Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)

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Vaccination and prevention

Ocular disease can be severe. Vesicles on the tip of the nose Hutchinson sign indicate involvement of the nasociliary branch and a higher risk of severe ocular disease. However, the eye may be involved in the absence of lesions on the tip of the nose. Intraoral zoster is uncommon but may produce a sharp unilateral distribution of lesions. No intraoral prodromal symptoms occur. However, many patients, particularly the elderly, have persistent or recurrent pain in the involved distribution postherpetic neuralgia , which may persist for months or years or permanently.

The pain of postherpetic neuralgia may be sharp and intermittent or constant and may be debilitating. Herpes zoster is suspected in patients with the characteristic rash and sometimes even before the rash appears if patients have typical pain in a dermatomal distribution. Diagnosis is usually based on the virtually pathognomonic rash. If the diagnosis is equivocal, detecting multinucleate giant cells with a Tzanck test can confirm infection, but the Tzanck test is positive with herpes zoster or herpes simplex.

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Herpes simplex virus HSV may cause nearly identical lesions, but unlike herpes zoster, HSV tends to recur and is not dermatomal. Viruses can be differentiated by culture or PCR. Antigen detection from a biopsy sample can be useful. Antivirals acyclovir , famciclovir , valacyclovir , especially for immunocompromised patients.

For treatment of ophthalmic herpes zoster , an ophthalmologist should be consulted. For treatment of otic herpes zoster , an otolaryngologist should be consulted.

Treatment with oral antivirals decreases the severity and duration of the acute eruption and the rate of serious complications in immunocompromised patients; it may decrease the incidence of postherpetic neuralgia. Corticosteroids do not decrease the incidence of postherpetic neuralgia.

For less severely immunocompromised patients, oral famciclovir , valacyclovir , or acyclovir see above is a reasonable option; famciclovir and valacyclovir are preferred.

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Although data concerning the safety of acyclovir and valacyclovir during pregnancy are reassuring, the safety of antiviral therapy during pregnancy is not firmly established. Because congenital varicella can result from maternal varicella but rarely results from maternal zoster, the potential benefit of treatment of pregnant patients should outweigh possible risks to the fetus.

Herpes Zoster - Infectious Diseases - MSD Manual Professional Edition

Pregnant patients with severe rash, severe acute pain, or ophthalmic zoster can be treated with valacyclovir or acyclovir , especially in later stages of pregnancy. Management of postherpetic neuralgia can be particularly difficult. Treatments include gabapentin , cyclic antidepressants, and topical capsaicin or lidocaine ointment. Opioid analgesics may be necessary. Intrathecal methylprednisolone may be of benefit. A recent study suggests that injecting the entire affected area with botulinum toxin A 40 injections in a chessboard pattern can reduce pain.

The newer, recombinant vaccine appears to provide better and longer-lasting protection than the older, single-dose, live-attenuated zoster vaccine. There are currently no data regarding the efficacy of the recombinant vaccine in immunocompromised patients and no recommendations for its use in immunocompromised patients.

The live-attenuated vaccine is contraindicated in immunocompromised patients.

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Herpes zoster is caused by reactivation of the varicella-zoster virus the cause of chickenpox from its latent phase. A painful rash, usually crops of vesicles on an erythematous base, develops on one or more adjacent dermatomes. Antivirals acyclovir , famciclovir , valacyclovir are beneficial, especially for immunocompromised patients.

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From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Manual was first published in as a service to the community. Learn more about our commitment to Global Medical Knowledge. If asked to define fever, most physicians would offer a thermal definition, such as "fever is a temperature greater than. Fewer still could cite the origin of the thermometer or trace the evolution of modern concepts of clinical thermometry.

Although many would have some knowledge of the fundamentals of thermoregulation and the role played by exogenous and endogenous pyrogens in the induction of fever, few would have more than a superficial knowledge of the broad biological activities of pyrogenic cytokines or know of the existence of an equally complex and important system of endogenous cryogens. A distinct minority would appreciate the obvious paradoxes inherent in an enlarging body of data concerned with the question of fever's adaptive value.

