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Urinary tract infection, most frequently caused by Escherichia coli , is one of the most common bacterial infections in humans. A vast amount of literature regarding the mechanisms through which E. coli induces pyelonephritis has accumulated. Although cystitis accounts for 95% of visits to physicians for symptoms of urinary tract infections, few in vivo studies have investigated possible differences between E. coli recovered from patients with clinical symptoms of cystitis and that from patients with symptoms of pyelonephritis. Epidemiological studies indicate that cystitis-associated strains appear to differ from pyelonephritis-associated strains in elaboration of some putative virulence factors. With transurethrally challenged mice we studied possible differences using three each of the most virulent pyelonephritis and cystitis E. coli strains in our collection. The results indicate that cystitis strains colonize the bladder more rapidly than do pyelonephritis strains, while the rates of kidney colonization are similar. Cystitis strains colonize the bladder in higher numbers, induce more pronounced histologic changes in the bladder, and are more rapidly eliminated from the mouse urinary tract than pyelonephritis strains. These results provide evidence that cystitis strains differ from pyelonephritis strains in this model, that this model is useful for the study of the uropathogenicity of cystitis strains, and that it would be unwise to use pyelonephritis strains to study putative virulence factors important in the development of cystitis.

Barnas, George M., Paul A. Delaney, Ileana Gheorghiu, Srinivas Mandava, Robert G. Russell, Renée Kahn, and Colin F. Mackenzie. Respiratory impedances and acinar gas transfer in a canine model for emphysema. J. Appl. Physiol. 83(1): 179–188, 1997.—We examined how the changes in the acini caused by emphysema affected gas transfer out of the acinus (Taci) and lung and chest wall mechanical properties. Measurements were taken from five dogs before and 3 mo after induction of severe bilateral emphysema by exposure to papain aerosol (170–350 mg/dose) for 4 consecutive wk. With the dogs anesthetized, paralyzed, and mechanically ventilated at 0.2 Hz and 20 ml/kg, we measured Taciby the rate of washout of133Xe from an area of the lung with occluded blood flow. Measurements were repeated at positive end-expiratory pressures (PEEP) of 10, 5, 15, 0, and 20 cmH2O. We also measured dynamic elastances and resistances of the lungs (El and Rl, respectively) and chest wall at the different PEEP and during sinusoidal forcing in the normal range of breathing frequency and tidal volume. After final measurements, tissue sections from five randomly selected areas of the lung each showed indications of emphysema. Taciduring emphysema was similar to that in control dogs. Eldecreased by ∼50% during emphysema ( P < 0.05) but did not change its dependence on frequency or tidal volume. Rl did not change ( P > 0.05) at the lowest frequency studied (0.2 Hz), but in some dogs it increased compared with control at the higher frequencies. Chest wall properties were not changed by emphysema ( P > 0.05). We suggest that although large changes in acinar structure and El occur during uncomplicated bilateral emphysema, secondary complications must be present to cause several of the characteristic dysfunctions seen in patients with emphysema.

To test the effects of three hemoglobin solutions on liver function and hepatic morphology after resuscitation from severe hemorrhagic shock.Prospective study.Laboratory.Thirty-three beagle dogs.Hemorrhagic shock was induced in anesthetized dogs by removal of blood at a rate of 2 mL/kg/min until systolic blood pressure (BP) reached 50 mm Hg. BP was maintained at this level 2 hrs by further withdrawing 5 to 10 mL aliquots whenever BP increased50 mm Hg. Resuscitation was then initiated with autologous whole blood (n = 7), 4% pyridoxalated-hemoglobin-polyoxyethylene conjugate (4% PHP [n = 6]), 8% pyridoxalated-hemoglobin-polyoxyethylene conjugate (8% PHP [n = 9], or 8% stroma-free hemoglobin (n = 7). Four dogs were managed identically but were not resuscitated. Gross necropsy and histologic examination of the liver were performed on all dogs after 7 days, or earlier if death occurred.In vitro interferences of PHP and stroma-free hemoglobin with liver function tests were determined and recommendations for interpretation of results from blood samples containing PHP and stroma-free hemoglobin were made. Blood was collected before, during, and after resuscitation from hemorrhagic shock. The dogs were then awakened and survivors were monitored daily with blood sampling until they were killed and necropsy was performed. After 7 days, the survival rate following hemorrhagic shock was 100% for whole blood and 4% PHP, 86% for stroma-free hemoglobin, and 33% for 8% PHP. Of the resuscitated dogs not surviving 7 days, all but one died within 27 hrs from coagulopathy. All dogs not resuscitated died within 1.75 hrs after 2 hrs of shock. Bilirubin, alkaline phosphatase, and lactic dehydrogenase concentrations could not be measured due to interferences of stroma-free hemoglobin and PHP. Aspartate (AST) and alanine (ALT) aminotransferase concentrations could be measured after dilution to overcome the interferences. Significant increases in AST and ALT values in all groups 24 hrs after resuscitation were attributed to hypoxic hepatocellular damage associated with the severity of the shock model rather than to the resuscitation fluid. Liver histology showed no changes attributed to toxic damage of hepatocytes in dogs resuscitated with stroma-free hemoglobin or PHP. However, changes, were less severe in dogs resuscitated with 4% PHP than in other groups.Morphologic studies at necropsy and liver function tests in dogs receiving hemoglobin solutions, compared with autologous blood, support the conclusion that the PHP and stroma-free hemoglobin solutions tested did not produce hepatic toxicity when used as resuscitation fluids in this model of severe shock.

