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Viral Infections of Cutaneous and Subcutaneous Tissues Prof. Arzu İlki, MD 0 Viruses are essential intracellular parasites. 1 Viruses attack the skin in 3 ways: direct inoculation systemic infection local spread from the inner focus 2 Dermatologically, viral diseases are often caused by DNA viruses....

Viral Infections of Cutaneous and Subcutaneous Tissues Prof. Arzu İlki, MD 0 Viruses are essential intracellular parasites. 1 Viruses attack the skin in 3 ways: direct inoculation systemic infection local spread from the inner focus 2 Dermatologically, viral diseases are often caused by DNA viruses. RNA group viruses cause diseases with general symptoms. 3 Viruses can act on skin cells : 1. Cytolytic-cytopathic effect: Through these effects, they can cause vesiclebulla formation. (Varicella zoster) 2. Proliferative effect: As a result of this effect, they can cause benign tissue hyperplasia. 3. Oncogenic effect: They can cause the formation of various malignant diseases. 4 Viral Exanthems Maculopapular Rash – Measles virus – Rubella virus – Parvovirus – Human Herpes v.6 5 Viral Exanthems Vesicular Rash – Herpes simplex virus – Varicella zoster virus – Coxsackie virus – Pox viruses 6 Measles q Measles virus (Rubeola) Genus:Morbillivirus à family:Paramyxoviridae q The virion structure includes: – Spikes – F protein – Matrix protein M, below the envelope q Only one serotype 7 Measles Disease q Humans are the only natural host for the virus q Measles is spread by direct contamination via air droplets of respiratory secretions. q Acute febrile illness, mostly in childhood q Incubation period: 10 – 14 days q Highly contagious 8 Measles Disease qProdromal phase: qHigh fever and 3 Cs: cough,coryza & conjunctivitis qKoplik's spots: red spots with bluish-white centre on the buccal mucos-Enanthem 9 Koplik’s spots 10 Measles Disease q1 – 2 days later, acute symptoms decline with appearance of a widespread maculopapular rash qMeasles rash appears on the face and then spreads down to body. Rash is generalized. Individual spots are irregular in shape and of variable size. q Over 10 – 14 days, recovery is usually complete as the rash fades 11 Maculopapular rash 12 Measles Disease Diagnosis: Specific antibody detection (IgM)-serum 13 Measles Complications q Pneumonia, more common in adults q Otitis media q Post-measles encephalitis q Subacute sclerosing panencephalitis (SSPE): For children 70% of babies will be affected Eyes: cataract, microophthalmia, glaucoma, retinopathy Ears: sensorineural deafness Heart: patent ductus arteriosus, pulmonary artery & valvular stenosis, ventricular septal defect Hepatosplenomegaly Low birth weight, thrombocytopenia Intrauterine death with abortion or stillbirth 20 Laboratory Diagnosis Clinical diagnosis is unreliable Serological diagnosis à the method of choice, detecting rubella specific IgG and rubella specific IgM. Congenital rubella syndrome: serological testing for specific IgM (Maternal IgM does not cross the placenta à diagnostic of intrauterine infection) 21 Control Attenuated live vaccine (MMR) Seroconversion occurs in over 95% Protection persists for more than 20 years Administration in pregnancy is contraindicated Pregnancy should be avoided for the month following vaccination NO SPECIFIC THERAPY FOR RUBELLA. 22 Human Parvovirus Genus: Erythrovirus ssDNA 23 Erythema infectiosumFifth disease infects only humans. symptoms depend on age and overall health. no symptoms/only mild, rash illness. 24 Erythema infectiosum Worldwide infection Seroprevalence increases with age (15-60% by age 5-9) 25 Transmission respiratory secretions, such as saliva, sputum, or nasal mucus, coughing or sneezing blood or blood products A pregnant woman who is infected with parvovirus B19 can pass the virus to her baby. often in late winter, spring, and early summer. Mini-outbreaks of parvovirus B19 infection occur about every 3 to 4 years. 26 Erythema infectiosum Fifth disease is seen usually in school aged children Incubation period:4-15 days Non specific symptoms(7-10 days) 27 Erythema infectiosum Maculopapular rash Distinct facial rash: “slapped cheek” Lacy pink rash of the extremities Peripheral rash settle , re appear with exercise,temperature, emotion 28 Other Parvovirus Infections Arthritis (painful&swollen joints) 80% in adult females 10% in childhood cases Aplastic crisis -Anemia A transient acute event which complicates chronic hemolytic anemia B19 infection à responsible for 90% of cases Occurs most commonly in children with sickle cell anemia B19 in the immunocompromized Persistent infection that leads to persistent anemia 29 B19 in pregnancy Transplacental infection occur during acute maternal infection when the fetus is not protected by passive antibody May affect the fetus: Spontaneous abortion à during 2. trimester Hydrops fetalis: chronic infection in the fetus causing anemia, myocarditis and heart failure leading to edema (hydrops) 30 Laboratory Diagnosis Virus detection – Serum, detecting viral antigens using ELISA detecting