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Non menstrual toxic shock syndrome: new insights into diagnosis cheapest generic toradol uk pain treatment with methadone, pathogenesis toradol 10 mg with amex wnc pain treatment center arden nc, and treatment. Toxic-shock syndrome: epidemiologic features, recurrence, risk factors, and prevention. Development of serum antibody to toxic shock toxin among individuals with toxic shock syndrome in Wisconsin. Epidemiologic analysis of group A Streptococcus serotypes associated with severe systemic infections, rheumatic fever, or uncomplicated pharyngitis. Evidence for superantigen involvement in severe group A streptococcal tissue infections. Streptococcal toxic shock syndrome: synthesis of tumor necrosis factor and interleukin-1 by monocytes stimulated with pyrogenic exotoxin A and streptolysin O. Toxin shock syndrome-associated staphylococcal and streptococcal pyrogenic toxins are potent inducers of tumor necrosis factor production. Streptococcal pyrogenic exotoxin B enhances tissue damage initiated by other Streptococcus pyogenes products. Clinical and microbiological characteristics of severe group A Streptococcus infections and streptococcal toxic shock syndrome. Differences in potency of intravenous polyspecific immunoglobulin G against streptococcal and staphylococcal superantigens: implications for therapy of toxic shock syndrome. The Eagle effect revisited: efficacy of clindamycin, erythromycin, and penicillin in the treatment of streptococcal myositis. Penicillin-binding protein expression at different growth stages determines penicillin efficacy in vitro and in vivo: an explanation for the inoculum effect. Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin. Impact of antibiotics on expression of virulence-associated exotoxin genes in methicillin-sensitive and methicillin-resistant Staphylococcus aureus. Intravenous immunoglobulin therapy for streptococcal toxic shock syndrome—a comparative observational study. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double blind, placebo controlled trial. Characterization of a strain of community-associated methicillin-resistant Staphylococcus aureus widely disseminated in the United States. Skin and soft-tissue infections caused by community-acquired methicillin-resistant Staphylococcus aureus. Necrotizing fasciitis caused by community associated methicillin resistant Staphylococcus aureus in Los Angeles. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. Comparative activity of telavancin against isolates of community-associated methicillin-resistant Staphylococcus aureus. Telavancin versus vancomycin for the treatment of complicated skin and skin-structure infections caused by gram-positive organisms. Results of a double-blind, randomized trial of ceftobiprole treatment of complicated skin and skin structure infections caused by gram positive bacteria. Tribble Enteric Diseases Department, Infectious Diseases Directorate, Naval Medical Research Institute, Silver Spring, Maryland, U. Sometimes symptoms begin as early as on the plane ride home, sometimes not until weeks later. In either case, the patient becomes progressively ill, critically so, all the while unknowingly infecting others. The disease spreads, chaos is loosed, and only the timely insight of an awkwardly introverted yet surprisingly attractive physician stands between armageddon and the return of normalcy. Nonetheless, the likelihood of today’s critical care physician having to manage patients with a tropical infection is increasing, as international travel has increased from an estimated 25 million border crossings in 1950 to over 806 million crossings in 2005 (1). To better prepare travelers prior to their trips abroad, the discipline of travel medicine has been refined over the past 25 years, with an increasing reliance upon evidence-based data and the recent publication of practice guidelines (2). This information assists the physician in determining not only what vaccines or prophylactic regimens may help prevent infection in the traveler, but also stresses the importance of safety awareness and environmental risk avoidance. It is no surprise, then, that each year four million travelers returning from developing countries become ill enough that medical intervention is required either en route or upon return home (4). That is not to say there are four million cases of Ebola or African trypanosomiasis every year, but how can the clinician know what illnesses are being seen, and more importantly, which to consider more likely in their patients? Established in 1995, it now comprises 41 travel or tropical medicine clinics (16 in the United States, 25 in other countries representing all continents) that not only report what diagnoses are seen in their facilities, but additional invaluable data such as time to presentation of illness, geographic exposures, adherence to prophylactic measures, etc. With now more than a decade of surveillance information available, it has been shown that febrile illness, dermatologic disorders (especially insect bites), and acute/chronic diarrheal