Rotavirus To Scrapies March 28,2007

Reoviridae Family Introduction

-Respiratory Enteric Orphan Viruses= REO viruses -Although found in the respiratory system they rarely cause respiratory disease mostly enteric disease!! -Includes: Orbiviruses, Coltiviruses (Colorado Tick Fever), Orthoreoviruses (asymptomatic infections); Rotaviruses #1 cause of infant diarrhea worldwide. -Double layered protein capsid that can undergo antigenic shift like influenza A. -Non-enveloped (resistant to detergents, acids, pH, drying, repeated freezing and thawing) -BUT enveloped virus-like properties: it acquires an envelope during assembly then looses it.

Rotavirus Pathogenesis

Immunity and Epidemiology

Clinical Syndromes

Lab Dx/ Tx/Control

-Spread is fecal-oral and maybe respiratory -Absorption to columnar epithelial cells of villi of SI shorten/blunt villi and promote mononuclear cell infiltrate into lamina propria (binds to them leading to problems with brush boarder) -8 hours after infection: -Notice cytoplasmic inclusions and huge numbers (billions) of virions/gm stool. (Only need 10 to cause an infection.) -NSP4 protein (like cholera toxin) watery diarrhea and severe dehydration (5 million children die ↓ age of 2 yrs) -Wheel like look to the bug. Immunity: -Abs from mothers colostrums/milk (sIgA) only prevents infection for 6 mos. (remember: sIgG crosses placenta) -Antigenic shift (like influenza) -Without Abs, even a small number of virions (10) can cause infection. Epidemiology: -Ubiquitous 95% of children worldwide are infected by age 3-5 -Very contagious; transmitted on furniture, fomites, toys, and hands -Two types cause two different diseases: Type A (infants > 24mos, + malnourished in developing nations gastroenteritis and potential dehydration); Type B (Chinese infants, older children, adults severe gastroenteritis. Gastroenteritis: -48hr incubation sudden onset of severe vomiting (PROJECTILE is KEY), watery diarrhea, fever, dehydration (electrolyte imbalance) -Self-limiting; usually recover 5-7days without sequelae Not distinguishable from other types of gastroenteritis (Norwalk virus, bacterial) by signs and Sx’s; no blood or leukocytes in stool. Diagnosis: stool samples; Electromicroscopy: Wheel like spokes (PATHONEUMONIC) ND TX: Bovine colostrums + probiotics (sacromices billardiae + lactobacillus)

Coltivirus Introduction

Epidemiology/ Lab Dx Colorado Tick Fever

-M/C tick borne viral disease in US (compare with Lyme Disease and Rocky Mountain Spotted Fever (RMSF) -Similar to other reoviruses but: infects RBC precursors survives in mature RBCs (NOTE: parvo virus B-19 and Dengue Virus also attack RBCs) -Vector wood tick (Dermacenter andersoni), reservoir squirrels/chipmunks, hosts humans -Invades vascular endothelium/vascular smooth mm and weakens capillaries leading to hemorrhage hypotension shock Wester/North western USA and CANADA (almost exclusively needs 4000-5000 ft elevation Rocky Mountains) -unlike other tick diseases, coltivirus must enter the blood stream quickly (KEY); RMSF1wk; Lyme Dz 24hrs 3-6day incubation Sx fever that is biphasic/saddle back fever (spike for 2-3days then none then again); maculopapular/petechial rash (like RMSF) but more generalized and shorter lived; hemorrhage hypotension shock (like dengue fever) Tx: none Prevention: same as for other tick borne Dz

Poxviridae Introduction

Smallpox Virus

2 Genus: Orthopoxvirus: variola (smallpox) Don’t mix with vericella!! Molluscipoxvirus: Molluscum contagiosum (cause warts) -one of the largest most complex viruses double layer envelope **Unlike other viruses pox viruses contain all the necessary information for their own DNA and RNA synthesis. Hx: Historical accounts for over 2000yrs. 1st live vaccine in 1796. 1967 WHO mandated that in 10 yrs they would vaccinate all susceptible people in the world; last reported case: October 1977, in Somalia Now: Thought of for bioterrorism.(good for it because- it kills only 30% but very infectious; aerosole stable, small infectious does needed, immunologically naïve population, no effective tx. Smallpox Vaccine: Live vaccine (modified cowpox) virus injected; SE vaccinia necrosum (can lead to eczema) Cannot be given to pregnant, HIV+, immunosuppressed or skin Dzes like eczema (even if skin condition is in the past!), children >12-18 yoa Virus: Variola major: 4 types Variola is inhaled 4-9days asymptomatic, not contagious in replication

Other Pox Viruses

Prodrome 2-4days Skin Rash: -thick opaque fluid filled center with “belly button like depression in center” -infectious until last scab falls off -Unlike chicken pox, in smallpox all the lesions are at the same stage at the same time DDX FEATURE DX & TX: M/c clinical only d/t very characteristic lesions. Molluscum contagiosum and other pox viruses are zoonoses. (ex: cowpox, monkey pox) Molluscum contagiosum: -STD, fomites, wrestling, rugby (also see herpes gladiatorium or HSV rugbytorium and ringworm) -Genital tumours or disseminated large skin tumours (immunocompromised most likely HIV+) or small benign warts, cutaneous papules in children/adults. SX: fleshy, pearl-like umbilicated nodules with central caseous plug good DDX from HPV DX: characteristic skin lesions (see above); molluscum bodies in biopsy (inclusion bodies) Orf/erythema contagiosum: -sheep/gaot farmers -DDX with herpetic witlow. -caused by direct contact with infected sheep/goats, or soil? -contagious pustular dermatitis (mostly hands)

Scrapies-like agent Introduction

Pathogenesis & Diagnosis

Creutzfeld-Jacob Disease-Sporatic form Creutzfeld-Jacob

Prions (proteinaceous infectious particles)filterable (size of viruses) but no DNA or RNA Replicate very slowly 5days to 1week doubling time Very resistant! (weird for a protein, it even resists proteinase) 2 Types: Sporadic Creutzfeld-Jakob Dz, Varient CJD Transmissible neurogenerative Dz to a variety of mammals including humans. Pathogenesis: Not very well known very closely associated with normal human protein PrPc (primary protein in cells) PrPsc some variation of PrPc that might be actual infective agent. Get aggregates of protease resistant hydrophobic glycoproteins in plaques/fibrils in CNS Diagnosis: Not cultivated in lab, no Abs produced, normal CT scan, normal MRI, abnormal EEG DX with: Western blot confirm diagnosis with proteinase K resistant PrPc Long incubation (up to 30 yrs) but rapid fatal once symptomatic (m/c only 1 yr) -rapidly progressing dementia; m/c after age 70; Genetic susceptibility 10% occurs in families. Young onset mean is 27yrs

Disease-Varient form

-pyschiatric/sensory symptoms dementia at final stage only -unlike sporadic CJD detect PrPsc in follicular dendritic cells (lymphoid tissue) Orally acquired (not just in brain) Strong laboratory and epidemiological link to BSE (eating contaminated meats)