{"id":5159,"date":"2011-07-14T20:24:01","date_gmt":"2011-07-14T20:24:01","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5159.htm\/"},"modified":"2012-07-25T18:01:42","modified_gmt":"2012-07-25T22:01:42","slug":"viral-infections","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/infectious-disease\/viral-infections.htm\/","title":{"rendered":"Viruses and Influenza"},"content":{"rendered":"

<\/span>Herpes<\/span><\/h2>\n

<\/span>Zoster (VZV)<\/span><\/h3>\n

aka Shingles<\/p>\n

vesicular rash on erythematous base along one dermatome.\u00a0 Usually does not cross the midline, though due to a small overlap of spinal nerves, may cross slightly.<\/p>\n

 <\/p>\n

It comes from the Latin \u0091cingulus\u0092 which means \u0091girdle\u0092. \u0091Gird\u0092 means to encircle as with a belt or band. A girdle is a device which encircles in such a fashion. With varicella\u0092s tendency to follow a dermatome around the body, it is clear to what \u0091cingulus\u0092 refers.<\/p>\n

 <\/p>\n

EMEDhome:<\/p>\n

The diagnosis of herpes zoster is based on clinical presentation. The primary differential diagnosis is zosteriform herpes simplex virus infection. \u00a0How does the clinician differentiate the two?Herpes simplex infection tends to produce a shorter and milder prodrome, followed by skin vesicles that are more uniform, smaller, and closely clustered. Herpes simplex is also more likely to be recurrent (Mayo Clin Proc, Vo. 79, pg. 1057).<\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

The immunocompromised can have multi-dermatomal involvement.<\/p>\n

Can give acyclovir if immunocompromised, eye involvement (suspect if nose affected), elderly, or disseminated<\/p>\n

Use acyclovir, fam, or val.\u00a0 Possible superiority of Valtrex, also less expensive (In long Run) and more compliance.\u00a0 Steroids do not help prevent post neuralgia or outcome (NEJM 330:896).\u00a0 The elderly should be treated with antivirals if less than 72 hours from rash onset as they will still derive benefit.<\/p>\n

 <\/p>\n

Acyclovir<\/strong> \u0097 Acyclovir (ACV) has an excellent safety profile but is only moderately active against VZV in vitro with a median effective concentration (EC50) of 2.3 to 4.0 \u00b5g\/mL against clinical viral isolates [5]. Although oral ACV (800 mg five times daily for 7-10 days) has been the mainstay of herpes zoster treatment, its poor bioavailability and need for frequent daily dosing has prompted the design of newer antiviral agents (valacyclovir and famciclovir) with improved pharmacokinetics [6-9].<\/p>\n

 <\/p>\n

Valacyclovir<\/strong> \u0097 Valacyclovir is well absorbed from the gastrointestinal tract and is rapidly converted to ACV in vivo, thereby providing a three- to five-fold increase in ACV bioavailability [9,13]. (See “Valacyclovir: An overview”). Valacyclovir is approved by the United States Food and Drug Administration (FDA) for the treatment of herpes zoster in immunocompetent adults. (1000 mg PO three times daily for 7 to 14 days)<\/p>\n

 <\/p>\n

Famciclovir<\/strong> \u0097 Famciclovir, the prodrug of penciclovir, is well absorbed from the gastrointestinal tract and is rapidly converted in the intestinal wall and liver to the active compound penciclovir that has broad activity against VZV (500 mg given three times daily)<\/p>\n

 <\/p>\n

 <\/p>\n

Localized herpes zoster in an immunocompetent host is only contagious from direct contact with open lesions. \"\"<\/a>\"\"<\/a><\/p>\n

The mechanism of zoster paresis has not been determined. Weakness develops abruptly within 2-3 weeks after the rash and can involve upper or lower extremities. The prognosis of zoster paresis is good (MMWR, June 6, 2008).<\/p>\n

<\/span>Herpes Zoster Keratitis<\/span><\/h3>\n

 <\/p>\n

Hutchinson’s Sign<\/h4>\n

herpetic involvement of tip of nose, V1 distribution<\/p>\n

treat c acycolvir, fam, or val.\u00a0 Get Optho consult<\/p>\n

can treat with oral if immunocompetent (N Engl J Med 2002 Aug 1;347(5):340-6.)<\/p>\n