Person-to-person transmission of influenza viruses occurs by contact (direct and fomites) and non-contact (droplet and small particle aerosol) routes, but the quantitative dynamics and relative contributions of these routes are incompletely understood. The transmissibility of influenza strains estimated from secondary attack rates in closed human populations is confounded by large variations in population susceptibilities. An experimental method to phenotype strains for transmissibility in an animal model could provide relative efficiencies of transmission. We developed an experimental method to detect exhaled viral aerosol transmission between unanesthetized infected and susceptible ferrets, measured aerosol particle size and number, and quantified the viral genomic RNA in the exhaled aerosol. During brief 3-hour exposures to exhaled viral aerosols in airflow-controlled chambers, three strains of pandemic 2009 H1N1 strains were frequently transmitted to susceptible ferrets. In contrast one seasonal H1N1 strain was not transmitted in spite of higher levels of viral RNA in the exhaled aerosol. Among three pandemic strains, the two strains causing weight loss and illness in the intranasally infected ‘donor’ ferrets were transmitted less efficiently from the donor than the strain causing no detectable illness, suggesting that the mucosal inflammatory response may attenuate viable exhaled virus. Although exhaled viral RNA remained constant, transmission efficiency diminished from day 1 to day 5 after donor infection. Thus, aerosol transmission between ferrets may be dependent on at least four characteristics of virus-host relationships including the level of exhaled virus, infectious particle size, mucosal inflammation, and viral replication efficiency in susceptible mucosa.

Diarrhea caused by Campylobacter jejuni results in soft mucoid feces that take the form of the container in which the fecal specimen is placed (grade 2 diarrhea). In more severe cases the feces are fluid, yellowish in color, and may be positive to tests for occult blood.

outbreak investigation: An outbreak of diarrhea, bloody diarrhea, and abdominal cramps occurred among persons undergoing flexable sigmoidoscopy at a branch clinic of a local health center. Illness was associated with use of sigmoidoscopes cleaned by one clinic assistant and appeared to be caused by 2% glutaraldehyde disinfectant solution left in the instruments after cleaning. animal studies: In subsequent animal studies, colonic instillation of 2 % glutaraldehyde solutions caused bloody diarrhea and a distinctive pattern of mucosal damage; similar changes were seen in a review of pathologic samples from other human cases of glutaraldehyde disinfectant-associated diarrhea. conclusion: Our data indicate that improper endoscopic reprocessing can result in serious illness and underscore the importance of adequate training and quality control in this area.

A prospective bacteriologic study of 18 infant pig-tailed macaques (Macaca nemestrina) housed in a nursery facility in which Campylobacter spp. are endemic was undertaken to determine the epidemiology of infection and reinfection. The isolates of Campylobacter jejuni and C. coli cultured from 8 of the 18 infants were characterized by serotyping, DNA hybridization, and polyacrylamide gel electrophoresis protein profiles. The chronology of infection was indicative of multiple reinfections with different strains of C. jejuni and C. coli during the 12-month study of each infant. The duration of infection with a particular strain was 3 to 4 weeks. Infants were also infected with nalidixic acid-resistant campylobacters. These observations indicated that long-term infections under endemic conditions are caused by continual reinfection. C. jejuni or C. coli infection correlated with diarrhea in 5 of the 18 infants at 1 to 4 months of age.

