Fixed Drug Eruption Caused by Tosufloxacin Tosilate

A 39-year-old woman presented with a purple-red macula, 2 cm in diameter, on the back of her right hand. She had had similar maculae at this location several times before and residual pigmentation had persisted for 6 months. Histopathological examination showed slight acanthosis of the epidermis and perivascular round-cell infiltration and melanophages in the dermis. Oral provocation tests with five drugs that the patient had received as common-cold treatments on different occasions were positive only in the case of tosufloxacin; after an hour the skin lesion reappeared. To our knowledge this is the first published report of a fixed drug eruption caused by tosufloxacin, although such eruptions have previously been reported for several other fluoroquinolones.

Thickening of the Synovium of the Digital Flexor Tendons: Cause or Consequence of the Carpal Tunnel Syndrome?

Using a monofilament wire suture, the radial and ulnar edges of the flexor retinaculum were approximated in 14 white New Zealand rabbits. As a result, the volume of the carpal tunnel was diminished, and “carpal tunnel syndrome” was produced. At various intervals after this procedure the animals were sacrificed. The median nerve and all the digital flexor tendons passing through the carpal tunnel were excised “en bloc”, and sent for histological examination. Vascular proliferation with perivascular round cell infiltration and oedema, and large areas of fibroblastic activity were observed around the digital flexor tendons. This was probably due to increased vascular permeability secondary to ischaemic endothelial damage. These findings are similar to those observed in the synovium of patients operated on for carpal tunnel syndrome.

Pathology of rats intranasally inoculated with the cilia-associated respiratory bacillus

Five-week-old Wistar/Ms rats were inoculated intranasally with a lung homogenate containing a strain of cilia-associated respiratory (CAR) bacillus and were examined on days 4, 7, 14, 21, 28 and 56 postinoculation (PI). Some rats showed clinical signs with wheezing and considerable body weight loss from day 21 PI. Gross lesions, including enlargement of lungs with focal atelectasis, bronchiectasis and emphysema, were observed from day 21 PI. Histologically, round cell infiltration was first present in the lamina propria of the nasal respiratory mucosa on day 7 PI. From day 14 PI, colonization of the CAR bacillus (4-8 µm in length), associated with round cell infiltration in the lamina propria and the peripheral regions, was observed in the ciliated mucosa of the bronchioles, bronchi, trachea and nasal cavities. Generally, the lesions progressed and expanded from upper to lower airways with time. Sporadic mucopurulent bronchopneumonia was observed from day 21 PI in some rats. The CAR bacilli (0·2-0·25 µm in diameter) were also demonstrated electron-microscopically in the ciliated epithelium of the intrapulmonary airways. The CAR bacillus antigen was demonstrated on the ciliated mucosa of the affected airways by the indirect immunofluorescence assay technique. Microbiological examination revealed that the rats used in this study were free from other known respiratory pathogens throughout the experimental period. Thus, it is suggested that the CAR bacillus alone can produce a murine respiratory disease. Fourteen days were needed for pathological lesions to develop.

Pathogenesis of Biliary Atresia

In Reply.— The letter of Esterly is an important one with some significant observations regarding a potential acquired inflammatory and viral etiology of biliary atresia. A marked and progressive inflammatory component of biliary atresia with extensive early round cell infiltration and progressive fibrosis was reported by one of the authors in 1953.1 This observation led to strong recommendations for early operation in biliary atresia.2,3 It has been suggested that biliary atresia, neonatal spontaneous perforation of the extrahepatic bile ducts, and choledochal cysts may be variants of an acquired infalmmatory process, possibly viral, such as cytomegalovirus, and possibly oncogenic.4

The Natural History of Haemophilic Arthritis

Surgical exploration of eight chronically afflicted haemophilic knee joints in patients aged 6 to 31 years, has revealed a pattern of progressive arthropathy.Significant synovial changes occurred very early. Cellular overgrowth produced thickening, convolution and increased vascularity. Haemosiderin was deposited heavily in all cell layers. Fibrosis ultimately contracted the synovium.Chronic inflammation produced epiphyseal overgrowth. Initially, articular cartilage changes resembled chondromalacia, but fissuring soon occurred and ultimately cartilage was totally lost over central weight-bearing areas and in the intercondylar region. Anomalies of matrix, chondrocyte aggregation and death, and subchondral round cell infiltration were features. Haemosiderin staining was sparse, occurring only in some chondrocytes and infiltrating cells.Biochemical analysis of articular cartilage biopsies revealed a severe depletion of glycosaminoglycans. There was no biochemical evidence of a reaction of repair.Articular cartilage damage occurred mainly between the ages of 6 and 10 years. This evidence suggests that early surgical synovectomy may arrest the process that produces progressive joint destruction.

