Postmortem histological freeze-thaw artifacts: a case report of a frozen infant and literature review.

Freezing and thawing have the potential to alter the gross and histologic appearance of tissues, causing damage to individual cells and disrupting the overall architecture. In forensic investigations, freezing and thawing can play a crucial role in cases of unknown cause of death. Perpetrators may use freezing preservation to conceal the body or obscure the time of death. Freezing can also occur naturally when a body is exposed to the elements, sometimes even leading to death itself. We present a case report involving an autopsy performed on an infant, who died of natural causes, after undergoing freezing and thawing. The objective of this study was to identify and discuss the histological artifacts observed in different tissues as a result of the freeze-thaw process. Histologically, the infant's tissues exhibited the most common features described in the literature. Ice crystal artifacts, characterized by expansion of the extracellular space and tissue clefts, were found in the heart, brain, liver, lungs, and kidneys. On the contrary, adipose tissue was not affected, likely due to the scarcity of water. Freeze-thaw artifacts should be taken into account whether a body is known to have been frozen or to add further data if found already defrosted.

Fulminant Sepsis and Perinatal Death at 23 Weeks Due to Fusobacterium nucleatum.

Introduction: Fusobacterium nucleatum is a gram-negative anaerobe, a constituent of the oral microflora, responsible for chronic periodontal diseases. Case Report: We describe a preterm infant with premature rupture of membranes at 23 weeks of gestational age due to F. nucleatum. The newborn died soon after birth. Placental histopathology showed severe necrotizing chorioamnionitis and funisitis with gram-negative bacilli. After autopsy, F. nucleatum was microbiologically isolated from the lung. The mother had dental hygiene 1 day before delivery, presenting mild and diffuse gingivitis. At admission, she had leukocytosis, foul-smelling vaginal discharge, but no fever. Conclusion: This case highlights the possibility of F. nucleatum spreading from oral cavity after a dental procedure to the placenta with chorioamnionitis and fetal infection. This raises the question of whether dental procedures during pregnancy should be accompanied by prophylactic antibiotics.

Second Trimester Fetal Loss Due to Citrobacter koseri Infection: A Rare Cause of Preterm Premature Rupture of Membranes (PPROM).

Citrobacter koseri is a facultative anaerobic, motile, non-spore-forming Gram-negative bacillus, which belongs to the family of Enterobacteriaceae. Severe infections due to Citrobacter spp. have been reported in the urinary tract, respiratory airways, intra-abdominal organs, skin and soft tissue, eye, bone, bloodstream, and central nervous system. In newborns, C. koseri is a well-known cause of meningitis, cerebral abscesses, brain adhesions, encephalitis, and pneumocephalus. Infection can be acquired through vertical maternal transmission or horizontal hospital settings; however, in many cases, the source is unknown. Preterm premature rupture of membranes (PPROM), caused by C. koseri, has rarely been described. Herein, we describe a case of PPROM at 16 weeks and 3 days of gestation, leading to anhydramnios. The parents opted for legal termination of the pregnancy, as the prognosis was very poor. C. koseri was isolated postmortem from a placental subamniotic swab and parenchymal sample, as well as fetal blood and lung. To the best of our knowledge, this is the first case of early second-trimester PPROM in which C. koseri infection was demonstrated.

Kingella kingae Intrauterine Infection: An Unusual Cause of Chorioamnionitis and Miscarriage in a Patient with Undifferentiated Connective Tissue Disease.

Kingella kingae is a Gram-negative coccobacillus belonging to the Neisseriaceae family. In children less than 4 years old, K. kingae invasive infection can induce septic arthritis and osteomyelitis, and more rarely endocarditis, meningitis, ocular infections, and pneumonia. In adults, it may be a cause of endocarditis. To date, K. kingae acute chorioamnionitis (AC) leading to preterm rupture of membranes (PPROM) and miscarriage has never been reported. Herein, we describe a case of intrauterine fetal death (IUFD) at 22 weeks' gestation due to K. kingae infection occurred in a patient affected by undifferentiated connective tissue disease (UCTD) in lupus erythematosus systemic (LES) evolution with severe neutropenia. K. kingae was isolated in placental subamnionic swab and tissue cultures as well as fetal ear, nose, and pharyngeal swabs. Placental histological examination showed necrotizing AC and funisitis. In the fetus, neutrophils were observed within the alveoli and in the gastrointestinal lumen. Maternal medical treatment for UCTD was modified according to the K. kingae invasive infection. In the event of IUFD due to AC, microbiological cultures on placenta and fetal tissues should always be carried out in order to isolate the etiologic agent and target the correct medical treatment.

Klebsiella pneumoniae Chorioamnionitis: An Underrecognized Cause of Preterm Premature Rupture of Membranes in the Second Trimester.