The differentiation of skeletal muscle was studied by electron microscopy in bovine fetuses from 47 days gestation to neonatal calves 3 days of age. Initially, the muscle was composed of clusters of myotubes with mononucleated myoblasts between them. In 2-month-old fetuses these myoblasts became apposed to the differentiating muscle cells and were enclosed within the rudimentary basal lamina of the myotubes. At this stage the clusters of myotubes consisted of central, larger diameter, more differentiated myotubes and also the mononucleated satellite cells. The differentiated myotubes separated from the clusters accompanied by satellite cells which continued proliferating and fused together to form new generations of satellite myotubes. In this manner new clusters of myotubes were formed. By 4-5 months some of the separating myotubes began to form individual myotubes and independent myofibers were prominent in fetuses of 5-8 months of age. The myofibers in the 8-month-old fetuses showed diversification into fiber types by differences in the thickness of the Z-line, the prominence of the sarcotubular system, the amount of glycogen and lipid droplets and also the number of mitochondria.

A paramyxovirus related to parainfluenza 2 (PI2) virus was recovered from the lungs of two dead Ottoman vipers from a zoological collection. Snakes of other species in the collection were unaffected. Histologic examination of the vipers' lungs revealed interstitial pneumonia, and degeneration and hyperplasia of bronchial and atrial epithelia. Scattered vacuoles, some of which contain eosinophilic inclusion bodies, were seen in the cytoplasm of several cells of affected epithelial tissues. The virus recovered from pulmonary tissues of the snakes replicated optimally at 30 C in a variety of cell cultures and hemagglutinated chicken erythrocytes. Viral hemagglutination was inhibited by PI2 virus antiserum, but not by antisera to PI1, PI3, respiratory syncytial, and canine distemper viruses. Indirect immunofluorescence with PI2 antiserum specifically stained inclusions in the epithelial cells of respiratory tissues and infected cell cultures.

Velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a human disorder characterized by a number of phenotypic features including cardiovascular defects. Most VCFS/DGS patients are hemizygous for a 1.5–3.0 Mb region of 22q11. To investigate the etiology of this disorder, we used a cre-loxP strategy to generate mice that are hemizygous for a 1.5 Mb deletion corresponding to that on 22q11. These mice exhibit significant perinatal lethality and have conotruncal and parathyroid defects. The conotruncal defects can be partially rescued by a human BAC containing the TBX1 gene. Mice heterozygous for a null mutation in Tbx1 develop conotruncal defects. These results together with the expression patterns of Tbx1 suggest a major role for this gene in the molecular etiology of VCFS/DGS.

The aims of diabetic treatment are: correction of hyperglycaemia; control of symptoms; prevention of complications; normal life and good health; and avoidance of any side-effects of treatment.

Experimental infection of four specific-pathogen-free Macaca nemestrina monkeys (aged 3.5 and 4.5 months) with Campylobacter jejuni 81-176 caused acute diarrheal illness, characterized by fluid diarrhea, bloody stools, and fecal leukocytes, which lasted for approximately 7 to 11 days. Histologic examination of intestinal biopsies showed acute colitis characterized by infiltration of the mucosa with neutrophils and lymphocytes, and cryptitis. There were no histologic changes in the small intestine. Excretion of C. jejuni was demonstrated for 2 to 4 weeks postchallenge. Plasma antibodies to C. jejuni group antigen were elevated after challenge. Only mild diarrhea occurred after rechallenge with the same strain or with a heterologous C. jejuni strain (79-168) followed by further elevation in specific immunoglobulins A, M, and G. Four 1-year-old juvenile M. nemestrina monkeys which had experienced multiple infections with Campylobacter spp. did not exhibit illness when challenged with C. jejuni 81-176. All had elevated immunoglobulin A, M, and G plasma antibodies prior to challenge, and these humoral antibody levels were indicative of the immunity to challenge. The results demonstrate that C. jejuni infection in M. nemestrina caused colitis with clinical and pathologic results similar to those found in humans and indicate that prior infection protects against subsequent challenge.