illnesses comprise almost 70% of all travel-related illness (4). An analysis of 6957 travelers with fever revealed that malaria (21%), acute diarrheal disease (15%), respiratory illness (14%), and dengue (6%) were the most commonly identified etiologies (6). Time to presentation can be helpful to the clinician when generating a differential diagnosis (see Table 1). It is helpful to realize that the familiar adage “common things are common” applies also to travel medicine. In a review of 25,023 patients within the GeoSentris database, there were no reported cases of travel-related anthrax, yellow fever, primary amebic meningoencephalitis, poliomyelitis, Rift Valley fever, tularemia, murine typhus, tetanus, diphtheria, rabies, Japanese encephalitis, or Ebola (4). In the same report, of 17,353 patients, only one case each of the following infections was identified: Angiostrongylus cantonensis, hantavirus, cholera, melioi- dosis, Ross River virus, legionellosis, meningococcal meningitis, and African trypanosomiasis. If any of these diagnoses is suspected, an infectious diseases consultation is recommended. As malaria is the single most common life-threatening infection in returning travelers (Table 2), it will be emphasized in this chapter. Other critical care infectious disease syndromes to be Table 2 General Considerations in Potentially Infected Critically Ill Returning Travelers Diagnostic consideration Comments Make accurate traveler- and itinerary-specific Obtain detailed history of sites visited, activities, and potential risk assessment. Incubation periods: short (<10 days); intermediate (10–14 days); prolonged (>21 days) A minimum period of 5–7 days before considering malaria. Narrow the differential diagnosis using clinical progression and specific findings (i. Always consider and perform diagnostic testing to evaluate for malaria if a traveler has been in a malarious region with an appropriate incubation period. Data from 1997–2002 collected through the GeoSentinel global sentinel surveillance identified malaria in 3. Patients with falciparum malaria were more likely to have traveled to sub-Saharan Africa (89%), with the majority (80%) presenting within four weeks of their return. Several important features are noted among those patients who died from their infection. These include: insufficient or inappropriate malaria chemoprophylaxis (90%) and delay in diagnosis and/or effective therapy (40%). Deaths were considered preventable in 85% of cases and were commonly attributed to patient-related decisions/actions and/or contributing medical errors (11). The current recommendations for malaria prophylaxis take into consideration regional antimalarial drug resistance (13). And so, as a result of our population’s increasing travel to malaria-endemic areas as well as oftentimes inadequate adherence to prescribed chemoprophylaxis, it is increasingly likely that today’s critical care physician will encounter patients with malaria.

In the very young child it is often impossible to carry out extensive operative treatment purchase toradol 10mg otc pain treatment research, but the placement of glass ionomer cement over areas of enamel hypoplasia is simple and effective order toradol paypal pain management in dogs. In older/more co-operative children stainless-steel (or nickel/chrome) preformed crowns should be placed on the second primary molars to minimize further wear due to tooth on tooth contact (Chapter 8587H ). It is advisable (and usually possible) to place such restorations with minimum tooth preparation because of the pre-existing tooth tissue loss. The teeth undergo such excessive wear that they become worn down to gingival level and are unrestorable. Teeth affected by dentinogenesis imperfecta are also prone to spontaneous abscesses due to the progressive obliteration of the pulp chambers. In these cases pulp therapy is unsuccessful and extraction of the affected teeth is necessary. As the permanent dentition develops close monitoring of the rate of tooth wear will guide the decision about what intervention is needed. Cast occlusal onlays on the first permanent molars not only protect the underlying tooth structure but also maintain function and control symptoms. The resulting increase in the vertical dimension is associated with a decrease in the vertical overlap of the incisors. Within a few weeks full occlusion is usually re-established, the whole procedure being well tolerated by young patients. Alternatively, localized composite or glass ionomer cement restorations may be placed over areas of hypoplasia. The emphasis should remain on minimal tooth preparation until the child gains adulthood. At this point, if clinically indicated, full mouth rehabilitation may be considered and should have a good prognosis in view of the conservative approach that has been adopted throughout the early years (Fig. The characteristic form of the teeth in this condition is unfavourable for crowning; the teeth being supported by short, thin roots. The permanent dentition, like the primary dentition, is prone to spontaneous abscesses and the prognosis for