Hemorrhagic Pneumonia Research Articles

ETIOLOGICAL STRUCTURE AND DIFFERENTIAL DIAGNOSTICS OF SALMONELLOSIS OF BIRDS

The article presents the results of a study of the etiological structure and differential diag-nostic signs of avian salmonellosis. When identifying bacteria isolated from 128 blood samples of chickens with the use of rapid test "Salmonella latex kit" established the dominance of cultures of the microorganisms Salmonella spp. - of 10.94% (14 samples); 10 strains (71,43%) were attributed to Salmonella gallinarum, 4 (of 28.57%) to Salmonella pullorum. The overall level of resistance of Salmonella to ampicillin - 57,58%; tetracycline - 60,61%; streptomycin - 66,67%; had to 57,58%; 60,61% and 66,67% are sensitivity to norfloxacin amounted to 69,70%, to ceftazidime - 78,79%, enrofloxacin - 57,58%, ciprofloxacin - 69,70% of the tested strains. At postmortem examination the most frequently detected signs of pericarditis, hemorrhagic pneumonia, aeroscout, catarrhal-hemorrhagic enteritis, perihepatitis, hyperplasia of the spleen. The most frequently detected signs of pericarditis, aeroscout, catarrhal-hemorrhagic gastroenterocolitis, perihepatitis, inflam-mation of the ovaries, hyperplasia of the spleen. Revealed signs of congestive hyperemia, macrophage reaction, hyperplasia and plasmocytomas of lymphocyte transformation, increase the permeability of microcirculatory vessels, lymphoid-cellular infil-tration of loose fibrous connective tissue, perivascular oedema, disseminated thrombosis, proliferation of lymphocytes from lymph nodes, spleen, liver, and pancreas. In violation of the porosity of the blood vessels of serous membranes of organs were observed extensive serous oedema, the output of the formed elements of blood and the loss of fibrinogen.

Epidemiology of porcine reproductive and respiratory syndrome (PRRS) outbreak in India

Porcine reproductive and respiratory syndrome (PRRS) is recognized as an economically important swine disease worldwide. India has reported the first outbreak of PRRS in pig populations of Mizoram stateto OIE (World Organization for Animal Health) on 26thJune, 2013. The outbreak was observed in an epizootic form in pig population of Mizoram and caused huge loss to the pig farmers. The disease was observed to affect all age groups including the pregnant sows with morbidity rate 44.01% - 80.29% and mortality rate 14.51% - 66.11%. However, the most severe acute respiratory disease with highest morbidity and mortality rate was recorded in preweaned piglets. Severe pathological lesions like hemorrhagic interstitial pneumonia, hemorrhagic lymphadenitis with lymphoid depletion, vasculitis and interstitial nephritis were observed in pigs of all age groups and reproductive failure in pregnant sows.Post outbreak serosurveillance revealed 28.26% seropositivity. Sequence and phylogenetic analysis of ORF-7 gene from field samples during the outbreak established the belonging of PRRSV in genotype II and revealed 99% sequence identity with the Chinese isolates characterized as highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV).

Therapeutic effect of Pseudomonas aeruginosa phage YH30 on mink hemorrhagic pneumonia

Hemorrhagic pneumonia caused by Pseudomonas aeruginosa remains one of the most costly infectious diseases among farmed mink and commonly leads to large economic losses during mink production. The objective of this study was to investigate the potential of using phages as a therapy against hemorrhagic pneumonia in mink. A broad-host-range phage from the Podoviridae family, YH30, was isolated using the mink-originating P. aeruginosa (serotype G) D7 strain as a host. The genome of YH30 was 72,192bp (54.92% G+C), contained 86 open reading frames and lacked regions encoding known virulence factors, integration-related proteins or antibiotic resistance determinants. These characteristics make YH30 eligible for use in phage therapy. The results of a curative treatment experiment demonstrated that a single intranasal administration of YH30 was sufficient to cure hemorrhagic pneumonia in mink. The mean colony count of P. aeruginosa in the blood and lung of YH30-protected mink was less than 103 CFU/mL (g) within 24h of bacterial challenge and ultimately became undetectable, whereas that in unprotected mink reached more than 108 CFU/mL (g). Additionally, YH30 dramatically improved the pathological manifestations of lung injury in mink with hemorrhagic pneumonia. Our work demonstrates the potential of phages to treat P. aeruginosa-caused hemorrhagic pneumonia in mink.

