Pulmonary inflammatory pseudotumor due to Coxiella burnetii. Case report and literature review.

A 58-year-old man was admitted because of respiratory failure, episodic fever with chilling, cough, malaise, fatigue, myalgia and weight loss lasting for at least one month. Chest x-rays and CT scan of the chest showed bilateral pulmonary consolidations in upper lobes, the left lower lobe, and mediastinal lymphadenopathy. Bronchoscopy with cytology was unremarkable. A needle CT-guided lung biopsy documented an inflammatory pseudotumor, lymphoplasmacytic type. Serology showed high titer antibodies to phase II Coxiella burnetii infection. Therapy with doxycycline and hydroxychloroquine for three months led to a complete resolution of symptoms and radiological findings, and a marked decrease in titers to Q fever.

A retrospective study on burden of human echinococcosis based on Hospital Discharge Records from 2001 to 2009 in Sardinia, Italy.

Cystic Echinococcosis (CE) is an infective zoonosis that represents a worldwide important public health problem. In humans, its manifestations may range from asymptomatic infection to severe disease and possible death, and lead to economic losses from treatment costs and lost wages. Recent studies suggest that this disease has a large social impact in endemic areas, and estimates of burden in terms of monetary and no-monetary impact on human health are essential to allocate financial and technical resources. In Sardinia, the most affected Italian region per number of inhabitants, CE is still endemic, although three eradication campaigns have been carried out in 1962, 1978, and 1987, respectively. To date, the burden of human CE in Sardinia remains poorly defined. In this work, a retrospective study was carried out using public Hospital Discharge Records spanning from 2001 to 2009. During these years, a total of 1409 discharges were recorded: 1196 (84.88%) records corresponding to patients hospitalized for symptoms directly correlated to CE (primary diagnosis), and 213 (15.11%) records corresponding to patients hospitalized for symptoms not directly correlated to CE and with an afterwards or concurrent diagnosis of echinococcosis made during the hospitalization (secondary diagnosis). The annual regional average record (discharge rate) was 9.3/100,000 inhabitants. Direct cost associated with diagnosis, surgery or chemotherapy, medical care, and hospitalization in humans were evaluated in this work. Furthermore, burden of disease was also evaluated by using the disability-adjusted life years (DALYs), the preferred disease-burden measure of the World Health Organization. Knowing the burden of human CE in Sardinia is extremely important to enable the prioritization of control measures for this preventable neglected disease. This is the first study describing the measure of the overall disease burden in an Italian region endemic for this disease, performed by calculating the number of CE patients from Hospital Discharge Records.

Two cases of human granulocytic ehrlichiosis in Sardinia, Italy confirmed by PCR.

In this work we report the first two cases of human granulocytic ehrlichiosis (HGE) in Sardinia. In early September 2004, a 69-year-old woman (patient 1) was admitted to the Infectious Diseases Institute of Sassari for rickettsiosis like-syndrome: high fever (39.5-40 degrees C), dyspnea, reduced consciousness, vomiting, and cutaneous rash. In late September 2004, a 30-year-old man (patient 2) with high fever was admitted for an evident palmar and oral erythema, edema of the labium, very intense arthralgia, myalgia, and dyspnea. In these two hospitalized patients, the diagnosis was made through indirect IgM and IgG immunofluorescent technique and confirmed by the presence of the specific DNA in the leukocytes. The two patients were A. phagocytophilum-PCR positive.

Molecular identification of pathogenicity genes and ERIC types in Vibrio cholerae O1 epidemic strains from Mozambique.

The phenotypic and genotypic profiles of the V. cholerae strains causing the Mozambican 1997-8 epidemic were characterized to provide a reference for comparison with other epidemic strains. A total of 75 strains of V. cholerae O1 isolated in different provinces, were analysed. Strains were characterized by PCR for detecting toxin genes (ctxA, zot and ace), virulence associated genes (tcpA. nanH, hlyA and torR) and ERIC sequences. All V. cholerae strains were serotype O1, Ogawa, biotype El Tor. MIC testing showed a high proportion of strains multi-resistant to drugs (100% to cotrimoxazole and 52% to tetracycline) and susceptibility to ciprofloxacin. The isolates contained two intact copies of the CTX genetic element and all other genes tested. PCR of restricted DNA revealed two ERIC types: the first in provincial isolates, also predominant in other African epidemic strains, and the second in Maputo isolates (the national capital).

Brucella abortus infection acquired in microbiology laboratories.

We report an outbreak of laboratory-acquired Brucella abortus infection originating in the accidental breakage of a centrifuge tube. A total of 12 laboratory workers were infected (attack rate of 31%), with an incubation time ranging from 6 weeks to 5 months. Antibody titers were evaluated weekly in all personnel exposed, allowing the diagnosis of the infection in most cases before the onset of clinical symptoms, so that specific therapy could be administrated.

Tracking of clinical and environmental Vibrio cholerae O1 strains by combined analysis of the presence of toxin cassette, plasmid content and ERIC PCR.

Clinical and environmental Vibrio cholerae O1 strains associated with the cholera epidemic in the Luanda province of Angola from 1991 to 1994 were tracked by toxin distribution, plasmid content and chromosomal polymorphism of the enterobacterial repetitive intergenic consensus (ERIC) sequences by PCR fingerprinting. To follow the distribution of ace, zot and ctxA toxin genes, 6 specific PCR tests were applied to 100 Vibrio strains, after preliminary hybridization experiments. Clinical isolates of Vibrio cholerae O1 were characterized by high stability of the toxigenic cassette and the presence of a large conjugative multi-resistant plasmid of incompatibility class C. Such characteristics were present in all isolates during the four years of the epidemic. Environmental strains, isolated from the river supplying water to the Luanda population showed three different genetic profiles: the presence of both cassette and plasmid, the presence of cassette only or absence of both. To assess the clonal relationship between the clinical isolates and the three groups of environmental strains, the strains were analyzed by PCR ERIC polymorphism. This analysis, supported by the toxin and plasmid content, suggested the stability of the epidemic strain in clinical cases during the epidemic and led to the finding that there was a strict genetic relationship of the epidemic strain with the environmental ones as characterized by the presence of the toxin cassette. The role of the water supply from Bengo River as a reservoir of the Vibrio epidemic strain is discussed.

Vibrio cholerae in the horn of Africa: epidemiology, plasmids, tetracycline resistance gene amplification, and comparison between O1 and non-O1 strains.

The prevalence of Vibrio cholerae O1 and non-O1 has been investigated in numerous Somali regions of the Horn of Africa from 1983 to 1990. From January 1983 to January 1985 and between December 1986 and December 1990, no strains of V. cholerae O1 and 226 strains (5.3%) of V. cholerae non-O1 were isolated from 4,295 diarrhea cases. During a cholera epidemic in 1985 and 1986, the overall case-fatality rate was 13% and the attack rate was 3-3.5 per 1,000 population. Matched case-control studies identified a waterborne route of transmission. A drug-susceptible Ogawa strain from Ethiopia caused the introduction of the disease into northern Somalia. There were two major resistant derivatives of the original strain, and the one resistant to ampicillin, kanamycin, streptomycin, sulfonamide, and tetracycline (TC) predominated in the spreading disease. In 1986, susceptible Ogawa strains quickly displaced this resistant strain. The two incompatibility group C plasmids responsible for the resistance patterns had complex and scattered differences in their structures. Physical analysis of the plasmid DNA region coding for TC resistance demonstrated its genetic amplification in highly resistant variants of Ogawa strains.