Clinical features fail to distinguish respiratory infections caused by Branhamella catarrhalis from those caused by Haemophilus influenzae

Branhamella catarrhalis is being isolated with increasing frequency from patients with symptoms and signs of respiratory tract infection. Records of 77 patients were reviewed to define the spectrum of respiratory illness and to compare clinical and laboratory features with those of respiratory infection due to Haemophilus influenzae. Both B catarrhalis and H influenzae caused respiratory infection predominantly in elderly males with underlying heart or lung disease. There were no clinical or laboratory features aside from sputum Gram stain and culture which differentiated the two groups. Although fewer than one-half of each group received antibiotics, no patient developed progressive respiratory disease.     

Across state lines: Fulminant Babesia microti infection in a liver transplant recipient

The potential for transmission of Babesia microti by blood transfusion is well recognized. Physicians may be unaware that products used for transfusion may be collected from geographically diverse regions. We describe a liver transplant recipient in South Carolina who likely acquired B. microti infection from a unit of blood collected in Minnesota.     

Effect of Sex Steroids on Babesia microti Infection in Mice

Sex-based-differences are known to affect susceptibility to protozoan infections, but their effects on parasitemia and clinical symptoms in Babesia infections remain unclear. We examined the sex-based susceptibility of various mouse strains to Babesia microti Munich strain infection. In all strains, male mice exhibited significantly higher peak parasitemia and more severe anemia than female mice. Testosterone and estradiol-17β treatment caused an increase in parasitemia and aggravation of anemia. Orchidectomized male mice receiving testosterone exhibited smaller splenic macrophage populations three days after infection, smaller B cell populations 10 days after infection, and reduced splenic tumor necrosis factor-α and interferon-γ mRNA expression than mice that did not receive testosterone. Mice receiving estradiol-17β did not exhibit immunosuppressive effects. Thus, a weakened and delayed innate immunity response may lead to acquired immunity failure. The results suggested that testosterone directly affects T or B cells, leading to delayed acquired immunity, dramatically increased parasitemia, and severe anemia.     

Role of Helicobacter pylori infection on nutrition and metabolism

Helicobacter pylori (H. pylori) is a gram-negative pathogen that is widespread all over the world, infecting more than 50% of the world’s population. It is etiologically associated with non-atrophic and atrophic gastritis, peptic ulcer and shows a deep association with primary gastric B-cell lymphoma and gastric adenocarcinoma. Recently, the medical research focused on the modification of the gastric environment induced by H. pylori infection, possibly affecting the absorption of nutrients and drugs as well as the production of hormones strongly implicated in the regulation of appetite and growth. Interestingly, the absorption of iron and vitamin B12 is impaired by H. pylori infection, while infected subjects have lower basal and fasting serum levels of ghrelin and higher concentration of leptin compared to controls. Since leptin is an anorexigenic hormone, and ghrelin stimulates powerfully the release of growth hormone in humans, H. pylori infection may finally induce growth retardation if acquired very early in the childhood and in malnourished children. This review is focused on the nutritional effects of H. pylori infection, such as the reduced bioavailability or the malabsorbption of essential nutrients, and of gastrointestinal hormones, as well as on the relationship between H. pylori and the metabolic syndrome.     

Combination of culture,antigen and toxin detection,and cytotoxin neutralization assay for optimal Clostridium difficile diagnostic testing

BACKGROUND:

There has been a growing interest in developing an appropriate laboratory diagnostic algorithm for Clostridium difficile, mainly as a result of increases in both the number and severity of cases of C difficile infection in the past decade. A C difficile diagnostic algorithm is necessary because diagnostic kits, mostly for the detection of toxins A and B or glutamate dehydrogenase (GDH) antigen, are not sufficient as stand-alone assays for optimal diagnosis of C difficile infection. In addition, conventional reference methods for C difficile detection (eg, toxigenic culture and cytotoxin neutralization [CTN] assays) are not routinely practiced in diagnostic laboratory settings.

OBJECTIVE:

To review the four-step algorithm used at Diagnostic Services of Manitoba sites for the laboratory diagnosis of toxigenic C difficile.

