Summary: Human infection with Fusobacterium necrophorum usually involves F. necrophorum subsp. funduliforme rather than F. necrophorum subsp. necrophorum, which is a common pathogen in animals. Lemierre9s syndrome, or postanginal sepsis, is the most common life-threatening manifestation. Tonsillitis is followed by septic thrombophlebitis of the internal jugular vein and then a septicemia with septic emboli in lungs and other sites. Recent evidence suggests that F. necrophorum can be limited to the throat and cause persistent or recurrent tonsillitis. F. necrophorum is unique among non-spore-forming anaerobes, first for its virulence and association with Lemierre9s syndrome as a monomicrobial infection and second because it seems probable that it is an exogenously acquired infection. The source of infection is unclear; suggestions include acquisition from animals or human-to-human transmission. Approximately 10% of published cases are associated with infectious mononucleosis, which may facilitate invasion. Recent work suggests that underlying thrombophilia may predispose to internal jugular vein thrombophlebitis. Lemierre9s syndrome was relatively common in the preantibiotic era but seemed to virtually disappear with widespread use of antibiotics for upper respiratory tract infection. In the last 15 years there has been a rise in incidence, possibly related to restriction in antibiotic use for sore throat.

Human Infection with Fusobacterium necrophorum (Necrobacillosis), with a Focus on Lemierre's Syndrome

SUMMARY This review begins with a discussion of the large family of Staphylococcus aureus and beta-hemolytic streptococcal pyrogenic toxin T lymphocyte superantigens from structural and immunobiological perspectives. With this as background, the review then discusses the major known and possible human disease associations with superantigens, including associations with toxic shock syndromes, atopic dermatitis, pneumonia, infective endocarditis, and autoimmune sequelae to streptococcal illnesses. Finally, the review addresses current and possible novel strategies to prevent superantigen production and passive and active immunization strategies.

Staphylococcal and Streptococcal Superantigen Exotoxins

It is commonly believed that the clinical and epidemiological characteristics of the next influenza pandemic will mimic those of the 1918 pandemic. Determinative beliefs regarding the 1918 pandemic include that infections were expressed as primary viral pneumonias and/or acute respiratory distress syndrome, that pandemic-related deaths were the end states of the natural progression of disease caused by the pandemic strain, and that bacterial superinfections caused relatively fewer deaths in 1918 than in subsequent pandemics. In turn, response plans are focused on developing and/or increasing inventories of a strain-specific vaccine, antivirals, intensive care beds, mechanical ventilators, and so on. Yet, there is strong and consistent evidence of epidemiologically and clinically important interactions between influenza and secondary bacterial respiratory pathogens, including during the 1918 pandemic. Countermeasures (eg, vaccination against pneumococcal and meningococcal disease before a pandemic; mass uses of antibiotic(s) with broad spectrums of activity against common bacterial respiratory pathogens during local epidemics) designed to prevent or mitigate the effects of influenza-bacterial interactions should be major focuses of pandemic-related research, prevention, and response planning.

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Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) strains have emerged as serious health threats in the last 15 years. They are associated with large numbers of atopic dermatitis skin and soft tissue infections, but when they originate from skin and mucous membranes, have the capacity to produce sepsis and highly fatal pulmonary infections characterized as necrotizing pneumonia, purpura fulminans, and postviral toxic shock syndrome. This review is a discussion of the emergence of 3 major CA-MRSA organisms, designated CA-MRSA USA400, followed by USA300, and most recently USA200. CA-MRSA USA300 and USA400 isolates and their methicillin-sensitive counterparts (community-associated methicillin-sensitive S aureus) typically produce highly inflammatory cytolysins α-toxin, γ-toxin, δ-toxin (as representative of the phenol soluble modulin family of cytolysins), and Panton Valentine leukocidin. USA300 isolates produce the superantigens enterotoxin-like Q and a highly pyrogenic deletion variant of toxic shock syndrome toxin 1 (TSST-1), whereas USA400 isolates produce the superantigens staphylococcal enterotoxin B or staphylococcal enterotoxin C. USA200 CA-MRSA isolates produce small amounts of cytolysins but produce high levels of TSST-1. In contrast, their methicillin-sensitive S aureus counterparts produce various cytolysins, apparently in part dependent on the niche occupied in the host and levels of TSST-1 expressed. Significant differences seen in production of secreted virulence factors by CA-MRSA versus hospital-associated methicillin-resistant S aureus and community-associated methicillin-sensitive S aureus strains appear to be a result of the need to specialize as the result of energy drains from both virulence factor production and methicillin resistance.

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Secreted virulence factor comparison between methicillin-resistant and methicillin-sensitive Staphylococcus aureus, and its relevance to atopic dermatitis

Staphylococcus aureus is a highly successful bacterial pathogen owing to its abundance of cell surface and secreted virulence factors. It is estimated that 30% of the population is colonized with S. aureus, usually on mucosal surfaces, and methicillin-resistant S. aureus is a major public health concern. There have been multiple attempts to develop an S. aureus vaccine using one or more cell surface virulence factors as antigens; all of these vaccine trials have failed. In this Opinion article, we suggest that an over-reliance on rodent models and a focus on targeting cell surface components have been major contributing factors to this failure.

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Papers

Toxic shock syndrome