Subacute Septicemia in a Leatherback Sea Turtle <i>(Dermocheleys Coriacea)</i> Rescued Ashore Northern Samar, Philippines

The leatherback sea turtle (Dermocheleys coriacea) is considered an endangered species here in the Philippines and around the world. In Northern Samar, a leatherback sea turtle reportedly found by local fisher folks along the rocky mangrove and coral reef areas was placed in a rescue confinement for treatment and observation. Upon retrieval, the left fore flipper was already missing and the lacerated, amputated area was then bleeding. Treatment to arrest hemorrhage was performed and antimicrobials were administered. Two days thereafter, the animal succumbed to death. Because the animal was recovered a day following a typhoon that hit the province, it was inferred that the injury might be attributed to calamity-induced trauma as the animal was recovered as it was trapped along the rock-strewn mangrove areas. Following death, necropsy examination presented findings of severe congestive pneumonia, hemorrhages along the intestinal serosa, severe hepatic congestion, pericarditis and pronounced disseminated intravascular coagulopathy. The prominent histopathological finding of sub-acute severe hemorrhagic pneumonia with infiltrates of mononuclear cells, red blood cells, hemosiderins and proteinaceous debris were discerned along the lung parenchyma. The hepatocytes are swollen, distended and some presented congestion and necrosis. The intestinal sub-mucosae are infiltrated with mononuclear cells. Smears from blood and liver showed variable Gram-negative organisms. It was impressed that the animal may have been suffering from an underlying subclinical septicemic infection even prior to traumatic injury. These findings underscore the need to further study the microbial profile of this endangered species and provide means to mitigate occurrence of septicemia cases that could further exacerbate its dwindling populace. This index case of septicemia affecting a leatherback sea turtle has been reported for the first time in the country.

Genetic characterization of classical swine fever virus detected in wild pigs (Sus scrofa) of Mizoram, India

Outbreak of Classical swine fever (CSF) in wild pigs of Mizoram, a far North Eastern state of India was confirmed by post mortem examination, histopathology and RT-PCR on tissue samples targeting the E2 glycoprotein and NS5B gene fragments of CSFV. Necropsy examination revealed typical button ulcers in large intestine and infarction on spleen with hemorrhagic pneumonia in lungs. Two isolates of CSFV from outbreaks were subjected to nucleotide sequencing of E2 and NS5B gene fragments for genetic typing. Phylogenetic analysis on 190 nucleotides region of E2 gene and 409 nucleotide region of NS5B gene revealed that both the isolates belonged to the group 2 and subgroup 2.1.

Pore-Forming Toxins Induce Macrophage Necroptosis during Acute Bacterial Pneumonia.

Necroptosis is a highly pro-inflammatory mode of cell death regulated by RIP (or RIPK)1 and RIP3 kinases and mediated by the effector MLKL. We report that diverse bacterial pathogens that produce a pore-forming toxin (PFT) induce necroptosis of macrophages and this can be blocked for protection against Serratia marcescens hemorrhagic pneumonia. Following challenge with S. marcescens, Staphylococcus aureus, Streptococcus pneumoniae, Listeria monocytogenes, uropathogenic Escherichia coli (UPEC), and purified recombinant pneumolysin, macrophages pretreated with inhibitors of RIP1, RIP3, and MLKL were protected against death. Alveolar macrophages in MLKL KO mice were also protected during S. marcescens pneumonia. Inhibition of caspases had no impact on macrophage death and caspase-1 and -3/7 were determined to be inactive following challenge despite the detection of IL-1β in supernatants. Bone marrow-derived macrophages from RIP3 KO, but not caspase-1/11 KO or caspase-3 KO mice, were resistant to PFT-induced death. We explored the mechanisms for PFT-induced necroptosis and determined that loss of ion homeostasis at the plasma membrane, mitochondrial damage, ATP depletion, and the generation of reactive oxygen species were together responsible. Treatment of mice with necrostatin-5, an inhibitor of RIP1; GW806742X, an inhibitor of MLKL; and necrostatin-5 along with co-enzyme Q10 (N5/C10), which enhances ATP production; reduced the severity of S. marcescens pneumonia in a mouse intratracheal challenge model. N5/C10 protected alveolar macrophages, reduced bacterial burden, and lessened hemorrhage in the lungs. We conclude that necroptosis is the major cell death pathway evoked by PFTs in macrophages and the necroptosis pathway can be targeted for disease intervention.

