Haemophilus Influenzae Infection Research Articles

Selection for Phase Variation of LOS Biosynthetic Genes Frequently Occurs in Progression of Non-Typeable Haemophilus influenzae Infection from the Nasopharynx to the Middle Ear of Human Patients

Surface structures in Haemophilus influenzae are subject to rapid ON/OFF switching of expression, a process termed phase variation. We analyse tetranucleotide repeats controlling phase variation in lipo-oligosaccharide (LOS) genes of H. influenzae in paired isolates from both the nasopharynx and middle ears of paediatric patients with chronic or recurrent otitis media. A change in expression of at least one of the seven phase variable LOS biosynthesis genes was seen in 12 of the 21 strain pairs. Several strains showed switching of expression in multiple LOS genes, consistent with a key role for phase variable LOS biosynthetic genes in human infection.

Early Onset Nontypable Haemophilus influenzae Sepsis in a Preterm Newborn Infant

We present a case of fulminant neonatal sepsis caused by nontypable Haemophilus influenzae and discuss some potential prevention measures. A 33-year-old pregnant woman delivered a 1,166 g male neonate at 27 weeks and 2 days of gestation. He died 5 hours after birth. Haemophilus influenzae was isolated from the amniotic fluid, maternal vaginal discharge, placenta, neonatal oral cavity, neonatal skin, and neonatal stool. These isolates were found to be nontypable by polymerase chain reaction and sensitive to ampicillin. Placental histopathology revealed acute chorioamnionitis without cord phlebitis or arteritis. An autopsy found no colonization of gram-negative cocobacilli in the organs including the lungs. These results suggest that acute intrapartum nontypable Haemophilus influenzae infection can cause fulminant and invasive neonatal sepsis. Intrapartum antibiotic prophylaxis may be useful for prevention.

S22 Analysis of the lung microbiome in human asthma using whole genome shot-gun metagenomics

Introduction and ObjectivesEvidence is accumulating for the presence of bacteria in the airways and the existence of a commensal airway microbiome. Molecular techniques reveal complex microbial assemblages in bronchiectasis and...

Mixed Pneumococcal–Nontypeable Haemophilus influenzae Otitis Media Is a Distinct Clinical Entity With Unique Epidemiologic Characteristics and Pneumococcal Serotype Distribution

Complex (ie, recurrent, nonresponsive, or chronic) otitis media (OM) is frequent and is often caused by a mixed-pathogen infection with biofilm formation. We conducted this study to characterize children with OM due to mixed Streptococcus pneumoniae and nontypeable Haemophilus influenzae (NTHi) infections (M-OM) and those with OM due to single, S. pneumoniae-only infections (S-OM) and to examine whether pneumococcal serotypes associated with M-OM differed from those associated with S-OM. In a 10-year prospective study in southern Israel, the clinical and demographic variables and pneumococcal serotypes associated with M-OM were compared to those associated with S-OM in children <3 years old. M-OM episodes were significantly more likely to be found in Bedouin children (for whom living conditions are crowded and colonization occurs during early life) and in older children with bilateral OM, recurrent OM, previous tympanocentesis, and lower body temperature, as well as during the winter, suggesting an association with recurrence/chronicity. M-OM was associated with pneumococcal serotypes most commonly carried by healthy children, whereas S-OM was associated with serotypes previously shown to have a higher disease potential. S-OM and M-OM differ clinically and epidemiologically, with overlapping characteristics. Our findings are in agreement with clinical and experimental reports associating respiratory tract biofilms and mixed infections with pneumococcal serotypes of lower virulence and higher capacity to colonize the nasopharynx in healthy individuals.

Nontypeable Haemophilus Influenzae Infection Upregulates the NLRP3 Inflammasome and Leads to Caspase-1-Dependent Secretion of Interleukin-1β — A Possible Pathway of Exacerbations in COPD