The present review considers many of these issues in the light of current data. The oldest known written reference to fever exists in Akkadian cuneiform inscriptions from the sixth century BC, which seem to have been derived from an ancient Sumerian pictogram of a flaming brazier that symbolized fever and the local warmth of inflammation.

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During the Middle Ages, demonic possession was added to the list of mechanisms believed responsible for fever. By the 18th century, Harvey's discovery of the circulation of blood and the birth of microbiology led iatrophysicists and iatrochemists to hypothesize, alternatively, that body heat and fever result from friction associated with the flow of blood through the vascular system and from fermentation and putrefaction occurring in the blood and intestines.

Subsequent work established that body temperature is tightly controlled within a narrow range by mechanisms regulating the rate at which such heat is allowed to dissipate from the body. The origin of the practice of monitoring body temperature as an aid to diagnosis is shrouded in uncertainty. The oldest known references to devices used to measure temperature date to the first or second century BC, when Philo of Byzantium and Hero of Alexandria are believed to have invented several such devices. In an analysis of a series of clinical thermometric measurements, the size of which has never been equaled estimated to have included some 1 million observations in as many as subjects , Wunderlich established Despite the fact that Wunderlich's work was published more than a century ago and was based primarily on axillary measurements generally taken no more often than twice daily, it has survived almost verbatim in modern day concepts of clinical thermometry.

Interestingly, recent tests conducted with one of Wunderlich's thermometers suggest that his instruments may have been calibrated by as much as 1. Fever has been defined as "a state of elevated core temperature, which is often, but not necessarily, part of the defensive responses of multicellular organisms host to the invasion of live microorganisms or inanimate matter recognized as pathogenic or alien by the host. The rise in temperature during fever is to be distinguished from that occurring during episodes of hyperthermia. Unlike fever, hyperthermia involves an unregulated rise in body temperature in which pyrogenic cytokines are not directly involved and against which standard antipyretics are ineffective.

It represents a failure of thermoregulatory homeostasis, in which there is uncontrolled heat production, inadequate heat dissipation, or defective hypothalamic thermoregulation. In the clinical setting, fever is typically defined as a pyrogen-mediated rise in body temperature above the normal range. Although useful as a descriptor for the febrile patient, the definition ignores the fact that a rise in body temperature is but one component of this multifaceted response. This standard clinical definition is further flawed, because it implies that "body temperature" is a single entity, when in fact, it is a pastiche of many different temperatures, each representative of a particular body part and each varying throughout the day in response to the activities of daily living and the influence of endogenous diurnal rhythms.

Heat is derived from biochemical reactions occurring in all living cells. At rest, more than half of the body's heat is generated as a result of the inefficiency of the biochemical processes that convert food energy into the free energy pool eg, adenosine triphosphate. In adult humans and most other large mammals, shivering is the primary means by which heat production is enhanced.

Nonshivering thermogenesis is more important in smaller mammals, newborns including humans , and cold-acclimated mammals. This highly specialized form of adipose tissue located near the shoulder blades, neck, adrenal glands, and deep blood vessels is characterized by its brownish color, a profuse vascular system, and an abundance of mitochondria. Heat, generated primarily by vital organs lying deep within the body core, is distributed throughout the body by the circulatory system.

In response to input from the nervous system, the circulatory system determines the temperature of the various body parts and the rate at which heat is lost from body surfaces to the environment via conduction, convection, radiation, and evaporation.

In anesthetized animals, although discrete hypothalamic warming increases such cutaneous blood flow, blood pressure is maintained because of a concomitant reduction in gastrointestinal blood flow. No single center within the nervous system controls body temperature.

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Rather, thermoregulation is a process that involves a continuum of neural structures and connections extending from the hypothalamus and limbic system through the lower brainstem and reticular formation to the spinal cord and sympathetic ganglia Figure 1. Although generally referred to as the preoptic region , it actually includes the medial and lateral aspects of the preoptic area, anterior hypothalamus, and septum. Numerous studies extending more than 60 years have established that neurons located in this region are thermosensitive and exert at least partial control over physiologic and behavioral thermoregulatory responses.