Pneumonia Caused by Klebsiella spp. in 46 Horses.

Background Klebsiella spp. are implicated as a common cause of bacterial pneumonia in horses, but few reports describe clinical presentation and disease progression.Hypothesis/ObjectivesTo describe the signalment, clinicopathologic data, radiographic and ultrasonographic findings, antimicrobial susceptibility, outcome, and pathologic lesions associated with Klebsiella spp. pneumonia in horses.AnimalsForty‐six horses from which Klebsiella spp. was isolated from the lower respiratory tract.MethodsRetrospective study. Medical records from 1993 to 2013 at the William R. Pritchard Veterinary Medical Teaching Hospital, University of California, Davis were reviewed. Exact logistic regression was performed to determine if any variables were associated with survival to hospital discharge.ResultsSurvival in horses <1 year old was 73%. Overall survival in adults was 63%. For adults in which Klebsiella pneumoniae was the primary isolate, survival was 52%. Mechanical ventilation preceded development of pneumonia in 11 horses. Complications occurred in 25/46 horses, with thrombophlebitis and laminitis occurring most frequently. Multi‐drug resistance was found in 47% of bacterial isolates. Variables that significantly impacted survival included hemorrhagic nasal discharge, laminitis, and thoracic radiographs with a sharp demarcation between marked caudal pulmonary alveolar infiltration and more normal‐appearing caudodorsal lung.Conclusions and Clinical Importance Klebsiella spp. should be considered as a differential diagnosis for horses presenting with hemorrhagic pneumonia and for horses developing pneumonia after mechanical ventilation. Multi‐drug resistance is common. Prognosis for survival generally is fair, but is guarded for adult horses in which K. pneumoniae is isolated as the primary organism.

Therapeutic effect of the YH6 phage in a murine hemorrhagic pneumonia model

The treatment, in farmed mink, of hemorrhagic pneumonia caused by multidrug-resistant Pseudomonas aeruginosa strains has become increasingly difficult. This study investigated the potential use of phages as a therapy against hemorrhagic pneumonia caused by P. aeruginosa in a murine hemorrhagic pneumonia model. An N4-like phage designated YH6 was isolated using P. aeruginosa strain D9. YH6 is a virulent phage with efficient and broad host lytic activity against P. aeruginosa. No bacterial virulence- or lysogenesis-related ORF is present in the YH6 genome, making it eligible for use in phage therapy. In our murine experiments, a single intranasal administration of YH6 (2 × 107 PFU) 2 h after D9 intranasal injections at double minimum lethal dose was sufficient to protect mice against hemorrhagic pneumonia. The bacterial load in the lungs of YH6-protected mice was less than 103 CFU/g within 24 h after challenge and ultimately became undetectable, whereas the amount of bacteria in the lung tissue derived from unprotected mice was more than 108 CFU/g within 24 h after challenge. In view of its protective efficacy in this murine hemorrhagic pneumonia model, YH6 may serve as an alternative treatment strategy for infections caused by multidrug-resistant P. aeruginosa.

Comparative pathogenicity of Trypanosoma brucei rhodesiense strains in Swiss white mice and Mastomys natalensis rats