RESULT:

One year of retrospective C difficile data using the proposed algorithm was reported. Of 5695 stool samples tested, 9.1% (n=517) had toxigenic C difficile. Sixty per cent (310 of 517) of toxigenic C difficile stools were detected following the first two steps of the algorithm. CTN confirmation of GDH-positive, toxin A- and B-negative assays resulted in detection of an additional 37.7% (198 of 517) of toxigenic C difficile. Culture of the third specimen, from patients who had two previous negative specimens, detected an additional 2.32% (12 of 517) of toxigenic C difficile samples.

DISCUSSION:

Using GDH antigen as the screening and toxin A and B as confirmatory test for C difficile, 85% of specimens were reported negative or positive within 4 h. Without CTN confirmation for GDH antigen and toxin A and B discordant results, 37% (195 of 517) of toxigenic C difficile stools would have been missed. Following the algorithm, culture was needed for only 2.72% of all specimens submitted for C difficile testing.

CONCLUSION:

The overview of the data illustrated the significance of each stage of this four-step C difficile algorithm and emphasized the value of using CTN assay and culture as parts of an algorithm that ensures accurate diagnosis of toxigenic C difficile.     

Hantavirus pulmonary syndrome in Manitoba

The first confirmed case of hantavirus pulmonary syndrome in Manitoba was diagnosed in 1999. To define better the risk of exposure to hantaviruses in this area, the clinical features and epidemiological factors pertaining to this case were described, and a serological survey of rodents collected near the patient''s residence was undertaken. Small mammals were collected using live traps, were anesthetized via inhalation of isoflurane and were bled. Human and mouse serologies were undertaken using an ELISA to detect hantavirus-specific immunoglobulin G and/or immunoglobulin M antibodies. In addition, a full medical and epidemiological assessment, as well as individual risk factor and exposure analysis, were conducted. A 27-year-old Manitoba woman presented with severe respiratory distress and diffuse bilateral air space disease radiologically. Despite extremely aggressive measures, including mechanical ventilation, antibiotics, fluid management and inotropic support, the patient''s condition rapidly deteriorated, and she died 8 h after admission. Hantavirus pulmonary syndrome was confirmed by the detection of immunoglobulin M and immunoglobulin G antibodies to the Sin Nombre virus (SNV) in her sera and by the demonstration of SNV genomic sequences in her lung tissue. Exposure to hantavirus likely occurred in and around the home or in the rural area in which she resided. A total of 252 small mammals, primarily deer mice (Peromyscus maniculatus), were collected from 17 different sites at or near where the patient lived. Antibodies to SNV were detected in 28 of 244 (11.5%) deer mice, which were collected within 9 km of the residence of the fatal case, indicating that these rodents are a significant reservoir for SNV in this area.Key Words: Deer mice, Hantavirus pulmonary syndrome, HPS, Peromyscus maniculatus, Rodents, Serosurvey, Sin Nombre virusHantavirus pulmonary syndrome (HPS) was initially recognized in the southwestern United States in 1993 (1). An outbreak of HPS was caused by a hantavirus originally called the ''Muerto Canyon'' or ''Four Corners'' virus (2), but which is now named the ''Sin Nombre'' virus (SNV) (3). Since the original identification of the SNV, at least 12 other species of hantavirus have been identified in the Americas, including six that are known to be the etiological agent of HPS (3). Cases of HPS have been recognized in Canada but, to date, SNV is the only species of hantavirus that has been documented to cause HPS in this country.Although the SNV has been shown to infect many rodent species, the deer mouse, Peromyscus maniculatus, is the primary reservoir of SNV in the southwestern United States (4). The deer mouse is widely distributed in Canada (5) and is believed to excrete SNV in urine, saliva and feces (6). Human infection usually occurs when aerosolized virus is inhaled (3,6).As of January 1, 2000, 32 Canadian cases of HPS had been confirmed in the laboratory. All cases were reported in British Columbia, Alberta, Saskatchewan or Manitoba, with a case fatality rate of 37.5%, including the case described below (7). Patients ranged in age from 15 to 62 years (mean 39 years), and the majority (19 of 32 [60%]) were male (7). Before 1999, human cases of HPS had not been recognized in Manitoba. However, in July 1999, a female died from HPS; she had recently relocated from McAuley, Manitoba to Brandon, Manitoba. To gain further information regarding this case, local public health authorities conducted a full medical and epidemiological assessment, as well as individual risk factor and exposure analysis. Personnel from the Zoonotic Diseases and Special Pathogens (ZDSP) program trapped and bled small mammals in and around the patient''s principal residence and at 17 other sites within 9 km of this residence in southwest Manitoba.The present paper describes the clinical presentation and laboratory findings for the first confirmed HPS case in Manitoba, as well as the distribution and prevalence of hantavirus infections in the small mammals collected at 17 sites in southwestern Manitoba.     