Many, although not all, thermophysiologists believe that the temperature-sensitive preoptic region "regulates" body temperature by integrating thermal input signals from thermosensors in the skin and core areas including the central nervous system. According to this theory, if the preoptic temperature rises above its set point for whatever reason eg, during exercise , heat loss responses are activated to lower body temperature and return the temperature of the preoptic region to the thermal set point eg, If, on the other hand, the preoptic temperature falls below its thermal set point eg, as a result of cold exposure , various heat retention and heat production responses are activated to raise body temperature and with it the temperature of the preoptic region to its thermal set point.

The thermal set point of a particular heat production response is thus the minimum temperature tolerated by the preoptic region before the response is evoked. Although useful in explaining the elevation of the thermal set point that occurs during fever, the concept of a single central set point temperature is regarded by many thermal physiologists as oversimplified. At least some of these physiologists prefer to think of body temperature as regulated within a narrow range of temperatures by a composite set point of several thermosensitive areas and several different thermoregulatory responses.

A variety of endogenous substances and drugs seem to affect temperature regulation by altering the activity of hypothalamic neurons. Perhaps the best examples of such substances are the pyrogenic cytokines in the next section. These are released by phagocytic leukocytes in response to a wide array of stimuli and have the capacity to raise the thermoregulatory center's thermal set point.

Whether they cross the blood-brain barrier to do so 22 , 23 or act by causing the release of other mediators eg, prostaglandin E 2 in circumventricular organs, such as the organum vasculosum laminae terminalis 22 is, as yet, uncertain. Whatever the precise endogenous mediators of fever, their primary effect seems to be to decrease the firing rate of preoptic warm-sensitive neurons, leading to activation of responses designed to decrease heat loss and increase heat production.

Pyrogens traditionally have been divided into 2 general categories: those that originate outside the body exogenous pyrogens and those derived from host cells endogenous pyrogens. Exogenous pyrogens are, for the most part, microbes, toxins, or other products of microbial origin, 24 whereas endogenous pyrogens are host cell—derived pyrogenic cytokines that are the principal central mediators of the febrile response. According to current concepts, exogenous pyrogens, regardless of physicochemical structure, initiate fever by inducing host cells primarily macrophages to produce endogenous pyrogens.

Such concepts notwithstanding, certain endogenous molecules also have the capacity to induce endogenous pyrogens. These include, among others, antigen-antibody complexes in the presence of complement, 25 , 26 certain androgenic corticosteroid metabolites, 27 - 29 inflammatory bile acids, 30 complement, 31 and various lymphocyte-derived molecules.

On occasion, a single cytokine, like a single word, may communicate a complete message. More often, however, complete messages received by cells probably resemble sentences, in which combinations and sequences of cytokines convey information. Because of such interactions, it has been difficult to ascertain the direct in vivo bioactivities of particular cytokines.

Nevertheless, several cytokines have in common the capacity to induce fever. Based on this characteristic, they have been codified as so-called pyrogenic cytokines. Undetectable under basal conditions in healthy subjects, they are produced by many different tissues in response to appropriate stimuli. Once released, pyrogenic cytokines have short intravascular half-lives. They are pleiotropic: they interact with receptors present on many different host cells. They are active in picomolar quantities, induce maximal cellular responses even at low receptor occupancy, and exert local autocrine or paracrine and systemic endocrine effects.

It has been theorized, although not proved, that interaction between pyrogenic cytokines and their receptors in the preoptic region of the anterior hypothalamus activates phospholipase A 2 , liberating plasma membrane arachidonic acid as substrate for the cyclooxygenase pathway. Some cytokines might do so by increasing cyclooxygenase expression directly, causing liberation of the arachidonate metabolite, prostaglandin E 2. Because this small lipid molecule easily diffuses across the blood-brain barrier, it might be the local mediator that actually activates thermosensitive neurons.

Although not discussed in this article, recent studies indicate that thermal information involved in the febrile response also might be transmitted from the periphery to the thermoregulatory center via peripheral nerves. Extensive work with pyrogenic cytokines during the last 2 decades has provided a hypothetical model for the febrile response Figure 2.

Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)
Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series) Understanding Herpes, 2nd Ed (Understanding Health and Sickness Series)

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