COXSACKIE/ECHO VIRUS

Clinical Coxsackie A: usually vesicular lesions

syndrome: Coxsackie B: myocarditis, pleurodynia
Herpangina: coxsackie A and echovirus (not HSV). No skin lesions – unlike hand-foot-mouth dz. DDx Apthous ulcers
Coxsackie A Hand-foot-mouth dx: mild febrile disease with vesicular lesions on hands, foot, tongue.
syndrome: Acute hemorrhagic conjunctivitis: extremely contagious.
Coxsackie B Pleurodynia (Bornholm’s dz): “devil’s grip” – severe pleuritic chest pain – unilateral intercostals myalgia – “stitch like pain”.
syndrome: Myocarditis/pericarditis: m/c in adult males. Mistaken for MI. Children – sudden unexplained heart failure.
IDDM
Aseptic meningitis: #1 cause is echovirus. Neonatial fulminant hepatitis.
Lab Dx: CPE on monkey KI tissue culture. RT-CPR in CSF/other fluids.
Tx: IPV (Jonas Salk 1956 – inactivated virus). OPV (Albert Sabin – 1962 – live attenuated virus.)
RHINOVIRUS
Introduction: Most common cause (>50%) of the common cold (coryza). Spread via aerosolized nasal droplets, fomites, hands (#1). Can’t grow in acid of stomach
(unlike enterovirus) and also grows best at 33 C (cooler in nasal mucosa). Gradual antigenic drift (like influenzae A). <winter. Deliberate exposure of
“volunteers” to wet and cold does not cause cold (b/c of low vitamin D).
Pathogenesis: Infection by as little as 1 infectious particle. Bind ICAM-1 receptor. Most replication is in the nose.
Immunity: IFN. Transient.
Clinical Rhinorrhea (clear, watery—purulent or mucoid if secondary bacterial infection)
syndrome:
Lab Dx: Usually not necessary. Characteristic S’s and Sx’s. Culture: characteristic CPE in human diploid fibroblast cell at 33 C and acid labile.
Tx: Hand washing/ disinfect contaminated surfaces.
Allopathic: ABC useless against primary infection – flu and cold are caused by virus NOT bacteria.
ZINC: important for immune system (IFN), decreases inflammation, decreases viral attachment to nasal mucosa, inhibit viral replication, Zn fingers
and Ab synthesis and many other fxn.

TOGAVIRUS and FLAVIVIRUS

Introduction: Enveloped. TOGAVIRUS: alphavirus (arborviruses – arthropod borne), rubivirus (Rubella - German measles). FLAVIVIRUS: arborvirus (west nile)
Pathogenesis: Arbovirus have similar pathogenesis and epidemiology. Cause lytic infections in vertebrate hosts.
Female mosquito takes blood meal from vertebrate host. Female mosquito bites another host. Enters  flu-like symptoms and majority of infection
stops here. Virus expresses Fc receptors – phagocytosis (increases infectivity).
Humoral (Ab) immunity: in subsequent infections – increase uptake of virus in macrophages and other cells with Fc receptors.
Cell-mediated immunity: delayed type hypersensitivity reaction, Ag/Ab complex can weaken vasculature leading to hemorrhagic symptoms.
Epidemiology: Zoonoses. Vectors: MOSQUITO. Reservoirs: “immunologically naïve” birds. Humans: dead end hosts.
Puddles, ditches. Artificial ponds, toys, trash cans.
Clinical Flu-like syndrome. 1) meningitis/encephalitis OR 2) hepatitis, hemorrhagic fever, shock, viral arthritis
syndrome:
Yellow Fever: Jungle fever (monkey reservoir). Aedes aegypti mosquito.
3-6 day incubation sudden onset of fever. Jaundice. Hemorrhage. Encephalitis is rare. “Black vomit”
Dengue (break Aedes aegypti mosquito.
bone) fever: Primary infection: 4-8 day incubation. Bone pain 6-7 days. Maculopapular rash. Hemorrhagic shock syndrome: hypersensitivity reactions—weaken,
rupture vasculature, NO bone pain.
Lab Dx: Serology: problem false (+) much cross-reactivity. RT-PCR: genomic/viral mRNA in blood
Tx & prevention: None. No vaccine for Dengue fever.
WEST NILE
Introduction: In infected areas < 1% of mosquitos are infected and < 1% of people bitten by infected mosquito get serious health affects (usually >55yoa)
Transmission and Mosquito larvae can overwinter. No person to person transmission (possibly breast feeding, blood products). Main reservoir is CORVID BIRDS
immunity: (common house sparrow). Immunity: not sure if causes chronic infection but unlikely.
Clinical Most infections are mild or sub-clinical. 3-14 days febrile disease of sudden onset. Severe disease  encephalitis. Most significant risk factor is
syndrome: advanced age (immunocomprimised).
Dx: ELISA for anti- WNV IgM in serum or CSF within 8 days of infection. RT- PCR for viral genome.
Tx: Supportive only. Regular mosquito protection – remove outside water containers.
Naturopathic: thymol (not too long), cinnamon oil, catnip oil.
RHABDOVIRUS
Introduction: Enveloped. One of the most deadly diseases – 100% mortality. Class 4 pathogen.
Transmission/ Zoonoses. Rabid dog (also cats, fox, raccoon, coyote, skunks, bat).
Epidemiology: Does not penetrate intact membranes.
Rabies Incubation phase: attach to nicotinic Ach/ ganglioside receptors at muscle/nerve at site of wound – local replication.
Pathogenesis: Prodrome: retrograde axoplasmic flow to dorsal root ganglia. No detectable Abs.
Neurologic phase: travel to infect brain / encephalitis, salivary glands.
Clinical dz: Incubation phase: asymptomatic – delay is important for treatment (1-12months after exposure)
Prodrome: 2-10 days of fever, malaise, H/A, pain, paresthesia.
Neurological: hydrophobia, aerophobia, hyperactivity, aggressiveness. Furious rabies (death in 1 week, like tetanus). 15-60% have symmetrical
ascending paralysis “dumb rabies”  progress to death by cardiac or respiratory arrest (only 3 known survivors).
Dx: Once there is evidence of infection (symptoms or Abs) it is too late for effective intervention.
Lab Dx: Negri bodies (post-mortem).
Tx: Aggressive post-exposure prophylaxis is only hope for overturning clinical illness. 1) wound management 2) immunization