clinically important viruses II

clinical presentation of viral hepatitis

symptomatic

• jaundice - build up of bilirubin

• fever

• malaise/flu like illness

• dark urine - bilirubin

• pale greasy stools - need to absorb fats

summary of hepatitis viruses

hepatitis D

small enveloped RNA virus

needs HBV to replicate so you cant have it unless you have hepatitis b - coinfection or superinfection, worse prognosis

transmission route as HBV but highest risk is bloodborne e.g. shared needles IVDU rather than sexual

prevention, treatment and management of Hepatitis A

immunization: inactivated (not live) vaccine, passive immunization indicated in those with no history of HepA (within 2 weeks of exposure)

prevention: avoiding risk factors e.g. contaminated food, water in endemic areas

prevention, treatment and management of Hepatitis E

immunization: only in China

antivirals: Ribavirin indicated in transplant patients, reduce immunosuppression also

prevention: avoiding risk factors (as above)

prevention, treatment and management of hepatitis B

varies from low to high prevalence

immunization: of cloned surface antigen (HBsAg), three shots required, requires antibody titer monitoring, booster in 10% needed, High risk groups e.g. HCWs

prevention: avoiding risk factors e.g. clean needles, condoms. Patient education

antivirals: role limited as cant eradicate - interferon alpha

patients are also monitored for cancer and ultimately may need transplant

prevention, treatment and management of Hepatitis C

immunization: none

prevention: avoiding risk factors e.g. clean needles, condoms. Patient education

antivirals: always changing - interferon combined with Ribavirin antiviral. Previous mainstay of treatment 6-12 months

Measles

measles is an RNA virus with 1 stereotype, a member of the genus morbillivirus

humans, the only natural host

measles transmitted by direct contact with infectious droplets or less commonly, by the airborne speed

measles clinical features

initial viraemia with increases temperature (39 degrees)

miserable child, sore eyes, Koplik spots

rash: 2-4 days after prodo,e or 14 days after exposure, becomes confluent, begins on face and head, persists for 5-6 days and fades in the order of its appearance

lab diagnosis involving PCR

Koplik spota

minute bluish-white spots on an erythematous base of the buccal mucosa

resembling salt crystals

complications of measles

morbidity is approx. 10% of cases

measles associated pneumonia

involvement of CNS resulting in encephalitis - can have neurological sequalae, fatality rates increase

mumps epidemiology

transmission - respiratory droplets

temporal pattern - peak in late winter/spring

incubation period - 16-18 days

communicability - 3 days before to 4 days after onset of illness

mumps clinical features

non-specific prodrome of low-grade fever, headache, malaise, myalgias

Parotitis (swelling of partoid gland) in 30%-40%

up to 20% of infections are asymptomatic

may present as lowers respiratory illness, particularly in pre-school childeren

lab diagnosis-PCR

complications of mumps

CNS involvement

orchitis

pancreatitis

deafness

death

Rubella clinical features

prodrome of low grade fever

lymphadenopathy in second week

maculopapular rash 14-17 days after exposure

rubella epidemiology

transmission - respiratory

temporal pattern - peak in late winter and spring

incubation period - 14-23 days

communicability - 7 days before to 5-7 days after rash onset

Rubella complications

arthralgia and arthritis (mainly adult females)

post-infectious encephalitis

hemorrhagic manifestations

conjunctivitis

orchitis

congenital rubella syndrome

prevention and management of measles, mumps and rubella

prevention

• measles: single room isolation, with air borne precautions as highly transmissible

• mumps and rubella: droplet precautions

vaccination

• live MMR vaccine highly protective against measles

• in childhood schedule of vaccinations

contradicted in

• patients that experienced allergic reaction to previous does noted

• pregnant women

  • immunosuppressed or immunocompromised

herpes viruses - classification

1. Herpes simplex virus, type 1 (HSV1)

2. Herpes simplex virus, type 2 (HSV2)

3. Varicella zoster virus (VZV)

4. Cytomegalovirus (CMV)

5. Epstein Barr virus (EBV)

6.Human herpes virus 6 (HHV 6)

7.Human herpes virus 7 (HHV 7)

8.Human herpes virus 8 (HHV 8)

herpes basic features

latency characteristic

re-activation and recurrent infections precipitated by immunosuppression, stress and other infections

HSV and VZV in nerve cells e.g. trigeminal

EBV and CMV in lymphocytes

large enveloped double standard DNA viruses

DNA core surrounded by icosahedral capsid

enclose by glycoprotein-containing envelope

herpes viruses genome encode enzymes e.g. DNA polymerase that promotes viral DNA replication

some genes homologous with human chromosome

DNA replication and assembly of capsid; nucleus

virus released by exocytosis or lysis of cell

can cause: lytic, latent or immortalizing (EBV) infections

huma hyperviruses

herpes simple virus 1

vesicular lesions

• painful and filled with white fluid

• the lesions ulcerate rapidly

• associated with painful local lymphadenopathy

primary herpes

• fever, malaise, myalgia, painful local lymphadenopathy; vesicular lesions can be widely distributed

recurrent herpes

• localized lesions typically at the mucutaneous junction. recurrent episodes are typically less severe than the primary episode