viral genome using nucleic acid hybridization and PCR Antibody detection – Recent infection B19-specific IgM or increasing amounts of specific IgG. 31 Human Herpesvirus 6 (HHV 6) Two variants: – HHV 6A: no clear disease association – HHV 6B: responsible for Exanthema subitum = Roseola infantum = Sixth Disease 32 Roseola Infantum Common between 6 months - 3 years 33 Roseola Infantum 1-Highfever ,sometimes with LAP,a few days As the Fever resolves, it is followed by a maculopapular rash (a few hours-a few days) Central distribution 34 Vesicular Rash Herpes simplex virus Varicella zoster virus Coxsackievirus Smallpox 35 Herpes Simplex Viruses ds DNA Lipoprotein envelope, derived from the nuclear membrane Replicate in the nucleus 36 The virus is unable to survive for long in the environment and does not penetrate intact keratinized skin. Transmission is by intimate contact 37 Herpes Simplex Viruses Infects the majority of world’s population Two types: HSV-1 and HSV-2 Type 1 à associated primarily with mouth, eye and CNS Type 2 à found mostly in the genital tract 38 Herpes Simplex Viruses During the replication phase, at the site of entry in the epithelium, virus particles à enter through the sensory nerve endings à transported along the axon to the neurone in the sensory ganglion by retrograde axonal flow. Latent infection: HSV-1 in trigeminal gangl. HSV-2 in sacral ganglion 39 Reactivation Reactivation can be induced by – UV light – Fever – Trauma – Stress Interval between the stimulus and lesion appearance à 2 – 5 d. Weakened CMI 40 Primary HSV skin infections: May occur at any site as a result of direct inoculation through traumatized skin Transfer of infection from oral sites to other areas by fingers 41 Clinical Features Oral infection Acute febrile gingivostomatitis in preschool children Vesicular lesions ulcerate rapidly Skin infections Herpetic whitlow: primary lesion on the fingers or thumb of the child with herpetic stomatitis, due to autoinoculation. It also occurs as accidental inoculation in health care workers. Cold sore Eczema herpeticum: severe form of cutaneous herpes. It may occur in children with atopic eczema. 42 Cold sore 43 Laboratory Diagnosis Isolation of HSV in cultures of human diploid fibroblast cells. Growth is rapid. CPE à rounded, ballooned cells in foci and giant cell formation-EM Detection of viral antigens in cell (by immunofluorescence), scraped from the base of lesions 44 Varicella Zoster Virus Herpesviridae Only one antigenic type 45 Varicella Zoster Virus Two forms of infection Primary infection is a generalized eruption (chicken pox = Varicella) Very infectious (90% of non-immune household contacts will become infected). Reactivation is localized to one or few dermatomes (shingles = Zoster) 46 Chicken Pox Pathogenesis enters through URT or conjunctiva causes viremia Seeded in the epidermis àVesicular eruption Incubation period: 14 – 15 days The patient is infectious for 2 days before and up to 5 days after onset 47 Vesicular fluid becomes cloudy with the influx of leucocytes (pustules) These pustules dry up crusts form & desquamate. most dense on the trunk and head Lesions in all stages are present at any time while new ones are appearing. Pruritis 48 Pathogenesis of Zoster VZV stays latent in the sensory ganglia Reactivation can occur at any age but the rate is much increased in persons aged 60 years or over. Zoster is usually limited to one dermatome 49 Herpes Zoster Localized eruption, unilateral, in adults most commonly in the thoracic or upper lumbar region. Postherpetic neuralgia – Most common complication of zoster – 50% risk in patients aged over 60 years – pain persisting for 1 month or more after the rash 50 Herpes Zoster 51 Laboratory Diagnosis Early vesicular lesions are the best diagnostic material Virus isolation takes from 5 days to 3 weeks More rapid detection is possible with centrifugation-enhanced cultures (shell vials) Direct immunofluorescence VZV DNA amplification by PCR 52 Epidemiology Spread: respiratory route, in winter and early spring Varicella is highly infectious to susceptible close contacts Mortality is high in normal adults, particularly in smokers who develop pneumonia Zoster is associated with decreased T cell function: – Old age – Pre-AIDS phase – Organ transplant recipients 53 Control Passive immunization: varicella zoster immunoglobulin (VZIG): – Neonates – Non-immune pregnant contacts – Immunocompromized contacts A live attenuated vaccine, IM injection 54 Coxsackie viruses ssRNA , Picornavirus Two groups: A and B Group A: – Herpangina (vesicular pharyngitis) – Hand – Foot – and – Mouth disease – Acute hemorrhagic conjunctivitis Group B: – Pleurodynia (epidemic myalgia) – Myocarditis – Meningoencephalitis 55 Coxsackievirus Infections Occur between June-October Transmission: fecal-oral 50-80% of infections are asymptomatic Can cause skin rash and can mimic other virus infections Hand-foot-and-mouth disease (vesicular type) – Usually secondary to Coxsackie A16 – Children

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