 <\/p>\n

<\/span>Ramsey Hunt Syndrome (Herpes Zoster Oticus)<\/span><\/h3>\n

Ramsey Hunt syndrome is characterized by unilateral facial paralysis, a herpetiform vesicular eruption, and vestibulocochlear dysfunction. Can see vesicles on ear drum and decreased taste.\u00a0 The vesicular eruption may occur on the pinna, external auditory canal, tympanic membrane, soft palate, oral cavity, face, and neck as far down as the shoulder. There is considerably more pain than is associated with Bell\u0092s palsy, and the pain is frequently out of proportion to physical findings. In addition, outcomes are worse than with Bell\u0092s palsy, with a lower incidence of complete facial recovery and the possibility of sensorineural hearing loss. Therapy is similar to that for Bell\u0092s palsy. Antiviral therapy for 7 to 10 days have been advocated, also steroids prednisone 60 mg c 3 week taper.<\/p>\n

RAMSAY HUNT SYNDROME –<\/p>\n

A Case Report<\/p>\n

 <\/p>\n

P.S. NAGAPUPRE<\/p>\n

 <\/p>\n

A Case Report<\/p>\n

 <\/p>\n

Prof & Head, Deptt of ENT, MGIMS Sevagram,<\/p>\n

 <\/p>\n

Wardha, Maharashtra -442102<\/p>\n

 <\/p>\n

Introduction :<\/p>\n

 <\/p>\n

In 1906 James Ramsay Hunt gave a classic<\/p>\n

 <\/p>\n

description of the syndrome consisting of blisters<\/p>\n

 <\/p>\n

facial paralysis, and inner ear disturbances due<\/p>\n

 <\/p>\n

to herpes zoster. Since his description, the name<\/p>\n

 <\/p>\n

Ramsay Hunt and the designation Herpes Zoster<\/p>\n

 <\/p>\n

Oticus have been synonymous.He felt the problem<\/p>\n

 <\/p>\n

to be geniculate ganglionitis due to the herpes<\/p>\n

 <\/p>\n

virus. Subsequent investigators with the benefit<\/p>\n

 <\/p>\n

of histopathologic studies of autopsy cases of<\/p>\n

 <\/p>\n

patients with herpes zoster oticus demonstrated<\/p>\n

 <\/p>\n

little, if any, ganglion involvement. They did find<\/p>\n

 <\/p>\n

heavy lymphocytic infiltration in the substance<\/p>\n

 <\/p>\n

of the facial nerve. These findings were present<\/p>\n

 <\/p>\n

in facial nerve in several patients with paralysis<\/p>\n

 <\/p>\n

who recovered (1).<\/p>\n

 <\/p>\n

Discussion :<\/p>\n

 <\/p>\n

Herpes zoster oticus or Ramsay Hunt<\/p>\n

 <\/p>\n

syndrome includes facial paralysis associated with<\/p>\n

 <\/p>\n

hearing loss, dizziness, and herpetic eruption<\/p>\n

 <\/p>\n

around the auricle (commonest site being the<\/p>\n

 <\/p>\n

concha of the auricle). Herpes zoster oticus is the<\/p>\n

 <\/p>\n

cause of 2 to 10% of all cases of facial paralysis,<\/p>\n

 <\/p>\n

including 3 to 12% of adults and approximately<\/p>\n

 <\/p>\n

5% of children.<\/p>\n

 <\/p>\n

The facial nerve is the commonest to be<\/p>\n

 <\/p>\n

involved followed by the ocular nerve. This is due<\/p>\n

 <\/p>\n

to the fact that these nerves pass through bony<\/p>\n

 <\/p>\n

canal in the skull. This course in the bony canal<\/p>\n

 <\/p>\n

increases the chances of entrapment.<\/p>\n

 <\/p>\n

Pathologically, the theory of inflammatory<\/p>\n

 <\/p>\n

changes as a cause of Bell\u0092s palsy or facial paralysis<\/p>\n

 <\/p>\n

has been proposed by many authors. Sade described<\/p>\n

