyclonal stimulation – B-cell immortalization – heterophil antibodies – Neoplasms
Abnormal B-cells with EBV
Infectious Mononucleosis • Incubation = 4-7 weeks • Results in IM syndrome – fever, sore throat, lymphadenopathy, hepatosplenomegaly, hepatitis – fevers last 1-3 wks – 50% splenomegaly – rash occurs with antibiotic treatment (for mistaken Strept infection) – Major problem in AIDS
IM inflamed throat
• Diagnosis: – lymphocytosis, atypical lymphocytes, heterophil antibody
Antibiotic induced rash in IM
Herpes Simplex 1 & 2 • • • •
Seemingly more cases in last 100 years HSV-I anciently noted, HSV-II since 1800s Similar viruses, but genetically distinct Biology is similar, lytic followed by neural latency • HSV-1 is virus of ‘cold sores’ • HSV-2 venereal disease – but can cross infect
Herpes Simplex, Epidemiology
• World -wide prevalence • lesions highly infectious – from lips to hands to eyes common (leave cold sores alone!) – antibodies will not prevent recurrence
• Pathogenesis: – Primary replication – Dorsal root ganglion – Recurrence from sensory neurons – may lead to viremia and systemic hemorrhagic necrosis
Gingivostomatitis, primary lesion
Herpes simplex clinical picture • Primary lesion: HSV-1 – children-asymptomatic – gingivostomatitis • drooling, fever, pain in mouth, edema, vesicles lymphadenopathy
– Recurrences: Herpes labialis • cold sores, fever blisters • stress, UV-light, menses, trauma • edge of lip • usually in same place • vesicular fluid is highly infectious • ulceration & healing takes about 10 days
Herpes labialis
•
Herpes simplex-2 Genital lesions – symptoms from notable to debilitating – modified by HSV-1 – 2-7 days incubation – multiple painful lesions • penile or vaginal • fevers, malaise, lymphadenopathy, • recurrences, 5-8/yr • viral shedding between lesions! (importance?) • rectal & perianal becoming common* • Psychological scarring – nothing can be done – endangers partners
Herpes on penis
Herpes, vulva
Herpes simplex-2, continued – Accelerates HIV to AIDS, – Enhances transmission – some implication in cervical cancers • cervical dysplasia*
– Serious complications in congenital infections • blindness, meningitis, disseminated necrosis of skin, • potentially fatal • abortions & premature births
Vulvovaginitis in a child
– C-section indicated Herpes on cervix, cancer? during active infections Eczema herpeticum, necrotic ulcers
Other Herpes Manifestations • Herpetic whitlow – herpes fingers • occupational hazard of dental & medical • CNS herpes – mortality=70% • Eye herpes – usually from lips via hands – causes blindness • Neonatal herpes – potentially fatal – C-section indicated in active genital herpes • Immunocompromised***
Herpetic whitlow
Eye herpes, from fingers
Varicella/Zoster • This herpes virus causes two distinct, but linked diseases: varicella (chickenpox) and herpes zoster (shingles) • In USA over 90% infection rate • Waiting for the other shoe to drop???
Epidemiology of varicella/zoster • Global transmission – winter/spring more – aerosolization – vesicular fluid viral rich,crusty lesion viral poor – Infections may be fatal • immunocompromised • hemorrhagic varicella
Varicella
– in utero transmission • initial = shingles
– Shingles all ages, but • by 85, 50% have had • alterations in CMI
Immunocompromised varicella Varicella scars
Pathogenesis of varicella/zoster • Respiratory>viremia>skin • Vesicles initially clear, then cloudy as PMNs clear virus, then crusts over • Virus retreats to basal ganglia = latency • reduced CMI = recurrence • virus travels along sensory nerves to form skin lesions • Nerves show extensive inflammation, neural hemorrhagic necrosis • Extremely painful – pain may last for months with nerve damage
Shingles along nerve tract
Shingles from facial nerve Shingles and leukemia
Clinical Picture
• Chickenpox: lesions: – skin, mouth, vagina, rectum, conjunctiva – average 200 – sore throat, fever, pruritus, anorexia
• Neonatal: in 1st trimester: – chorioretinitis, deafness, brain atrophy – if mother become infected within 5 days • 20% neonatal, of which 35% fatal
• Shingles: AIDS, bad!
Fatal varicella Trigeminal nerve, eye shingles Disseminated from Breast cancer