We evaluated Mastomys natelensis rat as an animal model for Rhodesian sleeping sickness. Parasitaemia, clinical and pathological characteristics induced by T. b. rhodesiense isolates, KETRI 3439, 3622 and 3637 were compared in Mastomys rats and Swiss white mice. Each isolate was intra-peritonially injected in mice and rat groups (n=12) at 1×104 trypanosomes/0.2mL. Pre-patent period (PP) range for KETRI 3439 and KETRI 3622-groups was 3–6 days for mice and 4–5 days for rats while for KETRI 3637-infected mice and rats was 5–9 and 4–12 days, respectively. Pairwise comparison between PP of mice and rats separately infected with either isolate showed no significant difference (p>0.05). The PP’s of KETRI 3637-infected mice were significantly (p>0.01) longer than those infected with KETRI 3439 or KETRI 3622, a trend also observed in rats. The second parasitaemic wave was more prominent in mice. Clinical signs included body weakness, dyspnoea, peri-orbital oedema and extreme emaciation which were more common in rats. Survival time for KETRI 3439 and 3622-infected groups was significantly (p<0.05) longer in mice than rats but similar in KETRI 3637-infected groups. Inflammatory lesions were more severe in rats than mice. All mice and KETRI 3622-infected rats had splenomegaly, organ congestion with rats additionally showing prominent lymphadenopathy. KETRI 3439-infected rats showed hemorrhagic pneumonia, enteritis with moderate splenomegaly and lymphadenopathy. KETRI 3637-infected rats had the most severe lesions characterized by prominent splenomegaly, lymphadenopathy, hepatomegaly, enlarged adrenal glands, organ congestion, generalized oedemas, gastroenteritis, pneumonia and brain congestion. KETRI 3637-infected Mastomys is a suitable model for studying pathophysiology of HAT.

Isolation and characterization of a "phiKMV-like" bacteriophage and its therapeutic effect on mink hemorrhagic pneumonia.

The objective of this study was to investigate the potential of using phages as a therapy against hemorrhagic pneumonia in mink both in vitro and in vivo. Five Pseudomonas aeruginosa (P. aeruginosa) strains were isolated from lungs of mink with suspected hemorrhagic pneumonia and their identity was confirmed by morphological observation and 16S rDNA sequence analysis. Compared to P. aeruginosa strains isolated from mink with hemorrhagic pneumonia in 2002, these isolates were more resistant to antibiotics selected. A lytic phage vB_PaeP_PPA-ABTNL (PPA-ABTNL) of the Podoviridae family was isolated from hospital sewage using a P. aeruginosa isolate as host, showing broad host range against P. aeruginosa. A one-step growth curve analysis of PPA-ABTNL revealed eclipse and latent periods of 20 and 35 min, respectively, with a burst size of about 110 PFU per infected cell. Phage PPA-ABTNL significantly reduced the growth of P. aeruginosa isolates in vitro. The genome of PPA-ABTNL was 43,227 bp (62.4% G+C) containing 54 open reading frames and lacked regions encoding known virulence factors, integration-related proteins and antibiotic resistance determinants. Genome architecture analysis showed that PPA-ABTNL belonged to the “phiKMV-like Viruses” group. A repeated dose inhalational toxicity study using PPA-ABTNL crude preparation was conducted in mice and no significantly abnormal histological changes, morbidity or mortality were observed. There was no indication of any potential risk associated with using PPA-ABTNL as a therapeutic agent. The results of a curative treatment experiment demonstrated that atomization by ultrasonic treatment could efficiently deliver phage to the lungs of mink and a dose of 10 multiplicity of infection was optimal for treating mink hemorrhagic pneumonia. Our work demonstrated the potential for phage to fight P. aeruginosa involved in mink lung infections when administered by means of ultrasonic nebulization.

Requirement for Serratia marcescens cytolysin in a murine model of hemorrhagic pneumonia.

Serratia marcescens, a member of the carbapenem-resistant Enterobacteriaceae, is an important emerging pathogen that causes a wide variety of nosocomial infections, spreads rapidly within hospitals, and has a systemic mortality rate of ≤41%. Despite multiple clinical descriptions of S. marcescens nosocomial pneumonia, little is known regarding the mechanisms of bacterial pathogenesis and the host immune response. To address this gap, we developed an oropharyngeal aspiration model of lethal and sublethal S. marcescens pneumonia in BALB/c mice and extensively characterized the latter. Lethal challenge (>4.0 × 10(6) CFU) was characterized by fulminate hemorrhagic pneumonia with rapid loss of lung function and death. Mice challenged with a sublethal dose (<2.0 × 10(6) CFU) rapidly lost weight, had diminished lung compliance, experienced lung hemorrhage, and responded to the infection with extensive neutrophil infiltration and histopathological changes in tissue architecture. Neutrophil extracellular trap formation and the expression of inflammatory cytokines occurred early after infection. Mice depleted of neutrophils were exquisitely susceptible to an otherwise nonlethal inoculum, thereby demonstrating the requirement for neutrophils in host protection. Mutation of the genes encoding the cytolysin ShlA and its transporter ShlB resulted in attenuated S. marcescens strains that failed to cause profound weight loss, extended illness, hemorrhage, and prolonged lung pathology in mice. This study describes a model of S. marcescens pneumonia that mimics known clinical features of human illness, identifies neutrophils and the toxin ShlA as a key factors important for defense and infection, respectively, and provides a solid foundation for future studies of novel therapeutics for this important opportunistic pathogen.