endodontic treatment is very poor. The long-term plan for these patients is often some form of removable prosthesis, either an overdenture placed over the worn permanent teeth or a more conventional complete denture. Where the child is sufficiently co-operative the use of glass ionomer cements to restore and improve the appearance of primary incisors can be useful in gaining the respect and support from the patient and parent. In a few exceptional cases the loss of primary teeth may cause upset, but can be compensated for by constructing dentures. In cases of dentinogenesis imperfecta where the teeth are very worn but remain asymptomatic, overdentures can be constructed to which young children adapt remarkably well. As the permanent incisors erupt they must be protected from chipping of the enamel. The placement of composite veneers not only improves the appearance but also promotes better gingival health and protects the teeth from further wear. In a few cases the quality of the enamel is so poor that the bond between composite and tooth will be unsuccessful. It should be noted that in these cases porcelain veneers are also likely to be unsuccessful and full coronal restorations are the only option. Early consultation with an orthodontist is advisable in order to keep the orthodontic requirements simple. Treatment for these patients is possible and in many cases proceeds without problems. The use of removable appliances, where appropriate, and orthodontic bands rather than brackets will minimize the risk of damage to the abnormal enamel. The problem is twofold: there may be frequent bond failure during active treatment or the enamel may be further damaged during debonding. Some orthodontists prefer to use bands even for anterior teeth, while others will use glass ionomer cement as the bonding agent in preference to more conventional resin-based agents. In other instances cosmetic restorative techniques (veneers and crowns) may be more appropriate than orthodontic treatment. Stainless- steel crowns were placed on the first permanent molars at 9 years of age (lower arch). A detailed discussion on the management of hypodontia is beyond the remit of this text, however, there are a few principles that can be considered. During infancy and early school years there is rarely a need for any active intervention. An exception may be infants with Ectodermal Dysplasia who can have multiple teeth missing. In such cases the provision of removable partial or even complete dentures can be highly successful. However, as children move through the mixed and permanent dentition phases, aesthetics become increasingly important. Replacing one or two teeth may be relatively straightforward using either removable partial dentures or adhesively retained bridges (Fig. However, those individuals with multiple missing teeth often have associated skeletal and dentoalveolar discrepancies which demand a multidisciplinary approach (Fig. The core to such a clinical team includes a paediatric dentist, orthodontist, and prosthodontist. In addition a periodontist and a maxillofacial surgeon may be required for implants, bone grafting, and/or orthognathic surgery in later years. Finally, access to a geneticist with expertise in orofacial anomalies can be beneficial as adolescents begin to contemplate the implications of their dental anomaly on family planning. Children with multiple missing teeth and their families should be referred early to a multidisciplinary team for discussion and preliminary planning. Consideration needs to be given to the number and position of the missing dental units, the age of the child, their level of and attitude towards oral health, and importantly the wishes and expectations of the individual and their family. The aim of orthodontic treatment is to consolidate the spacing and place the existing teeth in the optimum position to support the definitive restorations. However consideration also needs to be given to any underlying skeletal discrepancy or dentoalveolar deficiency that may require a more surgical approach. Interim restorative solutions, such as removable dentures, composite veneer, or partial veneer restorations, can be placed during the mixed dentition phase but will require maintenance throughout adolescence. Proactive preventive strategies need to be supported in order to achieve optimum dental and periodontal health. This is essential for the long-term success of definitive prosthodontic solutions which may include removable dentures, porcelain veneers or crowns, fixed conventional or adhesively retained bridges, and osseointegrated implants. Key Points • Children with multiple missing teeth should be: -referred early to a multidisciplinary clinical team; -exposed to proactive prevention to optimize their periodontal health. The management of children with advanced restorative problems should be viewed as a long-term commitment. Advanced restorative problems in children should be treated as conservatively as possible. Identification of the aetiology of tooth discolouration is essential for selecting the most appropriate treatment technique.

