Viral infections of the skin, muscle and blood stream. Flashcards
Measles (Rubeola virus)
CHARACTERISTICS
- Paramyxovirus
- Genus:Morbillivirus
- ss RNA
- important cause of vaccine preventable death. most cases in US were from imported measels and those caused secondary imported cases.
IMPORTANT PROTEINS
- hemagglutinin protein
- fusion protein
- matrix proteins
TRANSMISSION
contagious 5 days before rash to 4 days after
incubation 7-18 days. has a winter spring 1-3 year cycle
EPIDEMIOLOGY: infects young ages in developing world, infection rate 85 % 5% asymptomatic
- infects older age groups in USA,
PATHOGENESIS- Site of replication is the respiratory mucosal epithelium, 4 day viremia seeds into the skin, the lymphoid tissues and other organs.
CLINICAL DIAGNOSIS
- Prodromal fever + 3C’s Cough, Coryza(runny noselike a head cold), Conjunctivitis.
- Koplik’s spots, maculopapular rash- Rash on palms
- lymphadenopathy
- patient history- disease in community , known exposure.
- photophobia
COMPLICATIONS- post infectious encephalitis-matrix protein defect
- interstitial pneumonia
- bacterial superinfections with pneumonia, otitis meia
- subacute sclerosing panencephalitis- worst possible outcome in those that intially appear to recover, death years later.
FACTORS AFFECTIING MEASLES SEVERITY
- poor areas of world, malnutrition, overcrowding, intensive exposure 85% of deaths are secondary cases within households
- Death due to pneumonia and encephalitis.
DIAGNOSIS: Urine or pharyngeal cell sample must be taken early
- PCR will detect virus but requires monkey kidney cells,
- look for 4 fold rise in antibody titer between acute and convalescent sera
CONTROL: live attenuated vaccine is the best single disease control method, gives lifelong immunity in most people and is given to infants at 13-15 months, don’t give too early otherwise no immune reaction, don’t give to pregenant or immunocompromised because it is a live firus. Second dose is improtant for sustained immunity.
- problems- can have adverse reactions with Fever and rash and must prevent inactivation by heart ant time ( cold chain) Origingal killed vaccine was used and it was a short lasting immunity, atypical measles syndrome can occur in these people today. Their immunity drops and the person gets measles if exposed, but the case lacks some symptoms.
- lapse in immunization leads to disease, so it can come back if rates drop to less than 75% vaccinated.
Rubella Virus
CHARACTERISTICS- togavirus family- SS RNA one serotype with human reservoir only
TRANSMISSION–14-21 day incubation, period of contagion is 7 days before until 7 days after appearance of rash.
CLINCAL FEATURES- lymphadenopathy, Rash, low grade fever, catarrhal upper respiratory symptoms, palatial spots Day 1 of rash, Rubella Xanthem (macular rash) 1-2 days after onset of prodromal fever that lasts 1-3 days and is on the head neck and trunk.
- mild disease in adults, complications rare, and may be ignored because it only lasts a few days. - Maculopapular rash, transient arthralgia, transient arthritis, encephalitis, usually resolves within 3 weeks or less.
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Congential- unborn child is severe. High risk in FIRST trimester -25% - (80% affected in first 2 weeks of gestation, 10% affected by third month) 6% affected in 4-5 months, and no major threat to fetus after month 5. slight eye opacity, Anemia, Transient immunodeficiency, interstitial pneumonia, intravascular coagulation, hepatitis, other malformations. LATE COMPLICATIONS: increased risk of diabetes mellitus, chronic thyroiditis, sub acute panencephalitis
-RUBELLA SYNDROME- cardiac defects, eye defects, nerve deafness, enlargement of liver and spleen, thrombocytopenia, intrauterine growth retardation CNS defects and retardation, Microcephay, encephalitis.
CONGENITAL PATHOGENESIS- transplacental spread to fetus leads to chronic fetal infection, compromised fetal oxygenation, Disruption of normal organogenesis, permanent organ defects, impaired mitosis and cellular necrosis with chromosomal breakage.
- continued postnatal damage- they shed virus for years, the patients immune system begins to see virus as self. Antibody immmune complexes form, continuing tissue damage occurs.
DIAGNOSIS- acute infection of adults- PCR of respiratory secretions
- acute and convalescent serum samples looking for 4 fold rise in antibody
- IgM antibody- not perfect but OK
- Test for immunity in adults- screen for presence of IgG or total antibody of IgG + IgM. (don’t look only for IgM
CONGENITAL DIAGNOSIS- Titer comparison, if titer stays constant or goes up over months if bay was infected, if titer drops over 3-4 months baby was not infected. IgM specific antibody can help but sometimes inaccurate.