 <\/p>\n

casesoffacialparalysissecondarytoexternalotitis<\/p>\n

 <\/p>\n

with the inflammation traveling along the chorda<\/p>\n

 <\/p>\n

tympani or sensory anastomoses to the facial<\/p>\n

 <\/p>\n

nerve. Denny – Brown showed that pressure on a<\/p>\n

 <\/p>\n

nerve causes ischemic paralysis. Even a small<\/p>\n

 <\/p>\n

amount of inflammation will suffice to cause<\/p>\n

 <\/p>\n

pressure; thus, a relatively small amount of edema<\/p>\n

 <\/p>\n

or inflammatory exudates could cause strangulation<\/p>\n

 <\/p>\n

of the nerve. Fisch proved these changes<\/p>\n

 <\/p>\n

with photography of the inflammatory changes<\/p>\n

 <\/p>\n

in the labyrinthine portion of the facial nerve (1).<\/p>\n

 <\/p>\n

Hunt classified the disease into 4 grades<\/p>\n

 <\/p>\n

asfollow (7):<\/p>\n

(1) Disease affecting the sensory portion of<\/p>\n

the CN VII.<\/p>\n

(2) Disease affecting the sensory and motor<\/p>\n

divisions of the CN VII<\/p>\n

(3) Disease affecting the sensory and motor<\/p>\n

divisions of the CN VII with auditory<\/p>\n

symptoms<\/p>\n

(4) Disease affecting the sensory and motor<\/p>\n

divisions of the CN VIIwith both auditory<\/p>\n

and vestibular symptoms.<\/p>\n

Many authors have shown that there is no<\/p>\n

real difference between herpes zoster and Bell\u0092s<\/p>\n

palsy. Complement fixation test carried out by<\/p>\n

Tomita et al (3) in 1973 found that 25% of patients<\/p>\n

with Bell\u0092s palsy had positive for complement<\/p>\n

J MGIMS, January 2006, Vol 11, No (i), 55 – 57<\/p>\n

fixation tests. Paralysis of herpes zoster may more<\/p>\n

likely be a complete but predictability from<\/p>\n

electrical tests, and the time of recovery seem<\/p>\n

similar to those of Bell\u0092s palsy however the<\/p>\n

natural history between the two differs in several<\/p>\n

ways (2).<\/p>\n

1. Bell\u0092s palsy recurs in 12% of cases, but<\/p>\n

Herpes Zoster rarely recurs.<\/p>\n

2. With Bell\u0092s palsy the decrease in response<\/p>\n

to electrical testing peaks in 5-10 days<\/p>\n

but in Herpes zoster the peak is later<\/p>\n

(10-14days).<\/p>\n

3. 84% of those suffering from Bell\u0092s palsy<\/p>\n

have satisfactory recovery, but 60% of<\/p>\n

those with Herpes zoster oticus recover<\/p>\n

to a satisfactroy degree.<\/p>\n

The medical management for facial<\/p>\n

paralysis of herpes zoster is aimed at eliminating<\/p>\n

inflammation and ischemia of the nerve, thereby<\/p>\n

restoring facial function as quickly as possible.<\/p>\n

Steroid dose as recommended for adults is a<\/p>\n

daily total of 1mg\/kg body weight in divided<\/p>\n

dose. If the palsy is incomplete by the fifth day<\/p>\n

the dosage can be tapered to zero during the next<\/p>\n

5 days, if there is a question about the severity<\/p>\n

or the progression of severity full dosage is<\/p>\n

recommended for 10 days and then tapered<\/p>\n

over the next 5 days(4,5).<\/p>\n

Acyclovir, a virostatic drug developed<\/p>\n

for the use in the treatment of herpes simplex<\/p>\n

has been found to prevent replication of varicellazoster<\/p>\n