Rationale Nontypeable Haemophilus influenzae (NTHi) is the most common cause for bacterial exacerbations in chronic obstructive pulmonary disease (COPD). Recent investigations suggest the participation of the inflammasome in the pathomechanism of airway inflammation. The inflammasome is a cytosolic protein complex important for early inflammatory responses, by processing Interleukin-1β (IL-1β) to its active form.ObjectivesSince inflammasome activation has been described for a variety of inflammatory diseases, we investigated whether this pathway plays a role in NTHi infection of the airways.MethodsA murine macrophage cell line (RAW 264.7), human alveolar macrophages and human lung tissue (HLT) were stimulated with viable or non-viable NTHi and/or nigericin, a potassium ionophore. Secreted cytokines were measured with ELISA and participating proteins detected via Western Blot or immunohistochemistry.Measurements and Main ResultsWestern Blot analysis of cells and immunohistochemistry of lung tissue detected the inflammasome key components NLRP3 and caspase-1 after stimulation, leading to a significant induction of IL-1β expression (RAW: control at the lower detection limit vs. NTHi 505±111pg/ml, p<0.01). Inhibition of caspase-1 in human lung tissue led to a significant reduction of IL-1β and IL-18 levels (IL-1β: NTHi 24 h 17423±3198pg/ml vs. NTHi+Z-YVAD-FMK 6961±1751pg/ml, p<0.01).ConclusionOur data demonstrate the upregulation of the NRLP3-inflammasome during NTHi-induced inflammation in respiratory cells and tissues. Our findings concerning caspase-1 dependent IL-1β release suggest a role for the inflammasome in respiratory tract infections with NTHi which may be relevant for the pathogenesis of bacterial exacerbations in COPD.

Septic Arthritis Due to Haemophilus influenzae Serotype f in a Patient With Waldenström Macroglobulinemia

In Brief Haemophilus influenzae, a gram-negative pleomorphic bacillus, is a well- recognized pathogen in children. In recent years, it is increasingly recognized as an opportunistic pathogen in adults predominantly causing bacteremia, pneumonia, or meningitis. Impaired humoral immunity is a major factor in the development of more invasive infections. An extensive review of the literature reveals that it is infrequently identified as the etiologic agent of septic arthritis in adults. Initial management of septic arthritis includes surgical drainage and antibiotic therapy. We present a case of septic arthritis due to H influenzae serotype f in a patient with Waldenström macroglobulinemia. After surgical drainage and 3 weeks of antibiotic therapy, the patient resumed normal activity and has continued to do well after 1 year of follow-up. Physicians must be mindful of this invasive pathogen’s role in septic arthritis and the need for immediate surgical intervention and antibiotic administration so as to decrease associated morbidity and mortality. Since the introduction of the Hib vaccine, the overall incidence of Haemophilus influenzae infection has decreased among children with a subsequent increased incidence of invasive disease in adults. A majority of invasive infections are now identified as serotype f and other nontypable strains. Carlsen et al. present a case of septic arthritis due to H.influenzae, serotype f in a patient with Waldenström macroglobulinemia. Patients with underlying immunodeficiencies are especially prone to this relatively rare phenomenon. Physicians must remain vigilant in entertaining this diagnosis in patients with immunodeficiencies so as to prevent associated morbidity and mortality.

Epitope-specific immune recognition of the nontypeable Haemophilus influenzae outer membrane protein 26

Previous studies using rodent respiratory infection models of nontypeable Haemophilus influenzae (NTHi) infection have established the 26-kDa outer membrane protein of the bacterium, OMP26, as a potential vaccine antigen for NTHi. This study undertook a comprehensive immunological identification of OMP26 T- and B-cell epitopes. A series of OMP26 peptides were constructed and regions of the OMP26 antigen involved in recognition by lymphocyte receptors and induction of acquired immune responses were identified. The dominant T-cell epitopes for OMP26 were located toward the C-terminus between amino acid residues 95 and 197 (T3+T4 region) as mapped using antigen-specific lymphocyte proliferation assays. The newly identified T-cell epitopes exhibited strong capacity for efficient T-cell activation, suggesting that, compared with other OMP26 regions; epitopes within the T3+T4 region have the highest affinity for binding to major histocompatibility complex molecules. In contrast, the predominant B-cell epitopes of OMP26 were located more centrally within the molecule between amino acid residues 45 and 145 (T2+T3 region) as determined using enzyme-linked immunosorbent assay and surface plasmon resonance assays. The T2+T3 region was immunodominant in several species including chinchilla, mice and rats when assessed using both mucosal and parenteral immunization regimes. In addition, the antibodies directed against the T2+T3 region bound to intact NTHi cell surface, according to flow cytometry. Collectively, these results specifically locate the amino acid sequences containing the OMP26 T- and B-cell epitopes, which, as newly mapped antigenic epitopes for lymphocyte recognition, will be useful to improve existing NTHi vaccine strategies. Comprehensive definition of the minimum epitope length required for optimal B- and T-cell responses requires further study.