PREVENTION- LIVE vaccine, immunize children, check for immunity prior to pregnancy, if an adult female is seronegative, immunize but avoid pregnancy for months.
-If pregnant, test immunity, if positive, no problems, if negative, mom could get rubella, monitor mom’s titer, mom stays away from unimmunized children.
Parvovirus B19 ( Fifth Disease) (erythema infeciosum in kids)
Characterisitcs- No- envelope, SS DNA- codes for very few proteins, replicates in NUCLEUS of immuture ERYTHROCYTES and synovial fluid cells.
TRANSMISSION: spread by respiratory droplet inhaation. Pateint is infectious for 1 week, High rik areas of exposure are schools and day care during out breaks, homes with infected member, hospital caring for infected patients.
- serongative pregnant woman is at risk of acquiring the disease.
- focal outbreaks in spreing with a transmission rate of 2-5-%
- epidemics every 3-5 years
- 30-60% adults are seropositive.
INCUBATION- 4- 12 days
CLINICAL FEATURES- fever, malaise, headache, myalgia, slapped cheek rash on face, conflent indurated rash, also on arms and legs. itching, lymphadenopathy, leukopenia, anemia, arthralgia, arthritis later in females. illness lasts for 1-4 weeks.
Aplastic crisis- transient arrest of erythropoiesis, lasts for 7-10 days, happens in chronic anemia with chornic infection, in fetus with immature immune system, in adults with deficient immune system.
- B19 triggers crisis in patients needing increased production due to an underlying cause like sickle cell and thalassemia, virus halts normal RBC production, compounding the anemia problem for patients in crisis.
PREVENTION: pregnant women should avoid unnecessary contact with young children becasue it can cause congenital infection. (Hydrops fetalis)
DIAGNOSIS: DNA by PCR
- specimen- Viremia in blood 7-12 days after prodromal symptoms, culture of virus is not used.
- serological detection if viremic phase for PCR is missed, IgM for recent infection, IgG for past infection.
TREATMENT: transfusion of packed RBC for anemia, normal human immunoglobulin helps those with chornic infetion and may help aplastic crisis
-no antivirals or vaccine.
other causes of rubella like rashes or who may mimic rubella symptoms
17 echo viruses, 9 coxsackie viruses, adenoviru, arbovirus, epstein Barr virus, scarlet fever, toxic drug eruptions.
Hand Foot and Mouth disease
common in children,
Etiology: coxsackievirus A16, causes fever, blister like eruptions in mouth and or skin rash,
- no treatment.
Roseola Infantum syndrome ( 6th disease)
epidemiolgy- infants up to 4 years
ETIOLOGY: herpes virus 6B, adenoviruses, enteroviruses have similar symptoms.
Clinical symptoms- 3-5 days, abrupt onset, high fever, sometimes brief convulsion, leukopenia, Later symptoms after 3-5 days- fever subsides, macular rash that is faint and transient.
Rare complications affecting the CNS, Liver, Lungs
TREATMENT- no good clinical trials, in vitro data indicates susceptibilty to cirofovir and ganciclovir,both have been used together to help patients recover and cidofovir seemed to be the most potent.
HHV6
CHARACTERISITCSt-Cell lympohtropic virus that carries DNA structurally similar to CMV
HHV6B- casues roseola in most babies age 2
HHV6A- infects adults,virus found in lymph nodes of HIV-1 infected persons progressing to AIDS
HH7
Characteristics- Isolated from CD4 lympohcytes of healthy individuals, most closely related to HHV6
TRANSMISSION- 97% of all adults are serologically positive.
EPIDEMIOLOGY: children under 2 years become infected and clinical relevance unkown.
Other viruses tha can have a sash as one compenent of systemic infections in both children and adults
West nile virus, Dengue, chickengunya.
DIAGNOSIS- clinical suspicion, immunoassay for WNV antibody (4fold rise
-PCR detection, but have to have timing right. Virus is there for first 5 days at onset of symptoms.in both primary and secondary Dengue
in Primary, NS1 falls , IGM starts at the end of symptoms and makes a hump, IgG starts at the end of NS1 and stays increased.
Secondary, the same but IgG is already elevated from onset of symptoms.
HHV-1
3 major syndromes-
gingivostomatitis- primary infection often occurs in children age 1-5 years, icubation is 3-5 days, disease lasts 2-3 weeks.
-fever, sore throat, vesicular and ulcerative lesiions, edema, gingigostomatitis, submandibular lympohadenopthy and malaise.