ERIC-PCR genotyping of Pseudomonas aeruginosa isolates from haemorrhagic pneumonia cases in mink

BackgroundPseudomonas aeruginosa is a significant pathogen of mink and the cause of haemorrhagic pneumonia, an acute fatal disease in farmed mink.ResultsAmong 90 P. aeruginosa isolates from haemorrhagic pneumonia in mink...

Construction and Virulence of Filamentous Hemagglutinin Protein B1 Mutant of Pasteurella multocida in Chickens

Pasteurella multocida, a Gram-negative nonmotile coccobacillus, is the causative agent of fowl cholera, bovine hemorrhagic septicemia, enzoonotic pneumonia and swine atropic rhinitis. Two filamentous hemagglutinin genes, fhaB1 and fhaB2, are the potential virulence factors. In this study, an inactivation fhaB1 mutant of P. multocida in avian strain C48-102 was constructed by a kanamycin-resistance cassette. The virulence of the fhaB1 mutant and the wild type strain was assessed in chickens by intranasal and intramuscular challenge. The inactivation of fhaB1 resulted in a high degree of attenuation when the chickens were challenged intranasally and a lesser degree when challenged intramuscularly. The fhaB1 mutant and the wild type strain were investigated their sensitivity to the antibody-dependent classical complement-mediated killing pathway in 90% convalescent chicken serum. The fhaB1 mutant was serum sensitive as the viability has reduced between untreated serum and heat inactivated chicken serum (P<0.007). These results confirmed that FhaB1 played the critical roles in the bacterial pathogenesis and further studies were needed to investigate the mechanism which caused reduced virulence of the fhaB1 mutant.

Bacillus calmette-guerin infection in NADPH oxidase deficiency: defective mycobacterial sequestration and granuloma formation.

Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. CGD is an immune deficiency that leads to frequent infections with certain pathogens; this is well documented for S. aureus and A. fumigatus, but less clear for mycobacteria. We therefore performed an extensive literature search which yielded 297 cases of CGD patients with mycobacterial infections; M. bovis BCG was most commonly described (74%). The relationship between NOX2 deficiency and BCG infection however has never been studied in a mouse model. We therefore investigated BCG infection in three different mouse models of CGD: Ncf1 mutants in two different genetic backgrounds and Cybb knock-out mice. In addition, we investigated a macrophage-specific rescue (transgenic expression of Ncf1 under the control of the CD68 promoter). Wild-type mice did not develop severe disease upon BCG injection. In contrast, all three types of CGD mice were highly susceptible to BCG, as witnessed by a severe weight loss, development of hemorrhagic pneumonia, and a high mortality (∼50%). Rescue of NOX2 activity in macrophages restored BCG resistance, similar as seen in wild-type mice. Granulomas from mycobacteria-infected wild-type mice generated ROS, while granulomas from CGD mice did not. Bacterial load in CGD mice was only moderately increased, suggesting that it was not crucial for the observed phenotype. CGD mice responded with massively enhanced cytokine release (TNF-α, IFN-γ, IL-17 and IL-12) early after BCG infection, which might account for severity of the disease. Finally, in wild-type mice, macrophages formed clusters and restricted mycobacteria to granulomas, while macrophages and mycobacteria were diffusely distributed in lung tissue from CGD mice. Our results demonstrate that lack of the NADPH oxidase leads to a markedly increased severity of BCG infection through mechanisms including increased cytokine production and impaired granuloma formation.