virus. Acyclovir in the host cell is converted<\/p>\n

to acyclovir triphosphate and gets incorporated<\/p>\n

in the newly formed viral DNA, resulting in<\/p>\n

termination of the DNA molecular chain. Because<\/p>\n

VZV is generally less sensitive to acyclovir than<\/p>\n

is HSV, higher dose must be used to treat VZV<\/p>\n

infection. Oral Acyclovir is available; however,<\/p>\n

absorption from the gastrointestinal tract is only<\/p>\n

15% – 25% of the ingested dose. A dose of 800mg<\/p>\n

five times a day has a modest beneficial effect to<\/p>\n

localize the lesion. For these reason intravenous<\/p>\n

dose of 10 mg\/kg every 8 hours over a 7 days<\/p>\n

hospitalization has been recommended. This<\/p>\n

intravenous route has more inherent expenses<\/p>\n

than an oral route of administration. Prognosis<\/p>\n

depends primarily on immediate initiation of<\/p>\n

therapy(6). Alternate antiviral agents such as<\/p>\n

valacyclovir (1 g orally three times a day for 10<\/p>\n

to 14 days) or famciclovir (500mg orally three<\/p>\n

times a day for 10 days), which achieve adequate<\/p>\n

levels by an oral route, are now available as an<\/p>\n

alternative to intra-venous.<\/p>\n

Bibliography :<\/p>\n

1. Crabtree, J.A., Herpes Zoster Oticus and Facial<\/p>\n

paralysis.<\/p>\n

Otolarygologic clinnic of North America, <\/em><\/p>\n

June 1974.<\/p>\n

7(2)<\/strong>: p. 369-373.<\/p>\n

2. May, B.S.a.M., Disorder of the facial nerve. sixth<\/p>\n

ed. Scott-Brown\u0092s Otolaryngology, ed. A.G.<\/p>\n

Kerr. Vol. vol. 3. 1997, Jordan Hill, Oxford:<\/p>\n

Butterworth-Heinmann. 3\/24\/25.<\/p>\n

3. Tomita, H., Hayakawa, W. and Hondo, R.,<\/p>\n

varizella-Zoster virus in idiopathic facial palsy.<\/p>\n

Archives otolayngology,<\/p>\n

1972. 95<\/strong>: p. 364.<\/p>\n

4. May, B.S.a.M., Causes and management of facial<\/p>\n

paralysis. sixth edition ed. Disease of the ear, ed.<\/p>\n

L.a. Wright, 198 madison avenue, New York:<\/p>\n

Georgina Bentloff. 261.<\/p>\n

5. Adour, k.K., Facial paralysis.<\/p>\n

Trans. Am. Acad. <\/em><\/p>\n

Ophthal. Otolaryng.,<\/p>\n

1971. 76<\/strong>: p. 1284.<\/p>\n

6. John R.E. Dickins, J.T., Sharon S. Graham,<\/p>\n

Herpes zoster oticus : Treatment with intravenous<\/p>\n

Acyclovir.<\/p>\n

Laryngoscope, <\/em>july 1988. 98<\/strong>: p.776-779.<\/p>\n

7. Phillip A. Wackym, John S. Rhee., facial paralysis<\/p>\n

sixteen ed. Ballenger\u0092s Otorhinolaryngology<\/p>\n

Head and Neck surgery, ed. Snow, J.B.Jr.,<\/p>\n

Ballenger, J.J, 2003, BC Decker Inc., Hamilton.<\/p>\n

Ontario: 492-494.<\/p>\n

J MGIMS, January 2006, Vol 11, No (i), 55 – 57<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Post-Herpetic Neuralgia<\/span><\/h3>\n

After zoster attack.<\/p>\n

Persistent pain, Try TCAs.<\/p>\n

Amitriptyline<\/p>\n

10-25 mg PO OD<\/p>\n

Gabapentin<\/strong> Postherpetic neuralgia: Day 1: 300 mg, Day 2: 300 mg twice daily, Day 3: 300 mg 3 times\/day; dose may be titrated as needed for pain relief (range: 1800-3600 mg\/day, daily doses >1800 mg do not generally show greater benefit)<\/p>\n

 <\/p>\n

Treatment of Herpes Zoster (EMEDhome)<\/strong><\/p>\n