Pathogenesis of salmonellosis. Studies of fluid secretion, mucosal invasion, and morphologic reaction in the rabbit ileum.

Strains of Salmonella typhimurium were studied in the ligated rabbit ileal loop model to gain insight into the mechanisms whereby bacteria which invade the gastrointestinal mucosa evoke fluid exsorption. The organisms employed differed in various biologic attributes including the ability to invade the ileal epithelium, multiply within the mucosa, elicit an acute inflammatory reaction, and disseminate across the intestinal wall. Some strains provoked small intestinal fluid exsorption although these did not elaborate enterotoxin. Only those strains which invaded the mucosa were accompanied by either mucosal inflammation or fluid exsorption. Noninvasive strains produced neither histologic abnormalities nor fluid secretion. While strains which invaded the mucosa caused an acute inflammatory reaction, not all such strains evoked fluid secretion. Furthermore, there was no correlation in ability of invasive organisms to evoke fluid secretion or in the intensity of mucosal inflammation, number of intramucosal salmonellae, or in ability to disseminate from the rabbit ileum. These observations suggest that, as is the case in shigellosis, mucosal invasion may be a necessary factor for the intestinal fluid loss in salmonellosis. A bacterial property or factor, in addition to invasion of the gastrointestinal mucosa, seems to be responsible for fluid exsorptin. However, it is unlikely that a salmonella enterotoxin comparable to that elaborated by Vibrio cholerae, toxigenic Escherichia coli, or Shigella dysenteriae 1 is related to fluid secretion in salmonellosis.

Transmissible spongiform encephalopathy (Creutzfeldt-Jakob disease). Atypical clinical and pathological findings.

A middle-aged neurosurgeon had an 18-month illness characterized by abnormal sleep patterns, paresthesias, and necrotizing cutaneous lesions with vasculitis and signs of cerebral, brainstem, vestibulocerebellar, and progressive spinal cord involvement. Biopsy specimens of nerve and skin showed an acute vasculitis with endovascular cellular proliferation in the pattern of a Köhlmeier-Degos lesion and focal epidermal necrosis. Mental changes and cranial-nerve signs developed. Myoclonus occurred occasionally during sleep. Akinetic mutism ensued. At autopsy, major abnormalities were limited to the nervous system and skin. Spongiform encephalopathy typical of Creutzfeldt-Jakob disease was found with amyloid kuru plaques. A cribriform change distinct from the spongiform change was seen focally in the white matter. Scarred skin lesions and a healed, partially obliterative arteritis were noted. Inoculation of brain and lung into nonhuman primates resulted in a spongiform encephalopathy.

Small vessel replacement with gore-tex (expanded polytetrafluoroethylene).

Conduits of expanded, fibrillated polytetrafluoroethylene (PTFE [Gore-tex]) have been evaluated as small vessel prostheses in dogs during a 6-month period. A configuration of high porosity and low density, long fibril Gore-tex was found to yield the best patency in canine arteries (femoral and carotid) and veins (femoral) as compared with more dense, less porous PTFE with shorter fibrils. Host tissue reaction showed minimal inflammation, excellent infiltration, and formation of a smooth neointima, which suggested satisfactory acceptance of the prosthesis.

Erythema migrans: a chronicle.

Arvid Afzelius first described and named erythema migrans (EM), a clinical entity that he assumed to be caused by an agent transmitted by the bite of a tick (Ixodes reduvius). Certain neurologic, cutaneous, and other syndromes observed in Europe were recognized in the 1920s and 1930s to be disabling sequelae of EM. In the 1940s and 1950s the effectiveness of penicillin as therapy for EM was demonstrated. In 1968 the first patient with EM and neurologic sequelae in North America benefited from treatment with penicillin. In 1975, an epidemic arthropathy appeared in the area of Lyme, Connecticut. Despite resemblance to EM (the initial appearance of cutaneous lesions), the complex was called Lyme disease because of the occurrence of cardiac, neurologic, and arthritic sequelae. The vector of Lyme disease, Ixodes dammini--a tick that harbors agents that cause Lyme disease and babesiosis--was identified and characterized in 1979. The spirochete that causes Lyme disease was designated Borrelia burgdorferi. The North American and European species of spirochete and the clinical syndromes to which they are related are described.

Effect of exogenous interferon on neonatal infection with murine cytomegalovirus.

One dose of interferon given before inoculation of MCMV to the neonatal mouse resulted in less virus in the submaxillary glands and reduced tissue damage due to MCMV infection, probably by modulating the immune system.

Protective effect of low-dose interferon against neonatal murine cytomegalovirus infection.

Mice were injected with 10 to 5,000 reference units of interferon intraperitoneally or subcutaneously within 24 h of birth and reinoculated intraperitoneally 24 h later with 200 plaque-forming units of murine cytomegalovirus. Mock interferon and virus diluent were the control inocula. Infection of mock interferon-treated mice resulted in significant retardation of growth, accompanied by tissue injury and a depressed blastogenic response of splenic lymphocytes. Prophylactic administration of interferon prevented growth retardation and resulted in lower tissue viral titers and diminished injurious effects of the virus. Intraperitoneal inoculation of interferon was more protective than was subcutaneous, and 10 U of interferon was often as effective as 5,000 U. Accelerated maturation and enhanced activity of lymphoid elements were observed histologically in spleens and lymph nodes of interferon-treated mice; supportive of these findings was the greater incorporation of [3H]thymidine of splenocytes from interferon-treated mice. The protective effect of interferon may, therefore, be due to stimulation or accelerated maturation of cellular immune functions.

Inoculation of guinea pigs with varicella-zoster virus via the respiratory route.

Guinea pigs were inoculated by the respiratory route with wild-type (Cyr) or vaccine (Oka) strain varicella zoster virus (VZV). Wild-type cell-free virus obtained by sonication produced neutralizing antibody responses in steroid-treated animals when given via the intratracheal route, and induced neutralizing antibody as well as a pneumonitis in normal animals when given via the intrabronchial (i.b.) route. A humoral response also followed i.b. instillation of cell-associated wild-type or vaccine strain VZV. Prior i.b. administration of thioglycollate or exposure to hyperoxia altered the number and function of pulmonary macrophages, respectively, but viral susceptibility of the guinea pigs was not enhanced. Both strains of VZV could be isolated from bronchial washings up to 48 hours after i.b. instillation of cell-associated virus, but neither strain was isolated thereafter from cultures of bronchial washings or explanted lung tissues.