Clones of Streptococcus zooepidemicus from outbreaks of hemorrhagic canine pneumonia and associated immune responses.

Acute hemorrhagic pneumonia caused by Streptococcus zooepidemicus has emerged as a major disease of shelter dogs and greyhounds. S. zooepidemicus strains differing in multilocus sequence typing (MLST), protective protein (SzP), and M-like protein (SzM) sequences were identified from 9 outbreaks in Texas, Kansas, Florida, Nevada, New Mexico, and Pennsylvania. Clonality based on 2 or more isolates was evident for 7 of these outbreaks. The Pennsylvania and Nevada outbreaks also involved cats. Goat antisera against acutely infected lung tissue as well as convalescent-phase sera reacted with a mucinase (Sz115), hyaluronidase (HylC), InlA domain-containing cell surface-anchored protein (INLA), membrane-anchored protein (MAP), SzP, SzM, and extracellular oligopeptide-binding protein (OppA). The amino acid sequences of SzP and SzM of the isolates varied greatly. The szp and szm alleles of the closely related Kansas clone (sequence type 129 [ST-129]) and United Kingdom isolate BHS5 (ST-123) were different, indicating that MLST was unreliable as a predictor of virulence phenotype. Combinations of conserved HylC and serine protease (ScpC) and variable SzM and SzP proteins of S. zooepidemicus strain NC78 were protectively immunogenic for mice challenged with a virulent canine strain. Thus, although canine pneumonia outbreaks are caused by different strains of S. zooepidemicus, protective immune responses were elicited in mice by combinations of conserved or variable S. zooepidemicus proteins from a single strain.

Bacteriological and pathological investigation of goat lungs in Mymensingh and determination of antibiotic sensitivity

The foremost important goal of the present study was to investigate the bacteriological and pathological conditions in lungs of goats slaughtered in four different slaughter houses/places of Mymensingh Sadar, Mymensingh and in addition to it, antibiotic sensitivity test of commonly used antibiotics in Veterinary practices were performed on isolated bacteria. A total of 75 lungs of slaughtered goats were examined individually and out of which 20 affected lungs were collected for histopathology and bacterial isolation respectively from Mymensingh Sadar, Mymensingh in Bangladesh, during the period from January to May 2013.The lung lesions was grossly recorded 40% in goats (30 out of 75 lungs examined). Grossly, the lung lesions were categorized into (a) hemorrhages 35% (b) congestion 25% (c) hemorrhage and congestion 15% (d) emphysematous lung 15% and (e) hepatization in lung10%. In histopathology, lung lesions were categorized into (a) bronchopneumonia 30%, (b) pneumonia 25% (c) hemorrhagic pneumonia 20% (d) emphysema 15%, (e) purulent pneumonia 10%. Pasteurella sp. (15%) was isolated from the lung lesions of hemorrhagic pneumonia, E. coli. (25%) from bronchopneumonia and Staphylococcus sp. (40%) from purulent pneumonia, focal pneumonia and emphysema, and mixed infection (Staphylococcus sp. and E. coli) 20%. Finally antibiotics sensitivity test was performed on isolated bacteria to which ciprofloxacin was more powerful than others (penicillin, amoxicillin, streptomycin, nalidixic acid and kanamycin) tested and the second one was oxytetracyclin.DOI: http://dx.doi.org/10.3329/bjvm.v11i2.19142Bangl. J. Vet. Med. (2013).11(2): 159-166

The identification, typing, and antimicrobial susceptibility of Pseudomonas aeruginosa isolated from mink with hemorrhagic pneumonia