Quantitative PCR confirms culture as the gold standard for detection of lower airway infection by nontypeable Haemophilus influenzae in Australian Indigenous children with bronchiectasis

Correlation was observed between quantitative PCR and semi-quantitative culture for definition of Haemophilus influenzae infection in bronchoalveolar lavage specimens from 81 children with bronchiectasis. However, qPCR data correlated less well with airway neutrophilia, and supports continued use of culture as the gold standard for defining H. influenzae lower airway infection.

Thin-section CT findings of patients with acute Streptococcus pneumoniae pneumonia with and without concurrent infection

The aim of this study was to compare the pulmonary thin-section CT findings of patients with acute Streptococcus pneumoniae pneumonia with and without concurrent infection. The study group comprised 86 patients with acute S. pneumoniae pneumonia, 36 patients with S. pneumoniae pneumonia combined with Haemophilus influenzae infection, 26 patients with S. pneumoniae pneumonia combined with Pseudomonas aeruginosa infection and 22 patients with S. pneumoniae pneumonia combined with methicillin-susceptible Staphylococcus aureus (MSSA) infection. We compared the thin-section CT findings among the groups. Centrilobular nodules and bronchial wall thickening were significantly more frequent in patients with pneumonia caused by concurrent infection (H. influenzae: p<0.001 and p<0.001, P. aeruginosa: p<0.001 and p<0.001, MSSA: p<0.001 and p<0.001, respectively) than in those infected with S. pneumoniae alone. Cavity and bilateral pleural effusions were significantly more frequent in cases of S. pneumoniae pneumonia with concurrent P. aeruginosa infection than in cases of S. pneumoniae pneumonia alone (p<0.001 and p<0.001, respectively) or with concurrent H. influenzae (p<0.05 and p<0.001, respectively) or MSSA infection (p<0.05 and p<0.05, respectively). When a patient with S. pneumoniae pneumonia has centrilobular nodules, bronchial wall thickening, cavity or bilateral pleural effusions on CT images, concurrent infection should be considered.

InvasiveHaemophilus influenzaeSerotype e and f Disease, England and Wales

Haemophilus influenzae infection causes serious invasive disease, but incidence of the most virulent serotype, Hib, has dropped since introduction of routine Hib vaccination. In England and Wales, the incidence of 2 other serotypes, Hie and Hif, is increasing; during 2001-2010, there was an 11.0% year-on-year increase in Hif and a 7.4% increase in Hie. In 2009-2010, Hif incidence was 0.090/100,000 persons and Hie incidence 0.030/100,000, with higher rates among infants and older adults. Hie had a more severe clinical course; although outcome at 6 months was comparable for the 2 serotypes, case-fatality rate within 7 days of diagnosis was higher for Hie, even after adjustment for age and comorbidities. Multilocus sequence typing revealed a single major circulating clone for both Hif (sequence type 124; 89/99 isolates, 90%) and Hie (sequence type 18; 21/33, 64%), but no association between type and clinical disease or outcome was found.

Haemophilus influenzae Sepsis and Placental Abruption in an Unvaccinated Immigrant

BackgroundHaemophilus influenzae infections have declined dramatically in the United States since implementation of the conjugate vaccine. However, in countries where widespread immunization is not routine, H influenzae remains a significant cause of morbidity and mortality. We report a case of a previously unvaccinated immigrant with confirmed H influenzae sepsis and placental abruption leading to spontaneous abortion.ObjectivesTo alert emergency medicine practitioners that H influenzae should be recognized as a maternal, fetal, and neonatal pathogen. Clinicians should consider this diagnosis in immigrants presenting with uncertain vaccination history, as H influenzae can cause significant morbidity and mortality.Case PresentationA 36-year-old female was referred to our emergency department (ED) with lower abdominal pain with some vaginal spotting. The patient had an initial visit with normal laboratory investigations and normal imaging results, with complete resolution of symptoms. The patient returned to the ED with sudden onset of vaginal bleeding and abdominal pain. She presented at this time with sepsis, which progressed to septic shock, causing placental abruption and ultimately, spontaneous abortion. The patient was treated with pressors and antibiotics and was admitted to the medical intensive care unit where she received ampicillin, gentamycin, and clindamycin for suspected chorioamnionitis. The patient's blood cultures came back positive after 1 day for H influenzae. The patient did well and was discharged from the hospital 4 days later.ConclusionHaemophilus influenzae should be recognized as a neonatal and maternal pathogen. Clinicians should consider this diagnosis in immigrants presenting with uncertain vaccination history, especially in pregnant females, as H influenzae can cause significant morbidity and mortality.

