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Leslie Barker, Tring HP23 The V&A exhibition Modernism 1914-1939 has been acclaimed, and it was instructive to see the part played by the performing arts, designer clothing, and the pursuit [...]

ABSTRACTBetween October 2005 and May 2006, a total of 727 badgers found dead in Wales were reported, and 550 were delivered to the Regional Laboratories of the Veterinary Laboratories Agency (VLA). Of the 459 carcasses suitable for examination, 55 were deemed to be infected with Mycobacterium bovison the basis of culture, spoligotyping, and variable-number tandem repeat typing. Acid-fast bacteria were observed histologically in a further six badgers, but these bacteria were not confirmed as M. bovisby culture. A rapid serological test (BrockTB Stat-Pak) performed on thoracic blood showed a sensitivity of 35% and a specificity of 99%. Presence of M. bovisinfection was 45 times more likely to be confirmed postmortem by culture in BrockTB Stat-Pak-reactive animals than in seronegative ones. Using visible carcass lesions as a marker of bovine tuberculosis (bTB) infection had a similar sensitivity (38%) but was significantly less specific (84%) than serology. The overall accuracy of the antibody detection was 93% (346 correct results from 374 tests), whereas the accuracy of regarding visible lesions as a marker for bTB infection was 78% (354 correct from 453 carcasses examined). Culture remains the gold standard method for detecting M. bovisinfection in badgers. However, where resources are limited and/or an instant result is preferred, the BrockTB Stat-Pak could be used in field surveillance efforts to identify animals which should be examined further by only submitting test-negative animals to more detailed postmortem examination and culture.

Nine epidemiologically unrelated isolates {1 Salmonella Bredeney from turkeys, and 8 Escherichia coli [3 environmental isolates (2 from chickens, 1 from pigs), and 5 isolates from cattle with neonatal diarrhea]} were examined both pheno- and genotypically for extended-spectrum β-lactam (ESBL) resistance. Resistance phenotypes (ampicillin, aztreonam, cefotaxime, cefpodoxime, ceftazidime, and ceftriaxone) suggested the presence of an ESBL enzyme, but cefoxitin MICs (≥ 32 mg/L) suggested the presence of an AmpC-like enzyme. Synergism experiments with benzo(b)thiophene-2-boronic acid (BZBTH2B) and isoelectric focusing (IEF) revealed the presence of an AmpC β-lactamase with a pI ≥ 9. amp C multiplex PCR, sequence, and Southern analyses indicated that only the Salmonella isolate had a plasmid-encoded AmpC β-lactamase CMY-2 on a nonconjugative 60-MDa plasmid. PCR and sequence analysis of the E. coli ampC promoter identified mutations at positions -88(T), -82(G), -42(T), -18(A), -1(T) and +58(T) in all the isolates. In addition one strain had two extra-mutations at positions +23(A) and +49(G), and another strain had one extra-mutation at position +32(A). DNA fingerprinting revealed that all the E. coli isolates were different clones. It also showed that the U.K. Salmonella isolate was indistinguisable from a Canadian Salmonella isolate from turkeys; both had identical resistance phenotypes and produced CMY-2. This is the first report of a CMY-2 Salmonella isolate in the United Kingdom. These data imply that β-lactam resistance in animal isolates can be generated de novo as evidenced by the E. coli strains, or in the case of the Salmonella strains be the result of intercontinental transmission due to an acquired resistance mechanism.

During the warm seasons, physicians throughout the United States should be alerted to a recently recognized murine rickettsial disease, known as rickettsialpox, which to date has been reported only from the city of New York. Because the disease is harbored by the common house mouse (Mus musculus), is transferred to humans by the rodent mite (Allodermanyssus sanguineous) and because it has not subsided in incidence in the New York area for the past two years, the possibility of the spread of rickettsialpox to other cities is highly probable.The first cases of rickettsialpox1 were discovered in the spring of 1946 among a group of persons residing in a housing development in the Queens section of New York. Since then about 150 cases a year, from Queens and three other boroughs, have been reported to the New York City Department of Health. N[ill] fatalities have been recorded.The causative agent

Since the development of laboratory procedures which demonstrate its presence, the virus of herpes simplex has been found to be the cause of a wide range of infections. It has been demonstrated in such localized lesions as the common fever blister, aphthous stomatitis, acute herpetic gingivostomatitis1 and paronychia. It has also been recovered from the spinal fluid2 and brain substance3 of patients with encephalitis. Since 1941 the virus of herpes simplex has been demonstrated in the cutaneous lesions of those infrequent and grave systemic infections known as Kaposi's varicelliform eruption.This uncommon syndrome which bears Kaposi's name was first clinically described by him in 18874 as a disease resembling chickenpox and occurring in children with allergic eczema. His description of the disease follows:The vesicles are as large as a lentil, filled with clear serum, and the majority are umbilicated. They look like varicella vesicles but

During the past few years there has been a renewed interest in organic luetin in relation to the cutaneous reactions to its injection in syphilis. Several writers have given encouraging reports, the most optimistic of which have come from abroad.Noguchi,1 in 1911, using a luetin prepared from an extract of killed ascites agar cultures of Spirochaeta pallida, found that the skin of untreated patients with primary and secondary syphilis reacted negatively, while 70 per cent of those who had received arsphenamine gave positive reactions. In cases of congenital and late syphilis, almost 100 per cent of the patients gave positive reactions. The luetin reaction often remained positive after the Wassermann reaction of the blood became negative.Cohen,2 Ziegel,3 Wolfsohn,4 Pusey,5 Brown6 and others reported almost equally good results with Noguchi's luetin.The culture luetin continued to have many supporters until Clausz,7 Sherrick,

LETTERER-SIWE DISEASE (MALIGNANT, NONLIPID RETICULOENDOTHELIOSIS). PRESENTED BY DR. GEORGE C. ANDEREWS. HISTORY.— The patients were 8-month-old white male infants, identical twins. At the age of 4 months, both developed a skin eruption which persisted in spite of local use of steroids. There were involvement of the scalp consisting of a dry, scaly eruption which looked like "cradle cap" and also involvement of the mouth.They developed "ear infections" which cleared up after a while on antibiotics. PHYSICAL EXAMINATION.— On physical examination both infants present more or less the same clinical picture. The scalp is involved with a yellowish-brown crust which simulates seborrheic dermatitis. The skin, especially trunk and abdomen, presents a reddish-brown to orange-colored papular scaly eruption. Some of the papules look hemorrhagic; others are like xanthoma. Some are petechiae. There are small ulcerations in the oral mucosa.There is no lymphadenopathy, and spleen and liver cannot be palpated.

Since Hallopeau1,2 (1887) first described "lichen planus atrophicus,'' now known as lichen sclerosus et atrophicus,* there has been a plethora of confusing information regarding the segregation of this eruption as an authentic disease. The dermatosis has been placed in such various categories as lichen planus sclerosus, atrophic lichenoid dermatitis, white-spot disease, lichen albus, card-like scleroderma, morphea guttata— and many others. It was not until Kogoj3,4 (1934), Montgomery and Hill,5 (1940) and subsequent contributors brought out its specific clinical and histological features that the criteria for a classification of LSA were finally clarified.Although information on the general characteristics of LSA has been developed in the past years, there is still a lack of specific knowledge of the clinicopathologic features of the disease as it manifests itself on the female genitalia. Cases are often erroneously diagnosed as kraurosis vulvae, leukoplakia, and other precanceroses. As the consequence of incomplete

DIAGNOSIS: PROGRESSIVE LIPODYSTROPHY; CHRONIC URTICARIA AND ARTHRALGIA. PRESENTED BY DR. CARL T. NELSON. PATIENT: Eleven-year-old white female. HISTORY: Four years ago, the child developed intermittent pain in the lower limbs and a diagnosis of Legg-Perthes disease was documented by roentgenograms of the hip. Two and one-half years ago, she developed urticarial lesions of the lower limbs, accompanied by swelling of the ankles and knees and high fever. Hives and arthralgia appeared intermittently with periods of remission lasting no more than one month. Shortly after the onset of the above symptoms, a definite change in facial appearance occurred, but this was soon masked by mooning which appeared after the institution of steroid therapy 18 months ago. The child has been treated with desensitization injections, corticosteroids, a host of antihistaminics and antibiotics with no permanent relief. She was admitted to the Babies Hospital 12 days ago, and therapy consisting of Chlor-Trimeton, cyproheptadine,

Darier's Disease Resembling Linear Verrucous Epidermal Nevus. Presented by Dr. Benjamin J. Chester and (by invitation) Dr. Leonard Brown.The patient was a white girl, 25 years old.History: Patches of verrucous lesions on the right shoulder and right side of the chest, extending over the abdomen, were first noted at about 15 years of age. She saw a dermatologist in Cleveland, who biopsied the lesions on the right side and gave her oral vitamin A tablets for approximately nine months, which gave her no relief. During the next few years, she noted new lesions behind the right ear and within the right ear. She has had almost complete remission of these lesions at times. She noted exacerbations during pregnancy, four times, in 1953, 1954, 1956, and 1957. During these times, she has noted lesions bilaterally on forehead, flexor surfaces of right arm, and axilla. She developed

Under the title of "Chondrodermatitis Nodularis Chronica Helicis," Winkler1 in 1916 published the first study of painful nodules of the helix. The lesions of his eight cases were described as being cherryseed size with firmly attached central crusts which were painful under pressure. Upon removal of the crusts a small well-defined ulcer with an erythematous base remained. The skin lesions were attached to the cartilage. Episodes of infection beneath the crusts were common. Winkler believed that the cartilage had been damaged by traumatic, chemical, or thermal influence to the extent that it acted as a foreign body, provoking an inflammatory reaction in the skin.Foerster's2 (1918) findings on nodules of the helix, the first report in American literature, were in essential agreement with those of Winkler.In a 1929 report, Fox3 classified similar nodules of the anthelix as chondrodermatitis nodularis chronica helicis. Lane and Bechet, in their

MYCOSIS FUNGOIDES. PRESENTED BY DR. ALVIN M. LASHINSKY. Reason for presentation: Response of mycosis fungoides to teleroentgen therapy.History: The patient, a 70-year-old white man, was in excellent health until the onset of his disease 12 to 13 years ago, when he first began to have pruritus of the groin, without visible cutaneous changes. After six months, he developed redness and itching of the back of the left shoulder and left arm. The eruption gradually spread and new plaques appeared and coalesced over the ensuing twelve years, until most of his body was covered with lesions at the time he was first seen by us on May 15, 1958.He presented a generalized pruritic eruption consisting of many, large, confluent, brawny red, irregular-shaped plaques covering most of the body. Some of these lesions were crusted and most were infiltrated. On the left wrist there was a lesion which was markedly

DURING the past year, isonicotinic acid hydrazide (isoniazid) has been employed widely in the treatment of various types of systemic tuberculosis.1 Because of the favorable nature of preliminary studies, a trial of the drug seemed warranted in the treatment of tuberculosis involving the skin. This report summarizes observations on 7 patients with lupus vulgaris, 2 with scrofuloderma, 11 with erythema induratum (Bazin's disease), and 3 with papulonecrotic tuberculid. Two patients are reported on in detail. Four patients with sarcoidosis and one with the so-called rosacea-like tuberculid have been included. Leprosy has many clinical, pathological, and immunological similarities to tuberculosis; accordingly, a trial of isoniazid in the treatment of this disease was deemed important. Seven patients with leprosy were treated, three with the lepromatous, three with the tuberculoid, and one with the indeterminate form of the disease. Finally, a group of patients with miscellaneous skin diseases, including eight

OPINIONS differ as to the nosology of the bullous type of congenital ichthyosiform erythroderma. The pertinent questions that arise regarding this disease are the following: Is it a variant of the nonbullous type? Are the bullae due to a superimposed infection ? How is it clinically and histologically related to other dermatoses of the ichthyosis group? Or, finally, is the infection a combination of ichthyosis and epidermolysis bullosa?In an endeavor to answer these questions we have searched the literature on congenital ichthyosiform erythroderma for examples of the bullous form and have found only 19 such cases reported. Presented here is a history of a typical bullous case which has been under our observation for the past 18 months. A synopsis of the clinical and pathological findings in the 19 cases previously reported is also given.CASES IN THE LITERATUREAs first described by Brocq,1 in 1902, congenital ichthyosiform