Changes in neurologic function are generally nonfocal and simply reflect the fact that the patient is ill and very uncomfortable toradol 10mg sale lower back pain treatment left side. This infection starts in the subarachnoid space purchase toradol cheap online pain treatment center franklin tn, but bacteria then invade and damage the arteries and veins passing into the adjacent brain, and invade the brain directly. This, in combination with the systemic effects of the bacteremia, can result in a lethal outcome. Most often infectious, there are also rare disorders in which this occurs on a primarily immunologic basis. Fortunately encephalitis of all types is quite rare (10,000 to 20,000 cases per year in the United States). Brain infections of all types are uncommon, in large part because the nervous system is so well protected. Bacterial infection, which most typically starts as a meningitis, occurs primarily in three settings—mechanical injury to the skull (traumatic or surgical), contiguous untreated infection in the sinuses or mastoids, eroding through bone, or bacteremia with an organism able to cross the blood–brain barrier. Herpes simplex is thought to use one of two routes—either tracking from the olfactory epithelium to the olfactory tracts and then into the medial temporal lobes or binding peripheral sensory nerve terminals, migrating intra-axonally to the sensory ganglia, then tracking centrally along trigeminal branches innervating the meninges (1). Poliovirus specifically binds receptors on motor neuron terminals, then migrates centrally within axons (2). Other strains of organisms have developed mechanisms to cross the blood–brain barrier, but lack the ability to bind to neurons or glia; these cause infections limited to the meninges, and not encephalitis. In most instances alterations of consciousness and cognitive function will be a nonspecific response to the febrile state, probably caused by circulating cytokines or other small molecules that cross the blood– brain barrier and are then neuroactive (3). Two key elements are involved in differentiating between such encephalopathies and primary brain processes. From the systemic perspective, identification of a specific underlying medical abnormality is the key. Neurologically, it is essential to establish whether the observed changes are focal or not—brain disorders resulting from localized damage to the brain cause abnormalities of function related to the site of damage. Damage to the cerebral cortex can cause seizures, an altered level of consciousness, and cognitive difficulty. Damage to the deep white matter causes spasticity, ataxia, visual and sensory problems, but not seizures and has a less severe impact on alertness and cognition. Damage to the brainstem can affect level of consciousness, long tracts that pass through the brainstem, but most importantly cranial nerve function. Damage to the temporal lobes can cause memory and olfactory problems, frontal lobe damage affects behavior, occipital lobe damage affects vision, etc. Typically if there is a brain-damaging process, functions that are affected remain affected throughout. In contrast, in patients with an encephalopathy abnormalities fluctuate in space and time. Hence a detailed clinical neurologic assessment can help differentiate between a structural process—i. In assessing patients’ mental status, one of the first steps must be assessing language. Without establishing meaningful communication with the patient, further assessment of brain function can be uninterpretable. Aphasic patients are commonly described as “confused” because what they say makes no sense. If a patient’s language sounds fluent but its content is incomprehensible, it is understandable to interpret this as evidence of confusion. However, several simple steps—asking the patient to follow several simple verbal commands (without helpful gesticulations), asking him/her to name a few objects or repeat a few words—should readily differentiate between a language disorder and a confusional state. Similarly, the behavior of a patient with psychosis may seem inexplicable and may be interpreted as evidence of confusion. Remarkably, although psychotic patients may Encephalitis and Its Mimics in Critical Care 155 demonstrate extraordinarily bizarre behavior, they almost always retain orientation and memory. Many disorders other than infections can produce focal brain damage—strokes and tumors being the most common. Differentiating between these disorders and infections should usually be straightforward, based on the clinical context. Stroke usually has a virtually instantaneous onset and causes abnormalities related to the specific blood vessel involved. Tumors typically cause symptoms that develop insidiously (over weeks or longer) and