Eczema herpeticum- intact skn is normaly resistant to HHV-1 and 2- in patients with skin disorders, cutaneous infections are severe and widespread
Herpes Labials( MOST COMMON) (fever blisters, cold sores) is a recurrent infection, localized to the lips, fades over 4-5 days and is a painful lesion. lesions progress through pustular forms, then crusting and are healed in 8-10 days leaving no scars. Lesions may recur repeatedly at various intervals,
HHV2
Infections of baby in Pre- Natal and Post Natal- period
Pre: transplacental infections in utero cause congenital malformation- ( similar to rubella), occasionally fetus is aborted.
Post- about 75% occurs during birth exposure to mother’s virus. There is a 50% mortality, survivors often have permanent neurological impairment.
Best tests for HHV1/2 are viral culture or PCR, detected in skin, organs and in saliva of primary infection of HHV-1, direct stains of tissues is just OK
- HHV confirmed using a specific monoclonal fluorescent antibody stain for either HHv-2 or HHv-1
- surgical path tissue sections OK, observe multinucleated giant cells and Cowdry Type A intranuclear inclsions.
CMV
Primary and reactivaion occurs within 2 months of transplantation. don’t transplant CMV positive organ
-Leukemia and lymphoma pateints ar at low risk of CMV complications, Aids patietnts it is devastating and causes retinitis, colitis, and pneumonia.
DIAGNOSIS- Transplant patients and organ donors are tested for presence of CMV antibody- in bone marrow transplant, patients perform baseline and weekly quantitative PCR titers and using whole blood.
HHV8
Kaposi’s sarcoma realted, affects connective tissues such as cartilage bone, fat, muscle and blood vessels , majority have associated HIV infection and AIDS
Diagnosis- skin leasions can resemble other skin disorders like inflammation, bacterial or fungal infections, non hodgkin lymphoma or a benign tumor of the blood vessels (hemangioma)
- punch biopsy is sent to surgical pathology lab, under microscope the kaposi sarcoma’s cells usually have a distinctive shape and pattern of arrangement. Sometimes , thoguh, early lesions may not reveal the characteristic cell patterns
Herpesvirus varicellae
Characteristics:
Varicella-zoster virus- DNA virus- Chicken pox
-bleongs to herpes group, not resistant to drying and survival outside the body like true pox viruses.
TRANSMISSION: reservoir is infected person, spread by direct contact and aersol. communicable from 5 days before eruption to 6 days after last crop of vesicles appear, immunosuppressed cases contagious longer.
INCUBATION: 10-23 days
EPIDEM: 805 of susceptibles get disease if exposed,
PATHGENESIS: virus enters through URT, carried by phagocyti cells to local lymph nodes for primary replication. Some may occur in respiratory tract.
COURSE: Macular phase, papular phase, vesicular phase(fluid collects in cellular interspaces and lifts the superficial cornified layer to form a delicat vesicle), scab phase.
CLINICAL FEATURES- Dewdrop on Rose petal- early lesion- vesicular often 1 or 2 crops of lesions occuring 2-3 days after the first so will be in different phases.
-Near eye, avoid scratching to prevent complications.
COMPLICATIONS:- 250 deaths/ year highest in children with leukemia (7-10% mortality)
-in pregnancy- during 1st trimester causes fetal abnormalities in 3% cataracts, microcephaly, fatality(50%). in babies 5 days or less before delivery there is a high infant mortality risk, vaccinate susceptible women after their first pregnancy, stop transmission from children to mom which is how most adults get chickenpox.
DIAGNOSIS_ ELISA testing for atnibody to determine if susceptiple to chickenpox, and see if significant rise in titer, check skin scrapings, using PCR but cultre is ok
PREVENTION- prevent exopsure to immunocompromised leukemia patients,
- Hyper immune immunoglobulin VZIG can be given if accidentally exposed
- LIVE VIRUS vaccine is available give to young children before they are exposed after expusre won’t work. give 1 year old and then a booster after 4-6 years.
- given to adults who never had chicken pox- immunity 4-6 weks after 2nd dose, does not prevent primary infection after exposure, common reactions are fever soreness, rash, headache, vaccine also for older adults to prevent zoster attacks in old age.
Herpes Zoster
Latent varicellae lives in dorsal root ganglion or extramedullary cranial nerve ganglia for decades, reactivates when host cell mediated immunity falls.
triggers- old age, trauma, stress, surgery, malignancy, immunosuppression, transplantataion.
SPREAD- spreads peripherally from involved ganglia along sensory nerves to skin, typically unilateral and restricted to skin asupplied by sensory nerves of sinlge or associated group of dorsal root ganglia ( dermatome)
-CLINICAL-
Vesicles- erymthamtous base appear in crops and in irregular fasion along nere pathway, usually deepr seated and more closely aggregated than chickenpox, the vesicles evolve to healing crusted lesion over a period of 1-3 weeks.
-PAIN- sever in 66% of cases, may cause diagnositic dilemma before lesions appear.