Klebsiella pneumoniae is a Gram-negative, rod-shaped bacterium, responsible for hospital and community acquired pneumonia, urinary tract and wound infections, and bloodstream dissemination. K. pneumoniae infection in pregnancy, leading to acute chorioamnionitis (AC), preterm premature rupture of membranes (PPROM) and early pregnancy loss in the second trimester, has been rarely reported. Herein, we present a case of K. pneumoniae AC that caused intrauterine fetal demise (IUFD) at 19 weeks + 5 days. The 36-year-old mother was admitted at 18 weeks + 1 day of gestation for threatened abortion. IUFD occurred 11 days after. Fetal postmortem showed severe AC and funisitis, neutrophils within alveoli and intestinal lumen, associated with rod-like bacteria. Fetal blood and lung cultures grew K. pneumoniae, ß-lactamase-non-producing strain. Antibiogram revealed sensitivity for piperacillin/tazobactam. Three days after IUFD, the mother presented with fever (37.8 °C) which persisted for one week. Maternal blood and urine cultures were negative. According to fetal microbiological results, available 6 days after IUFD, initial treatment with amoxicillin/clavulanic acid was replaced with piperacillin/tazobactam with full patient recovery. Therefore, in the event of PPROM and IUFD, fetal microbiological investigations should always be performed to isolate the proper etiologic agent and start the correct medical treatment.

Asaia lannensis bacteremia in a 'needle freak' patient.

The genus Asaia has gained much interest lately owing to constant new species discoveries and its role as a potential opportunistic pathogen to humans. Here we describe a transient bacteremia due to Asaia lannensis in a patient with a psychiatric disorder (compulsive self-injection of different substances). Common phenotypic methods of identification failed to identify this organism, and only restriction fragment lenght polymorphism of PCR-amplified 16S rRNA gene allowed for proper identification. The isolate was highly resistant to most antibiotics. The paper also discusses the currently available medical literature, acknowledges the potential problems linked to the isolation of these strains and proposes an approach to species identification that can be applied in a clinical microbiology laboratory.

[Treating Clostridium difficile infection with faecal transplantation: donor microbiological testing]. / Terapia delle infezioni da Clostridium difficile con trapianto di feci: controlli microbiologici sul donatore.

Clostridium difficile associated diseases (CDADs) or C. difficile infections (CDIs) are increasing in incidence, severity and mortality. Among patients with CDIs, those with recurrent disease are less responsive to traditional therapies with commonly used drugs, such as metronidazole and vancomycin. Faecal microbiota transplantation is an old therapeutic procedure that has been recently proposed as a safe and effective treatment for CDI patients non-responsive to antibiotic therapy. In this paper we discuss the microbiological procedures that should be performed on faecal microbiota donors.

Regulation and differential expression of gdhA encoding NADP-specific glutamate dehydrogenase in Neisseria meningitidis clinical isolates.

Meningococcal gdhA, encoding the NADP-specific l-glutamate dehydrogenase (NADP-GDH), is essential for systemic infection in an infant rat model. In this paper, a limited transcriptional analysis detected differences in gdhA expression among clinical isolates. In strains expressing high levels of gdhA mRNA, two promoters, gdhA P1 and gdhA P2, initiated transcription of gdhA. In contrast, in strains expressing low mRNA levels, gdhA P2 was not active because of weak expression of gdhR, an associated regulatory gene. Gene knock-out and complementation of a gdhR-defective mutant confirmed that GdhR is a positive regulator for gdhA P2. Trans-activation of gdhA P2 was maximal in complex medium during late logarithmic growth phase and in chemical defined medium (MCDA) when glucose (MCDA-glucose) instead of lactate (MCDA-lactate) was used as a carbon source in the presence of glutamate. gdhR knock-out mutants lost both growth phase and carbon source regulation, and exhibited a growth defect more severe in MCDA-glucose than in MCDA-lactate. DNA-protein interaction studies demonstrated that 2-oxoglutarate, a product of the catabolic reaction of the NADP-GDH and an intermediate of the tricarboxylic acid (TCA) cycle, inhibits binding of GdhR to gdhA P2.

Phenotypes of a naturally defective recB allele in Neisseria meningitidis clinical isolates.

Neisseria meningitidis strains belonging to the hypervirulent lineage ET-37 and several unrelated strains are extremely UV sensitive. The phenotype is consequent to the presence of a nonfunctional recB(ET-37) allele carrying multiple missense mutations. Phenotypic analysis has been performed with congenic meningococcal strains harboring either the wild-type recB allele or the recB(ET-37) allele. Congenic recB(ET-37) meningococci, in addition to being sensitive to UV, were defective both in repair of DNA lesions induced by UV treatment and, partially, in recombination-mediated transformation. Consistently, the wild-type, but not the recB(ET-37), allele was able to complement the Escherichia coli recB21 mutation to UV resistance and proficiency in recombination. recB(ET-37) meningococci did not exhibit higher frequencies of spontaneous mutation to rifampin resistance than recB-proficient strains. However, mutation rates were enhanced following UV treatment, a phenomenon not observed in the recB-proficient counterpart. Interestingly, the results of PCR-based assays demonstrated that the presence of the recB(ET-37) allele considerably increased the frequency of recombination at the pilin loci. The main conclusion that can be drawn is that the presence of the defective recB(ET-37) allele in N. meningitidis isolates causes an increase in genetic diversity, due to an ineffective RecBCD-dependent DNA repair and recombination pathway, and an increase in pilin antigenic variation.