Haemophilus influenzae infection drives IL-17-mediated neutrophilic allergic airways disease.

A subset of patients with stable asthma has prominent neutrophilic and reduced eosinophilic inflammation, which is associated with attenuated airways hyper-responsiveness (AHR). Haemophilus influenzae has been isolated from the airways of neutrophilic asthmatics; however, the nature of the association between infection and the development of neutrophilic asthma is not understood. Our aim was to investigate the effects of H. influenzae respiratory infection on the development of hallmark features of asthma in a mouse model of allergic airways disease (AAD). BALB/c mice were intraperitoneally sensitized to ovalbumin (OVA) and intranasally challenged with OVA 12–15 days later to induce AAD. Mice were infected with non-typeable H. influenzae during or 10 days after sensitization, and the effects of infection on the development of key features of AAD were assessed on day 16. T-helper 17 cells were enumerated by fluorescent-activated cell sorting and depleted with anti-IL-17 neutralizing antibody. We show that infection in AAD significantly reduced eosinophilic inflammation, OVA-induced IL-5, IL-13 and IFN-γ responses and AHR; however, infection increased airway neutrophil influx in response to OVA challenge. Augmented neutrophilic inflammation correlated with increased IL-17 responses and IL-17 expressing macrophages and neutrophils (early, innate) and T lymphocytes (late, adaptive) in the lung. Significantly, depletion of IL-17 completely abrogated infection-induced neutrophilic inflammation during AAD. In conclusion, H. influenzae infection synergizes with AAD to induce Th17 immune responses that drive the development of neutrophilic and suppress eosinophilic inflammation during AAD. This results in a phenotype that is similar to neutrophilic asthma. Infection-induced neutrophilic inflammation in AAD is mediated by IL-17 responses.

Critical role of type 1 plasminogen activator inhibitor (PAI-1) in early host defense against nontypeable Haemophilus influenzae (NTHi) infection

Respiratory systems are constantly being challenged by pathogens. Lung epithelial cells serve as a first line of defense against microbial pathogens by detecting pathogen-associated molecular patterns (PAMPs) and activating downstream signaling pathways, leading to a plethora of biological responses required for shaping both the innate and adaptive arms of the immune response. Acute-phase proteins (APPs), such as type 1 plasminogen activator inhibitor (PAI-1), play important roles in immune/inflammatory responses. PAI-1, a key regulator for fibrinolysis and coagulation, acts as an APP during acute phase response (APR) such as acute lung injury (ALI), inflammation, and sepsis. However, the role of PAI-1 in the pathogenesis of these diseases still remains unclear, especially in bacterial pneumonia. In this study, we showed that PAI-1 expression is upregulated following nontypeable Haemophilus influenzae (NTHi) infection. PAI-1 knockout (KO) mice failed to generate early immune responses against NTHi. Failure of generating early immune responses in PAI-1 KO mice resulted in reduced bacterial clearance and prolonged disease process, which in turn led to enhanced inflammation at late stage of infection. Moreover, we also found that NTHi induces PAI-1 via activation of TLR2–MyD88–MKK3–p38 MAPK signaling pathway. These data suggest that PAI-1 plays critical role in earl host defense response against NTHi infection. Our study thus reveals a novel role of PAI-1 in infection caused by NTHi, one of the most common gram-negative bacterial pathogens in respiratory systems.

無莢膜型インフルエンザ菌（NTHi）の疫学

While most systemic pediatric Haemophilus influenzae infections are caused by the type b strain (Hib), nontypeable H. influenzae: (NTHi) has been considered a respiratory tract pathogen common in local infection such as acute otitis media, acute pneumonia, secondary chronic respiratory disease and other otorhinolaryngologic infections. Recent findings show, however, that NTHi also causes invasive infections such as meningitis, bacteremia, and lower respiratory tract infections such as pneumonia. A review of NTHi epidemiology from the 1990s onward shows that NTHi causes significant morbidity in pediatric acute otitis media, sinusitis, conjunctivitis and lower respiratory diseases such as pneumonia in Japan. This summary also reviews the worldwide influence of Streptococcus pneumoniae and Hib vaccines on causative pathogens, and several studies about increasing incidence of invasive infections due to NTHi. This review also touches on the emergence of treatment- and drug-resistant H. influenzae, which are now major public health challenges. As a cause of bacterial pediatric infection, NTHi is an important target for prevention.

Role of pneumococcal pneumolysin in the induction of an inflammatory response in human epithelial cells

Epithelial cells act as the first line of host defense against microorganisms by producing a range of molecules for clearance. Proinflammatory cytokines facilitate the clearance of invaders by the recruitment and activation of leukocytes. Upregulation of cytokine expression thus represents an important host innate defense response against invading microorganisms such as Streptococcus pneumoniae. Histological analysis of the airway revealed less leukocyte infiltration during the early stage of pneumococcal infection, when compared with nontypable Haemophilus influenzae (NTHi) infection. Here, we report that S. pneumoniae is less potent in inducing proinflammatory cytokine expression compared with NTHi. Among numerous virulence factors, pneumococcal pneumolysin was found to be the major factor responsible for the induction of inflammation. Interestingly, pneumolysin induces cytokine expression to a lesser extent at the early stage of infection, but becomes more potent in inducing inflammation at the late stage. Thus, this study reveals that pneumolysin induces the proinflammatory cytokine expression in a time-dependent manner.

Do New Zealand children with non‐cystic fibrosis bronchiectasis show disease progression?

There is minimal literature available on the long-term outcome of pediatric non-cystic fibrosis (CF) bronchiectasis. To document 5-year outcomes of children with chest computerized tomography (CT) scan diagnosed bronchiectasis from a tertiary New Zealand (NZ) respiratory clinic. Review of a clinical database identified 91 children. Demographics, clinical data, lung function, chest X-ray (CXR), sputum, presumed etiology, admission data, and the NZ deprivation index (NZDep) were collected. Univariate and multivariate regression were used to correlate clinical findings with lung function data and CXR scores using the Brasfield Scoring System. Of the 91 children, 53 (59%) were Pacific Island, 22 (24%) Maori, 14 (15%) European, and 2 (2%) Other. The median follow-up period was 6.7 years (range 5.0-15.3 years) and median age at diagnosis was 7.3 years (range 11 months-16 years). Lung function data (n = 64) showed a mean decline of -1.6% predicted/year. In 30 children lung function declined (mean FEV(1) -4.4% predicted/year, range 1-17%), remained stable in 13 and improved in 21 children (mean FEV(1) of +3% predicted/year, range 1-15%). Reduced lung function was associated with male gender, chronic Haemophilus influenzae infection, longevity of disease, and Maori and Pacific Island ethnicity. There was a significant correlation with FEV(1) and CXR score at beginning (n = 47, r = 0.45, P = 0.001) and end (n = 26, r = 0.59, P = 0.002) of the follow-up period. The only variable consistently related to CXR score was chronic Haemophilus influenzae infection occurring in 27 (30%) (r(2) = 0.52, P = <0.0001). Only four children were chronically infected with Pseudomonas species. Six children died. In our experience despite management in a tertiary multidisciplinary bronchiectasis clinic, progression of lung disease continues in a group of children and young adults.

Changing epidemiology of invasive Haemophilus influenzae in Ontario, Canada: Evidence for herd effects and strain replacement due to Hib vaccination

The epidemiology of invasive Haemophilus influenzae infections was evaluated in Ontario between 1989 and 2007 to assess the impact of the introduction of the conjugate H. influenzae serotype b (Hib) vaccine in the early 1990s on Hib and non-Hib serotypes in both vaccinated and unvaccinated cohorts as well as the possibility of “strain replacement” with non-vaccine H. influenzae strains. Data were collected by the provincial Public Health Laboratories-Toronto, Ontario Agency for Health Protection and Promotion, which performed almost all serotyping on invasive (blood, CSF, other sterile sites) H. influenzae strains isolated in the province during the study period. Temporal trends for Hib, other typeable strains, and non-typeable H. influenzae were evaluated by Poisson regression, controlling for the specimen submissions. Prior to infant Hib vaccination, the most commonly observed serotype was serotype b (64.9%). Subsequently, 70.3%, 13.6%, and 9.4% of isolates were non-typeable, serotype f, and serotype b, respectively. Infant Hib vaccination resulted in a decrease in Hib incidence in all age groups (pooled IRR 0.432) and marked increases of non-typeable and serotype f H. influenzae in children aged <5 years (IRR 2.4 and 3.0, respectively). Vaccination against Hib has altered the epidemiology of invasive H. influenzae infections in Ontario. Prevention of invasive Hib disease was observed in both vaccinated and unvaccinated age groups. Invasive H. influenzae infection now commonly presents as sepsis due to non-typeable H. influenzae in older individuals. However, strain replacement of Hib with serotype f and non-typeable strains in children under 5 years was documented.

Index of Suspicion in the Nursery

A 2,435-g male infant is born at 38 weeks gestational age to a 22-year-old G2P1001 woman who is blood group O+ and negative for group B Streptococcus. Labor had been induced for intrauterine growth restriction. Rupture of membranes with clear fluid occurred 3 hours before delivery, and the baby is delivered by emergency cesarean section for fetal bradycardia. Apgar scores are 8 at 1 minute and 8 at 5 minutes. The baby is suctioned by bulb and nasogastric tube. At 8 minutes of age, the baby's lungs sound wet, with a pulse oximetry reading of 68%, and 40% blow-by oxygen is started. By 15 minutes of age, he is breathing room air with a pulse oximetry reading of 98%. Physical examination in the newborn nursery yields normal results, with a Ballard score of 39 weeks, weight between the 10th and 25th percentiles, length at the 75th percentile, and head circumference at the 25th percentile. He has one low temperature of 35.4°C initially, but the capillary blood glucose measurements are 59 mg/dL (3.3 mmol/L) or more. He does well on formula feedings, with a weight loss of 15 g at 12 hours and 40 g at 36 hours. At 45 hours of age, after an uneventful hospital stay, the baby develops tachypnea and moderate intercostal and subcostal retractions. His pulse oximetry reading is 85% to 89%. He is placed on oxygen by nasal cannula, and an evaluation is undertaken that reveals the source of his respiratory distress. A 23-day-old male infant presents to the clinic because of persistent crying. Yesterday, he was seen in the emergency department, where colic was diagnosed. Today, his mother appears overwhelmed, stating that the baby cries throughout the day and night. She is concerned that the infant has abdominal pain or pain in his left …

InvasiveHaemophilus influenzaeDisease in Utah Children: An 11‐Year Population‐Based Study in the Era of Conjugate Vaccine

The incidence of invasive Haemophilus influenzae infection decreased dramatically since the introduction of the H. influenzae serotype b (Hib) conjugate vaccine. H. influenzae invasive disease continues to occur and cause significant morbidity and mortality in children aged <5 years. We aimed to report the epidemiology and serotypes of invasive H. influenzae disease in children from Utah in the post-Hib vaccine era. We identified all cases of invasive H. influenzae disease, defined as H. influenzae isolated from a sterile site, during the period 1998-2008 among children aged <18 years who were living in Utah. We identified 91 cases of invasive H. influenzae disease in children. Children aged <5 years accounted for 78 cases (86%). H. influenzae serotype a (Hia) was the most common serotype (22 cases), representing 28% of all cases of invasive disease among children aged <5 years. The majority (15 cases [93%]) of Hib disease cases occurred among children aged <5 years and accounted for 18% of all cases of H. influenzae invasive disease in this age group. The mean incidence of Hia disease increased from 0.8 cases per 100,000 child-years in 1998 to 2.6 cases per 100,000 child-years in 2008. The incidence of Hib disease among children aged <5 years remained steady at 0.5 cases per 100,000 child-years. Bacteremia accounted for 61% of all cases of invasive disease. One-half (13 of 26) of cases of H. influenzae meningitis were due to Hia. H. influenzae continues to cause invasive disease in Utah children. Hia is the primary cause of the overall increased incidence of invasive H. influenzae disease and leads to disease similar to Hib. Isolated cases of Hib disease demonstrate a continued reservoir. The success of the Hib conjugate vaccine may therefore be vulnerable to vaccine shortages and refusal of vaccination.

Necrotising fasciitis complicating Haemophilus influenzae type b epiglottitis in an adult

To present the first reported case of Haemophilus influenzae type b epiglottitis leading to necrotising fasciitis. Case report and review of the literature regarding the association of necrotising fasciitis with Haemophilus influenzae infection and with epiglottitis. A previously well, 64-year-old woman presented with epiglottitis, and subsequently developed necrotising fasciitis of her chest wall. The cause of both infections was Haemophilus influenzae serotype b. This organism has frequently been implicated in epiglottitis, but has not previously been reported to cause simultaneous necrotising fasciitis. The patient became critically ill, requiring intensive care management, but following surgical debridement and antibiotic treatment she made a full recovery. Although increasingly uncommon, clinicians must continue to be proficient in the diagnosis and management of epiglottitis, and to be aware of its full range of possible complications. This case report highlights a previously unknown and potentially fatal complication of Haemophilus influenzae type b epiglottitis.