Laboratory Biosafety: Sentinel surveillance of Lyme disease risk in Canada, 2019: Results from the first year of the Canadian Lyme Sentinel Network (CaLSeN)

BackgroundLyme disease is an emerging vector-borne zoonotic disease of increasing public health importance in Canada. As part of its mandate, the Canadian Lyme Disease Research Network (CLyDRN) launched a pan-Canadian sentinel surveillance initiative, the Canadian Lyme Sentinel Network (CaLSeN), in 2019.ObjectivesTo create a standardized, national sentinel surveillance network providing a real-time portrait of the evolving environmental risk of Lyme disease in each province.MethodsA multicriteria decision analysis (MCDA) approach was used in the selection of sentinel regions. Within each sentinel region, a systematic drag sampling protocol was performed in selected sampling sites. Ticks collected during these active surveillance visits were identified to species, and Ixodes spp. ticks were tested for infection with Borrelia burgdorferi, Borrelia miyamotoi, Anaplasma phagocytophilum, Babesia microti and Powassan virus.ResultsIn 2019, a total of 567 Ixodes spp. ticks (I. scapularis [n=550]; I. pacificus [n=10]; and I. angustus [n=7]) were collected in seven provinces: British Columbia, Manitoba, Ontario, Québec, New Brunswick, Nova Scotia and Prince Edward Island. The highest mean tick densities (nymphs/100 m²) were found in sentinel regions of Lunenburg (0.45), Montréal (0.43) and Granby (0.38). Overall, the Borrelia burgdorferi prevalence in ticks was 25.2% (0%–45.0%). One I. angustus nymph from British Columbia was positive for Babesia microti, a first for the province. The deer tick lineage of Powassan virus was detected in one adult I. scapularis in Nova Scotia.ConclusionCaLSeN provides the first coordinated national active surveillance initiative for tick-borne disease in Canada. Through multidisciplinary collaborations between experts in each province, the pilot year was successful in establishing a baseline for Lyme disease risk across the country, allowing future trends to be detected and studied.     

Detection of Clostridium difficile in retail ground meat products in Manitoba

The aim of the present study was to determine whether Clostridium difficile was present in uncooked retail ground beef and ground pork products sold in Winnipeg, Manitoba. Using an alcohol treatment protocol and inoculation of cultures on C difficile Moxalactam Norfloxacin (CDMN), toxigenic C difficile was found in 6.3% of 48 meat samples. The C difficile isolates belonged to different pulsotypes, all of which had been previously isolated from the stool of Manitoba patients with C difficile disease. Because cooking of meat will not eradicate C difficile spores, this raises a concern regarding potential foodborne transmissibility of this organism.     

Penicillium marneffei chylous ascites in acquired immune deficiency syndrome: A case report

Penicillium marneffei (P. marneffei) infection usually occurs with skin, bone marrow, lung or hepatic involvement. However, no cases of P. marneffei infection with chylous ascites have been reported thus far. In this report, we describe the first case of acquired immune deficiency syndrome (AIDS) which has been complicated by a P. marneffei infection causing chylous ascites. We describe the details of the case, with an emphasis on treatment regimen. This patient was treated with amphotericin B for 3 mo, while receiving concomitant therapy with an efavirenz-containing antiretroviral regimen, but cultures in ascitic fluid were persistently positive for P. marneffei. The infection resolved after treatment with high-dose voriconazole (400 mg every 12 h) for 3 mo. P. marneffei should be considered in the differential diagnosis of chylous ascites in human immunodeficiency virus patients. High-dose voriconazole is an effective, well-tolerated and convenient option for the treatment of systemic infections with P. marneffei in AIDS patients on an efavirenz-containing antiretroviral regimen.     