are not usually accompanied by systemic symptoms of infection. If there is no past history of epilepsy, and if no motor seizure activity was witnessed, these can be particularly perplexing. Post-ictal confusional states usually clarify themselves by resolving over minutes to hours. Although, as in patients with brain tumors, these patients do not typically have systemic symptoms of infection, assuming that this excludes encephalitis can be dangerous—not all patients with encephalitis have systemic signs at the onset, and encephalitis can present as non-convulsive status! All are potentially devastating and much-feared diseases—think of rabies or “sleeping sickness” as just two examples. On the other hand, most of the viruses that can cause encephalitis cause many more asymptomatic infections than symptomatic ones, and typically even among patients with symptomatic infection only a small subset develops neuroinvasive disease (2). The initial presentation of these infections is often unimpressive—typically much less dramatic than that of meningitis, where infection of the brain lining causes severe pain, sensitivity to light and sound, and reflex protective neck stiffness. The meninges and cortical blood vessels have nociceptive receptors, so inflammation is painful; the brain itself has no nociceptors. Fever, often low grade, is common—but less so in the very young, the elderly, and the immunocompromised. Neurologic changes are often initially limited to subtle alterations of consciousness or cognition—easily confused with the mild changes typically seen as a nonspecific result of systemic infection. Enteroviruses and listeria often cause prominent associated gastrointestinal symptoms. Specific Encephalitides A consideration of the specific infections (Table 1) that cause encephalitis should begin with those that are most treatable—spirochetoses, mycobacteria, and herpes viruses—all of which cause meningitis with varying degrees of parenchymal brain involvement. Consideration should next turn to disorders with significant prevalence—the arboviruses and most specifically West Nile Virus. Finally, there is a broad array of other agents that must be identified—if for no other reason than for epidemiologic recognition and prevention of additional victims (e. Although this infection is typically controlled by cell-mediated immunity, some degree of hematogenous dissem- ination occurs frequently. At some point long after initial infection, a tuberculoma may rupture into the subarachnoid space causing meningitis. This meningitis tends to involve the meninges at the base of the brain (regardless of where the tuberculoma was), where involvement of the cranial nerves and blood vessels that pass through the subarachnoid space is commonplace. In a small percentage of patients, brain imaging will demonstrate thick enhancement of the basilar meninges. The latter, indicative of a vigorous T-cell response, is said to have approximately 90% sensitivity Encephalitis and Its Mimics in Critical Care 157 and specificity. Outcome is heavily dependent on the patient’s level of function at the time treatment is initiated.

Now discount toradol 10 mg with visa jaw pain treatment medications, this is not to suggest that the author of On the Sacred Disease order 10 mg toradol fast delivery pain solutions treatment center atlanta, who has always been hailed as one of the first champions of an emancipated science of medicine, actually was a physician serving in the cult of Asclepius46 – even though the borderlines between secular 43 See Nestle (1938) 2; Edelstein (1967a) 223, 237. The reason for not accepting this suggestion is simply that the text does not support it (on 1. Yet what it does show is that the author has definite ideas on what one should do when invoking the help of the gods for the healing of a disease, and he may very well be thinking of the particular situation of temple medicine, with which he was no doubt famil- iar (which does not, of course, imply that he was involved in these practices or approved). One may point to this hypothetical ‘should’ and object, as I suggested at the beginning of this chapter, that these remarks need not imply the author’s personal involvement, but are solely used as arguments ad hominem. He may, for the purpose of criticising and discrediting his opponents, point out how a man ought to act when making an appeal to divine help for the cure of a disease, but this need not imply that he himself takes this way of healing seriously (after all, invoking the gods for healing presupposes the belief in a ‘supernatural’ intervention in natural processes). In this way one might say that all the preceding stipulations about impiety and piety are just made for the sake of argument and do not reveal any of the author’s own religious convictions: he may be perfectly aware of the truly pious thing to do without being himself a pious man. On the Sacred Disease 65 But I hold that the body of a man is not polluted by a god, that which is most corruptible by that which is most holy, but that even when it happens to be polluted oraffectedbysomethingelse,itismorelikelytobecleansedfromthisbythegodand sanctified than to be polluted by him. Concerning the greatest and most impious of our transgressions it is the divine which purifies and sanctifies us and washes them away from us; and we ourselves mark the boundaries of the sanctuaries and the precincts of the gods, lest anyone who is not pure would transgress them, and when we enter the temple we sprinkle ourselves, not as polluting ourselves thereby, but in order to be cleansed from an earlier pollution we might have contracted. It seems that if we are looking for the writer’s religious convictions we may find them here. The first sentence shows that the author rejects the presuppositions of his opponents, namely that a god is the cause of a disease; on the contrary, he says, it is more likely that if a man is polluted by something else (™teron, i. There is no reason to doubt the author’s sincerity here: the belief that a god should pollute a man with a disease is obviously blasphemous to him; and the point of the apposition ‘that which is most corruptible by that which is most holy’ (t¼ –pikhr»taton Ëp¼ toÓ ‰gnot†tou) is clearly that no ‘pollution’ (miasma) can come from such a holy and pure being as a god. As for the positive part of the statement, that a god is more likely to cleanse people of their pollutions than to bestow these to them, one may still doubt whether this is just hypothetical (‘more likely’) or whether the author takes this as applying to a real situation. This sentence shows that the author believes in the purifying and cleansing working of the divine. I do not think that the shift of ‘the god’ (¾ qe»v) to ‘the divine’ (t¼ qe±on) is significant here as expressing a reluctance to believe in ‘personal’ or concrete gods, for in the course of the sentence he uses the expression ‘the gods’ (to±si qeo±si). In fact, this whole sentence breathes an unmistakably polemical atmosphere: the marking off of sacred places for the worship of the gods was 48 But ‹n kaqa©resqai represents a potential optative rather than an unfulfilled condition. The distribution of ¾ qe»v, o¬ qeo© and t¼ qe±on in this context does not admit of being used as proof that the author does not believe in ‘personal’ gods. The use of the word ‘sprinkle’ (perirrain»meqa), which means ritual cleansing with water,50 is opposed to the ‘impious’ use of blood in the purificatory rituals of the magicians (1. Does this mean that he believes, after all, in the divine healing of diseases as taking place in temple medicine? One cannot be sure here, for the divine purification is explicitly defined by the author as applying to moral trangressions (tän ‰marthm†twn), indeed to the greatest of these. This restriction is significant in that it may indicate that in the author’s opinion an appeal to divine cleansing is only (or pri- marily) appropriate in cases of moral transgressions. I would suggest, as a hypothesis, that the author of On the Sacred Disease here aims at marking off the vague boundaries between medicine and religion: in his opinion it 50 See Parker (1983) 19; Ginouves (` 1962) 299–310. At any rate, the phrase oÉc Þv miain»menoi obviously expresses a reaction against the admittedly strange idea that the sprinkling of water entails pollution (on the prohibition to take baths see Ginouves (` 1962) 395 n. However, as Ginouves points out, there is a difference between a` loutr»n and a perirrantžrion. Versnel has suggested to me, to interpret the sentence as an extreme statement of the author’s belief (expressed in 1. There is still another possible interpretation which might be considered, which makes the sentence apply to the practice of temple medicine: ‘while entering the temple [for the healing of a disease], we sprinkle ourselves, not as if we were polluted [by the disease, i. This would suit the author’s aim of distinguishing between moral transgressions (which are, in his opinion, forms of pollution, mi†smata) and physical diseases (which are not) and would make sense of the words ¢ ti peponq»v in 1. However, on this interpretation pr»teron is difficult, and it would presumably require a perfect participle (memiasm”noi) instead of the present miain»menoi. On the Sacred Disease 67 is wrong to regard epilepsy (or any other disease) as a pollution (this seems to be the point of the words ãsper m©asm† ti ›contav in 1. He obviously thinks that no moral factor (punishment for crime or transgressions) is involved,53 and that, as a consequence, one should not believe that it can be cured by the gods alone. As for the author’s religious notions, we may deduce from these passages that he believes in gods who grant men purification of their moral trans- gressions and who are to be worshipped in temples by means of prayer and sacrifice. It is difficult to see how this conception of ‘the divine’ (to theion) can be incorporated within the naturalistic theology with which he has often been credited. But instead of concluding, therefore, that the statements of the first chapter are merely rhetorical remarks which do not reflect the author’s own religious opinion (which is apparently the course taken by most interpreters), I would throw doubt on the reality of this ‘naturalistic theology’ – for which I have given other reasons as well. It seems better to proceed in the opposite direction, which means starting from the religious assertions of the first chapter and then trying to understand the statements about the divine character of the disease. In this way, the text can be un- derstood as motivated by two interrelated purposes. First, by claiming that epilepsy is not god-sent in the traditional sense, the author does not intend to reject the notion of divine dispensation as such; his statements are to be regarded as a form of corrective criticism of a traditional religious idea. The author claims that it is blasphemous to hold that a holy and pure being like a god would send diseases as a form of pollution; thus his re- marks may be compared with statements by Plato which aim at correcting and modifying the traditional concept of divine dispensation (theia moira) without questioning the existence of this divine dispensation as such. To a certain extent this may be viewed as an attempt to ‘secularise’ the sacred disease; and from this point of view the positive statements about the divine character of the disease may be regarded as reluctant or even derogatory concessions rather than as proclamations of a new advanced theology. And from this perspec- tive it can further be understood why the author states that epilepsy is not more divine than the other diseases instead of saying that all diseases are just as divine as epilepsy. As we have seen, on the first interpretation of the divine character of the disease (which posits its divine character in its being caused by climatic factors), this restricted con- ception of divinity may well be connected with the fact that the influence of these factors is rather limited (and with the use of the word prophasis). On the second interpretation (and on the reading taÅth€ d’–stª qe±a, ‘in this respect they [i. On both views the derogatory tone of the statements can be understood from the author’s attempt to mark off the boundaries between medicine and religion and to purify the concept of divine dispensation. And it can now also be understood why he defines the divinity of the disease only in those contexts where he tries to point out the difference between the sense in which his opponents believe it to be divine and the sense in which he himself believes it to be so. This does not imply that the sincerity of the author’s statements about the divine character of the disease should be doubted. Nor should their relationship with developments in natural philosophy and with other con- temporary ideas on religion and the divine be questioned. It is precisely the philosophical search for unity and regularity in natural phenomena, the enquiry into cause and effect, and the belief, expressed by at least some of these philosophers, that in manifesting regularity and constancy these phenomena have a divine aspect, which may have led the author to assign a divine character to the disease in question. But the danger of stressing this relationship with natural philosophy is that we read into the text ideas 56 Contra Norenberg (¨ 1968) 26 and 49, who ignores the rhetorical impact of these statements. This danger is increased when this reading is guided by modern ideas about what is ‘primitive’ or ‘mythic’ and what is ‘advanced’ and ‘rational’, so that by labelling an author as advanced or enlightened we are too much guided in our interpretation of the text by what we expect him to say. Nowhere in On the Sacred Disease do we find statements such as that ‘Nature is divine’; nowhere do we find an explicit rejection of divine intervention in natural processes or of divine dispen- sation as such. It is important to distinguish between the corrective, ‘cathartic’ criticism of traditional religious beliefs and the exposition of a positive theology. It seems that the author of On the Sacred Disease has been regarded too much as an exponent of the latter, and that he has been regarded more as a philosopher or a theologian than as a physician.