Viral Diseases Flashcards
What is the pathophysiology of Herpes Simplex?
Virus infects through mucosal membranes or abraded skin. Latent infections harbored in neuronal cells: Trigeminal ganglia and Pre-sacral ganglia
What are clinical presentations of herpes simplex?
Dew-drop on rose petal. Primary infections: Gingivostomatitis and pharyngitis most frequent. Commonly seen in children and young adults. Fever, malaise, myalgias, inability to eat, irritability and cervical adenopathy lasts 3-14 days
Recurrence: Herpes labialis (“Cold Sores”)
Describe the urogenital lesions caused by HSV-1 or HSV2?
Vesicular lesions of external genitalia with pain, itching, dysuria, vagina and urethral discharge, tender inguinal lymph adenopathy
What complications can herpes simplex lead to?
Ocular disease. Neonatal and Congenital infections. Bells Palsy (CN7, facial). Encephalitis and recurrent Meningitis (most common cause of viral encephalitis in US). Herpetic whitlow
What is the best diagnostic method for herpes?
real-time HSV PCR assays are more sensitive method to confirm HSV infection in clinical specimens. particularly useful for the detection of asymptomatic HSV shedding
What is a Tzanck smear?
demonstrates the cytopathic effect of the virus (multinucleate giant cells), and can be performed on lesion scrapings from patients with active genital lesions. is only helpful if positive
What are the two distinct clinical presentations of Varicella-Zoster?
Primary infection: Chickenpox, transmission is likely by respiratory route. Recurrent infections: Herpes zoster, probably infects dorsal root ganglia during primary infection
What is the infectious period of Varicella-Zoster virus?
Incubation period: 10-21 days. Infected persons are infectious ~48 h before onset of vesicular rash and until all vesicles are crusted
What is the clinical presentation of chickenpox?
Rash, fever (100-103F) lasting 3-5 days, malaise
Skin lesions: Maculopapules, vesicles, and scabs in varying stages of development
What is the clinical presentation of herpes zoster (“shingles”)?
Unilateral vesicular eruptions which develop within a single dermatome (T3 to L3 most common). Often associated with severe pain
What diagnostic tests are used to confirm varicella-zoster?
complement fixation and virus neutralization in cell culture or fluorescent antibody test of smear of lesions
Describe the progression of the varicella-zoster viral infection vesicles?
thin-walled vesicle w/clear fluid forms on a red base. Vesicle becomes cloudy and depressed in the center with irregular border. A crust forms in the center and replaces the vesicle
How is varicella-zoster managed?
Vaccination. Primary disease: Prevent secondary infections. Recurrent infection: Acyclovir or Famcyclorvir. Analgesics
What are the clinical presentations of infectious mononucleosis (EBV)?
Fever/chills: 7-14 days. Lymphadenopathy rarely exceed 3 weeks duration (Posterior chain***). Severe pharyngitis with exudates for 5-7 days. HA, malaise, anorexia, soft palatal petechiae, rash (especially with administration of amoxicillin/PCN). Splenomegaly and mild hepatic tenderness
What are laboratory findings of infectious mononucleosis (EBV)?
Throat culture. Monospot. Heterophil antibodies. Atypical lymphocytosis in about 75%. EBV antibody titers directed at
What are possible complications of infectious mononucleosis?
Bacterial Strep pharyngitis, thrombocytopenia, neutropenia, splenic rupture, Bell’s palsy, Guillain-Barre syndrome, encephalitis
How is infectious mononucleosis treated?
supportive therapy, Tyelonal/NSAIDs, salt water gargles, rest, avoid contact sports 6-8wks
What is the clinical presentation of congenital CMV?
Ranges from inapparent infection to severe. Petechiae, hepatosplenomegaly, jaundice, Microcephaly, growth retardation, prematurity
What is the clinical presentation of perinatal CMV?
poor weight gain, adenopathy, rash, hepatitis, anemia and atypical lymphocytosis
What is the clinical presentation of CMV mononucleosis?
Heterophil Ab negative mononucleosis syndrome. Prolonged high fevers, profound fatigue and malaise. Myalgias, HA, & splenomegaly. Exudative phayngitis, cervical adenopathy, rubelliform rash are rare
What is the most important diagnostic study in the evaluation of suspected CMV?
viral culture from any body fluid or organ system.
What is the epidemiology of 5th disease (erythema infectiosum)?
Etiologic agent: Human Parvovirus B19. Respiratory tract is probably route of transmission
What is the clinical presentation of 5th disease (erthyema infectiosum)?
Classic “slapped face.” circumoral pallor. Low-grade fever, varying degrees of conjunctivitis, upper respiratory complaints, cough, myalgia, itching, nausea and diarrhea. Bilateral blotchy areas with lacy pattern on extremities/trunk one day later
What is the epidemiology of Roseola (infantum)?
Etiologic agent: HHV6 (B cell lymphotopic virus). Benign disease of infants 6 months to 4 y/o.
What is the clinical presentation of Roseola (infantum)?
Major cause of infantile febrile seizures. abrupt onset, irritability, and fever (up to 105F) lasting 3-5 days. Faint small (2-3 mm) macules or maculopapules over neck and trunk extending to thighs and buttocks appear after drop in temp
What is the epidemiology of measles (Rubeola)?
Transmitted through nasopharyngeal secretions (directly or airborne droplets) to respiratory mucous membranes or conjunctivae. Highly contagious: infectious from 5 days after exposure to 5 days after skin lesions appear
What is the clinical presentation of measles (Rubeola)?
Acute febrile eruption. Koplik’s spots. Brick red, irregular rash that first appears on face and spreads downwards. Prodromal: malaise, irritability, fever (up to 105F), conjunctivitis with increased lacrimation, edema of eyelids, photophobia, hacking cough, rhinorrhea
How is measles (rubeola) diagnosed?
Usually clinical. Labs: Neutropenia. Detection for IgM antibodies with ELIZA
What is the treatment for measles (rubeola)?
Isolation of patient. Bedrest. Antipyuretics. Fluids. Is a vaccine preventable illness
What is the epidemiology of Rubella (german measles)?
caused by Togavirus. Nasopharyngeal secretions transmit virus. Transplacental transmission causes rubella syndrome
What is the clinical presentation of Rubella (german measles)?
malaise, HA, fever, lymphadenopathy (post-auricular, occipital). lesions have lighter hue than measles. Forchheimer’s spots small red lesions) may appear on soft palate.
What is the presentation of congenital rubella syndrome?
Heart malformations, Eye lesions, Microcephaly, Mental retardation, Deafness, Thrombocytopenic purpura, Heptosplenomegaly, Intrauterine growth retardation
What is prevention of rubella?
Attenuated virus immunization. Don’t give to pregnant person during 1st trimester. Wait 3 months to get pregnant
How is rubella (German measles diagnosed)?
leukopenia, virus isolation and serologic tests (antibody tests, IgM antibodies to Togavirus)
What is the epidemiology of mumps?
a paramyxovirus. occurs most frequently in spring. spread by respiratory route.
What is the clinical presentation of mumps?
parotitis*, malaise, anorexia, fever, pharyngitis. Possible pain and tenderness. Painful swollen testicle (epididymoorchitis)
What are the common viral respiratory infections?
common cold: rhinovirus, coronavirus, adenovirus. influenza-like illness: influenza A/B. Bronchiolitis: Respiratory syncytial virus (RSV). Croup: parainfluenza virus
Describe major characteristics of the influenza viruses
orthomyxoviridae family of viruses. Types A,B,C. Type A viruses are further classified by hemagglutinin (H) antigens (H1-3) and neuraminidase (N) antigens (N1-2). Type A have major antigenic shifts every 3 yrs and type B every 5 years
What is the clinical presentation of influenza?
abrupt onset HA, fever, chills, myalgia, malaise, cough, pharyngitis
What are possible complications of influenza?
pneumonia (most common), Reye’s syndrome, myositis, rhabdomyolysis, myoglobinuria, myocarditis, pericarditis
How is influenza diagnosed and treated?
Inactivated virus vaccine given Oct/Nov each yr. Rapid flu swab, leukopenia. Tx: acetaminophen, rest, fluids.
What is the epidemiology of bronchiolitis?
RSV is from the paramyxovirus genus. major respiratory pathogen of kids. disease is milder in older kids/adults. transmitted by contact with fingers or fomites.
What is the clinical presentation of bronchiolitis?
Infants: rhinorrhea, low-grade fever, cough, wheezing. If severe: Tachypnea, dyspnea, hypoxia, wheezing, rhonchi and rales. Adults: common cold presentation
How is bronchiolitis diagnosed/treated?
Rapid RSV, culture of nasopharyngeal secretions. Tx: Ribavirin, contact isolation, respiratory therapy, hydration, antibronchospastic agents
What is the epidemiology of croup?
Caused by the parainfluenza viruses. Type 1 is most common in children. Type 2 is similar but less severe. Type 3 causes bronchiolitis and pneumonia is infants
What is the clinical presentation of croup?
Acute fever, Coryza, sore throat, hoarseness, Breathing difficulty with a “barking” cough. worse at night.
How is croup diagnosed and treated?
cool or moist air, acetaminophen, avoid cough meds, ER treatment (aerosolized racemic epi and prednisone)
What is the epidemiology of rabies?
caused by rhabdovirus. Urban: caused by unimmunized domestic dogs/cats. Sylvatic: caused by skunks, foxes, raccoons, wolves and bats
What is the clinical presentation of the prodome phase of rabies?
Fever, HA, malaise, myalgias, fatigability, anorexia, n/v, pharyngitis, nonproductive cough. Paresthesias and/or fasciculations around site of inoculation.
What is the clinical presentation of the acute encephalitis phase of rabies?
excitation and agitation, confusion, hallucinations, muscle spasms, meningismus, seizures and focal paralysis. excessive sensitivity to bright light, noise or touch. High fever, dilated irregular pupils, increased lacrimation, salivation, perspiration, and postural hypotension
What is the clinical presentation of the profound brainstem dysfunction phase of rabies?
Difficulty swallowing, increased salvation, “foaming at the mouth”, involuntary contractions of diaphragm accessory respiratory, pharyngeal and laryngeal muscles. Coma and respiratory failure
How is rabies diagnosed and managed?
isolation of virus, direct antigen detection. Tx: pre-exposure vaccines and post-exposure prophylaxis
What are characteristics of the rash associated with variola (smallpox) virus?
starts on face, Lesions same stage, Deep lesions, Often palms/soles, Centrifugal rash, Back > Abdomen, Multiloculated vesicles
What is the progression of smallpox?
Fever, malaise, non-productive cough, headache, backache, joint pain. Papular rash on face –> extremities. Papular–>vesicular–>pustular. Crusted lesions
Describe the smallpox vaccine
dc’d in 1970s because disease was erradicated. Is a live vaccine. Injection site becomes red, itchy. Vesicle umbilicates and evolves into a pustule that scabs and leaves a scar