Characterization of invasive Neisseria meningitidis from Atlantic Canada, 2009 to 2013: With special reference to the nonpolysaccharide vaccine targets (PorA,factor H binding protein,Neisseria heparin-binding antigen and Neisseria adhesin A)

BACKGROUND:Serogroup B Neisseria meningitidis (MenB) has always been a major cause of invasive meningococcal disease (IMD) in Canada. With the successful implementation of a meningitis C conjugate vaccine, the majority of IMD in Canada is now caused by MenB.OBJECTIVE:To investigate IMD case isolates in Atlantic Canada from 2009 to 2013. Data were analyzed to determine the potential coverage of the newly licensed MenB vaccine.METHODS:Serogroup, serotype and serosubtype antigens were determined from IMD case isolates. Clonal analysis was performed using multilocus sequence typing. The protein-based vaccine antigen genes were sequenced and the predicted peptides were investigated.RESULTS:The majority of the IMD isolates were MenB (82.5%, 33 of 40) and, in particular, sequence type (ST)-154 B:4:P1.4 was responsible for 47.5% (19 of 40) of all IMD case isolates in Atlantic Canada. Isolates of this clone expressed the PorA antigen P1.4 and possessed the nhba genes encoding for Neisseria heparin-binding antigen peptide 2, which together matched exactly with two of the four components of the new four-component meningococcal B vaccine. Nineteen MenB isolates had two antigenic matches, another five MenB and one meningitis Y isolate had one antigenic match. This provided 75.8% (25 of 33) potential coverage for MenB, or a 62.5% (25 of 40) overall potential coverage for IMD.CONCLUSION:From 2009 to 2013, IMD in Atlantic Canada was mainly caused by MenB and, in particular, the B:4:P1.4 ST-154 clone, which accounted for 47.5% of all IMD case isolates. The new four-component meningococcal B vaccine appeared to offer adequate coverage against MenB in Atlantic Canada.     

A 10-year retrospective review of Salmonella infections at the Children��s Hospital in London, Ontario

OBJECTIVES:

To describe Salmonella infections in children presenting to the Children’s Hospital (London Health Sciences Centre, London, Ontario), to assess risk factors for infection and to examine whether younger children, particularly infants younger than 12 weeks of age, experience higher morbidity than older children.

METHODS:

A 10-year retrospective review of children with Salmonella infections at the Children’s Hospital was conducted. Patient demographics, risk factors for infection, clinical characteristics, bacteriology and outcome were collected from the hospital charts and laboratory records. Data were separated into groups based on age and recent use of antibiotics to analyze differences in outcomes.

RESULTS:

Sixty-six children with Salmonella infections presented to the Children’s Hospital over a 10-year period. Common risk factors for Salmonella infection included having sick contacts, living in a rural area, recent travel, contact with pets (especially reptiles) and exposure to local water. Younger age was associated with an increased likelihood of admission to hospital, treatment with antibiotics and a longer course of antibiotic therapy. This was true when comparing older infants with those younger than 12 weeks of age. Patients recently treated with antibiotics and those with significant underlying medical conditions were more likely to be admitted.

CONCLUSIONS:

A wider knowledge of the epidemiological risk factors for Salmonella infection may improve diagnosis. Higher admission rates were expected in children younger than 12 weeks of age, those recently treated with antibiotics and those who had a significant underlying medical condition. A prospective, multicentre study is needed to further address questions regarding increased illness severity and appropriate management of Salmonella infections in children younger than 12 weeks of age.     