The biological characteristics and molecular epidemiology of Pseudomonas aeruginosa associated with mink hemorrhagic pneumonia from Shandong province of eastern China were determined in this study. From 2010 to 2011, 30 mink P. aeruginosa isolates were identified from lung, fecal and feed samples of clinical cases and subjected to serotyping, antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE) using SpeI. The P. aeruginosa isolates belonged to four serotypes—21 of type G, four of type I, three of type M, one of type B, and one non-typable strain. The strains were divided into four large groups as determined by PFGE. Isolates from the group 2 were highly homologous and were obtained from the same region as an epidemic. All of the isolates were sensitive to piperacillin, piperacillin/tazobactam, ceftazidime, cefepime, imipenem, amikacin, gentamicin and tobramycin and resistant to ampicillin, cefuroxime and cefuroxime axetil. A high frequency of resistance was found to ampicillin/sulbactam, cefazolin, cefotetan, ceftriaxone, nitrofurantoin, and trimethoprim/sulfamethoxazole (96.7%). Resistance to ticarcillin/clavulanic acid, ciprofloxacin and levofloxacin was less common (13.3%). There was no relationship between antibiotic resistance and serotype distribution of the isolates. The epidemic serotype of P. aeruginosa from the mink hemorrhagic pneumonia in Shandong province was type G, which was a clone of commonly found in this province. These findings reveal the genetic similarities and antimicrobial susceptibility profiles of P. aeruginosa from clinical cases of mink hemorrhagic pneumonia and will facilitate the prevention and control of the disease in Shandong province of China.

Life-threatening hemorrhagic pneumonia caused by Stenotrophomonas maltophilia in the treatment of hematologic diseases

Since the late 1990s, Stenotrophomonas maltophilia (S. maltophilia) has become one of the most common nonfermenting Gram-negative bacilli that cause opportunistic infection. Patients with hematologic diseases are the most risky candidate for S. maltophilia pneumonia or sepsis because of chemotherapy-induced neutropenia or immunodeficiency. Frequent exposure to broad-spectrum antibiotics and prolonged insertion of central venous catheter further enhance the risk of S. maltophilia infection. One of the most severe S. maltophilia infections is hemorrhagic pneumonia. This type of infection is mostly fatal because of pulmonary alveolar hemorrhage that leads to acute respiratory failure. Furthermore, S. maltophilia exhibits a high-level intrinsic resistance to conventional antibiotics such as β-lactams and aminoglycosides and, more recently, the increasing acquired resistance to co-trimoxazole and quinolones. According to our experienced and previously reported cases, all of the patients with hemorrhagic pneumonia caused by S. maltophilia had a fatal course within a few days after the onset of the pneumonia. In this article, we perform a systematic review on a total 30 cases of hemorrhagic pneumonia induced by S. maltophilia from our institutions and the literature, and we describe its early diagnosis, prophylaxis, and recommended therapeutic strategy for the infection in the treatment of hematologic disease.

A Type III Secretion Negative Clinical Strain of Pseudomonas aeruginosa Employs a Two-Partner Secreted Exolysin to Induce Hemorrhagic Pneumonia

Virulence of Pseudomonas aeruginosa is typically attributed to its type III secretion system (T3SS). A taxonomic outlier, the P.aeruginosa PA7 strain, lacks a T3SS locus, and no virulence phenotype isattributed to PA7. We characterized a PA7-related, T3SS-negative P.aeruginosa strain, CLJ1, isolated from a patient with fatal hemorrhagic pneumonia. CLJ1 is highly virulent in mice, leading to lung hemorrhage and septicemia. CLJ1-infected primary endothelial cells display characteristics of membrane damage and permeabilization. Proteomic analysis of CLJ1 culture supernatants identified a hemolysin/hemagglutinin family pore-forming toxin, Exolysin (ExlA), that is exported via ExlB, representing aputative two-partner secretion system. A recombinant P.aeruginosa PAO1ΔpscD::exlBA strain, deficient for T3SS but engineered to express ExlA, gained lytic capacity on endothelial cells and full virulence in mice, demonstrating that ExlA is necessary and sufficient for pathogenicity. This highlights clinically relevant T3SS-independent hypervirulence, isolates, and points to a broader P.aeruginosa pathogenic repertoire.

Characterisation of bovine viral diarrhoea virus (BVDV) isolates from an outbreak with haemorrhagic enteritis and severe pneumonia

During 2007 a disease outbreak occurred in cattle in the Marmara region of western Turkey characterised by severe pneumonia and haemorrhagic enteritis in calves. Cases from three farms at different locations were examined and bovine viral diarrhoea virus (BVDV) isolated in all cases. Phylogenetic characterisation of the virus isolates allocated them in a new cluster tentatively named as BVDV-1r.