PIGEON BREEDER'S LUNG IN CHILDREN

Diffuse interstitial pneumonitis associated with the prolonged exposure to pigeons is described in five boys ages 7 to 15. The clinical characteristics include a gradual onset of cough, shortness of breath, and weight loss; in three cases, acute onset of fever, chills, cough, and muscle aches occurred within 12 hours after heavy exposure. Physical findings consisted only of occasional rales and wheezes. The chest x-rays in four cases showed a diffuse interstitial pneumonitis. A lung biopsy in one case disclosed interstitial inflammation, round cell infiltration, and giant cell formation. The patients improved when the birds were removed. One severely ill boy was treated successfully with steroids. Pulmonary function studies disclosed diminished vital capacity, absent or minimal airway obstruction, and a variable defect in diffusing capacity. Their sera contained normal or elevated complement levels, increased γG and γA globulin, and precipitating antibody to extracts of pigeon feathers, droppings, and plasma. Levels of precipitating antibody, measured by a new radial diffusion technique, tended to correlate with the severity of the disease and the degree of exposure to pigeons. Antibody levels fell progressively when pigeons were removed from the environment. Except that the specific antigens differ, pigeons breeder's lung, Farmer's lung, bagassosis, maple bark stripper's disease and other similar syndromes are identical. They all differ sharply from allergic bronchial asthma in the symptoms and the mechanisms of the hypersensitivity. The histopathology of the biopsy, the elevated serum complement, and the absence of disease in some exposed individuals who have precipitins favor the interpretation that the pathogenesis of this illness is a delayed hypersensitivity to the inhaled antigens; but participation of an Arthus-type reaction cannot be excluded.

THE ROLE OF PENICILLIN-INDUCED BACTERIAL VARIANTS IN EXPERIMENTAL PYELONEPHRITIS

1. After injection into the renal medulla of rats Escherichia coli 06 variants reverted rapidly in vivo in the absence of penicillin. These variants had previously been shown to be stable in vitro. 2. Variants failed to survive following intramedullary injection when animals were receiving penicillin. 3. Late reversion of variants also failed to occur in animals treated with penicillin for only 1 or 2 days. 4. Variants survived and reverted more readily when injected in the renal medulla, compared with liver and spleen. Classical bacteria injected into the kidney, liver, and spleen were recovered in approximately equal numbers. 5. The histologic response to nonreverting variants, medium not containing variants, and killed variants was similar and was characterized by a fibrotic reaction with moderate round cell infiltration. 6. In contrast, the histologic response to reverting variants and to classical E. coli was characterized by an intense, acute, polymorphonuclear leukocytosis typical of acute pyelonephritis.

ACUTE AND CHRONIC ENTEROTOXIN ENTERITIS

1. Dogs develop severe gastrointestinal symptoms in response to intraintestinal administration of staphylococcal enterotoxin. These symptoms are salivation, vomiting, and diarrhea. 2. Staphylococcal enterotoxin induces acute enteritis marked by edema, hyperemia, round cell infiltration, mucosal exudation, and destruction of intestinal villi. 3. Prolonged administration of enterotoxin into the lumen of the intestine produced thickening of the entire bowel wall, edema, dilatation of the lymphatics, and exaggeration of submucous lymphoid nodules. The hypertrophy of the lymphoid nodules is visible, in the gross, as enlarged longitudinal mucosal ridges. This abnormality is arranged in skip areas, not dissimilar to those observed in human regional enteritis. 4. Chronic enterotoxin enteritis is associated with mesenteric lymph node hypertrophy. 5. The intestinal mucosa shows minute ulcerations, loss of villi, submucous fibrosis, and evidence of chronic inflammation.