Mycobacterium marinum infection from sea monkeys

A case of cutaneous Mycobacterium marinum infection acquired from Artemia nyos (sea monkeys) is presented. The infection was unresponsive to initial antimicrobial therapies. A biopsy of a lesion revealed granulomatous inflammation with cultures that subsequently grew M marinum. A three-month course of clarithromycin provided complete resolution.     

Klebsiella pneumoniae invasive liver abscess syndrome with purulent meningitis and septic shock: A case from mainland China

We present a rare case of invasive liver abscess syndrome due to Klebsiella pneumoniae (K. pneumoniae) with metastatic meningitis and septic shock. A previously healthy, 55-year-old female patient developed fever, liver abscess, septic shock, purulent meningitis and metastatic hydrocephalus. Upon admission, the clinical manifestations, laboratory and imaging examinations were compatible with a diagnosis of K. pneumoniae primary liver abscess. Her distal metastasis infection involved meningitis and hydrocephalus, which could flare abruptly and be life threatening. Even with early adequate drainage and antibiotic therapy, the patient’s condition deteriorated and she ultimately died. To the best of our knowledge, this is the first case of K. pneumoniae invasive liver abscess syndrome with septic meningitis reported in mainland China. Our findings reflect the need for a better understanding of the epidemiology, risk factors, complications, comorbid medical conditions and treatment of this disease.     

Risk factors for de novo hepatitis B infection in pediatric living donor liver transplantation

AIM: To investigate the incidence of de novo hepatitis B virus (HBV) infection after pediatric living donor liver transplantation (LDLT) and to analyze the risk factors associated with this de novo HBV infection.METHODS: The clinical and laboratory data of children who underwent LDLT from June 2010 to September 2012 in First Center Hospital in Tianjin, China, were retrospectively included in the study. Intrahepatic HBV DNA in donors and recipients was quantified by real-time polymerase chain reaction using DNA extracted from formalin-fixed, paraffin-embedded tissues.RESULTS: Between June 2010 to September 2012, 32 consecutive pediatric patients underwent LDLT in our institute. Thirty LDLT patients (13 girls and 17 boys) were followed up for a median of 15 mo, of whom 53.3% (16/30) were hepatitis B core antibody (HBcAb) positive and 36.7% (11/30) were hepatitis B surface antibody (HBsAb)/HBcAb positive before transplantation. Sixteen of the children received HBcAb-positive allografts, and 43.7% (7/16) of the grafts were found to be intrahepatic HBV DNA positive. De novo HBV infection developed in 16.1% (5/30) of the children within a median of 11 mo after transplantation. All five of the HBV-infected children had received HBcAb-positive allografts, four of which were intrahepatic HBV DNA positive. Two of the children developed de novo HBV infection despite the preoperative presence of both HBsAb and HBcAbCONCLUSION: In pediatric recipients, positive intrahepatic HBV DNA in allografts could be a risk factor for de novo HBV infection from HBcAb-positive allografts. HBsAb/HBcAb positivity in pediatric LDLT patients before transplantation exhibited only weak effectiveness in protecting them against de novo HBV infection from HBcAb-positive allografts.     

A review of 11 years of Stenotrophomonas maltophilia blood isolates at a tertiary care institute in Canada

BACKGROUND:

Stenotrophomonas maltophilia has emerged as a significant nosocomial pathogen with increasing resistance to trimethoprim/sulphamethoxazole (TMP/SMX), the current drug of choice for treatment.

OBJECTIVES:

To describe the microbiological and clinical characteristics of S maltophilia bloodstream infections (BSIs) over an 11-year period at a tertiary care centre in Canada.

METHODS:

All adult S maltophilia BSIs from 1999 to 2009 in a 750-bed tertiary care teaching hospital (University of Alberta Hospital, Edmonton, Alberta) were identified through the infection control nosocomial infection surveillance program. Demographic and clinical data were extracted from the infection control database and from patient charts. Microbiological data were confirmed through the laboratory information system.

RESULTS:

Twenty-five episodes of S maltophilia BSI (0.9% of all BSIs) involving 24 patients were identified between 1999 and 2009. The patient age range was 18 to 83 years (average 45.7 years). The majority were men (14 of 24 [58.3%]). The mean length of hospital stay was 83.3 days (range eight to 310 days). The rate of S maltophilia BSIs per 1000 admissions ranged from 0.04 to 0.22 (average 0.09). Greater than one-half of the episodes (13 of 25 [52%]) were admitted to the intensive care unit before BSI onset. Laboratory data were available for 24 of the 25 isolates. Polymicrobial infections were present in 11 of 24 (45.8%) patients. Resistance to TMP/SMX occurred in 8.3% of all infections. Fifteen per cent of isolates were resistant to ticarcillin/clavulanate. Mortality attributed to bacteremia was 16.7%.

CONCLUSIONS:

In the University of Alberta Hospital, the rate of S maltophilia BSI remains low and constant, and TMP/SMX remains the drug of choice for treatment.     

Subacute bacterial endocarditis caused by Cardiobacterium hominis: A case report

Cardiobacterium hominis, a member of the HACEK group of organisms, is an uncommon but important cause of subacute bacterial endocarditis. First-line therapy is a third-generation cephalosporin due to rare beta-lactamase production. The authors report a case involving endovascular infection due to C hominis that initially tested resistant to third-generation cephalosporins using an antibiotic gradient strip susceptibility method (nitrocephin negative), but later proved to be susceptible using broth microdilution reference methods (a ‘major’ error). There are limited studies to guide susceptibility testing and interpretive breakpoints for C hominis in the medical literature, and the present case illustrates some of the issues that may arise when performing susceptibility testing for fastidious organisms in the clinical microbiology laboratory.     

Pets are ‘risky business’ for patients undergoing continuous ambulatory peritoneal dialysis

The authors report the first case in Manitoba of a patient undergoing continuous ambulatory peritoneal dialysis who experienced three successive infections with Pasteurella multocida and Capnocytophaga species over an eight-month period. These zoonotic infections were believed to originate from contact with the patient’s household pets. To prevent such infections, the authors recommend the development and implementation of hygiene guidelines outlining the risks associated with owning domestic pets for continuous ambulatory peritoneal dialysis patients.     

Eosinophilia: A poor predictor of Strongyloides infection in refugees

BACKGROUND:

Canada resettles 10,000 to 12,000 refugees annually. Despite this being a highly vulnerable population, there are little Canadian data on subclinical tropical diseases harboured in this population over the past 20 years.

OBJECTIVES:

To determine the seroprevalence and predictors of Strongyloides infection in refugees arriving in Edmonton, Alberta.

METHODS:

A retrospective chart review of all refugees seen at the New Canadians Clinic between March 2009 and April 2010 was performed. Demographic, symptom and physical examination data were collected from the charts. Laboratory results were obtained from the electronic laboratory records.

RESULTS:

A total of 350 subjects were studied. The overall seroprevalence of strongyloidiasis was 4.6%. Equivocal results were found in 6.3%. In the positive group, the majority were male (62.5%); 75% were born in Africa (P=0.004) and 81.2% lived in refugee camps in Africa (P=0.002). Eosinophilia was present in 25% of the positive subjects (P=0.05), in none of the equivocal group and in 8.7% of the negative group.

DISCUSSION:

Persistent asymptomatic Strongyloides infection is maintained for years through autoinfection. Traditionally, eosinophilia was used as one of the key tools to diagnose chronic but stable diseases, but it was shown to have a poor predictive value for strongyloidiasis in returning expatriates as well as in those presenting with a disseminated form of the disease. It is important to raise awareness of the severe limitations of eosinophilia as a marker for strongyloidiasis when managing patients who either are immunocompromised, or about to start immunosuppressive therapy.

CONCLUSIONS:

The present study indicated that eosinophilia is a poor predictor of seropositivity and, thus, Strongyloides infection. Residence in Africa (birth/refugee camps) proved to be a significantly better predictor of Strongyloides seropositivity.     

Immune evasion strategies used by Helicobacter pylori

Helicobacter pylori (H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival.