MicrobiologyBytes

Methicillin-resistant Staphylococcus aureus (MRSA) is usually associated with hospital infections, where it can cause severe illness in the immunocompromised and elderly, particularly people with wounds where the bacteria can get in. In this article in Microbiology Today (pdf) Jodi Lindsay tells us about a novel strain of MRSA found in the USA that is causing concern. Called Community-acquired-MRSA (CA-MRSA), the bacteria can cause infection in healthy people and several outbreaks in contact sports teams have been reported:

Staphylococcus aureus are bacteria that commonly live in the nose, and about 20% of us carry them all the time, with another 50% intermittently coloni-zed. We have all had an S. aureus infection, usually an infected cut or wound that became inflamed and maybe produced some pus. Because of our healthy immune response, predominantly the production of neutrophils, we didn’t need anti-biotics and the infection cleared itself. Very occasionally, a S. aureus infection can become more serious in a healthy person, but we don’t really know why. However, in the USA there have recently been out-breaks of a new type of meticillin-resistant S. aureus (MRSA), to which athletes are particularly vulnerable…

Read more

Related:

• MRSA: Methicillin-resistant Staphylococcus aureus
• Novel treatments for MRSA
• Evolution and pathogenesis of Staphylococcus aureus
• Maggots or MRSA?

Malaria counts among the worst scourges of humankind, accounting for some 500 million clinical cases per year and more than one million deaths, mostly children. It amounts to an immeasurable health burden and inhibits economic prosperity in numerous tropical countries, most extensively in Africa. Plasmodium falciparum is the most virulent among the four Plasmodium species parasitic to humans, accounting for 85% of all malaria cases, and nearly all of the mortality. The extreme pathogenicity of P. falciparum has suggested that it is a recent human parasite, acquired by transfer from a nonhuman host. Some early molecular phylogenies seemed to be consistent with this hypothesis, because they showed P. falciparum to be more closely related to Plasmodium gallinaceum, a chicken parasite, than to any of the other human parasite species. A considered possibility was that P. falciparum evolved from an avian parasite following a horizontal host transfer, perhaps in association with the Neolithic domestication of the chicken. It was recently shown that the closest relative of P. falciparum is P. reichenowi, a malaria parasite isolated from a captive chimpanzee that had not been included in earlier studies. The close phylogenetic relationship between P. falciparum and P. reichenowi, their distinctness from the other human malaria parasites, and their remoteness from bird or lizard parasites was soon confirmed by other studies.

The zoonotic origin of P. falciparum elevates interest in the possible ongoing transmission of other malaria parasites of primate origin into the human population. The repeated emergence of human malaria parasites from zoonotic reservoirs raises the question of whether ongoing transmission of P. reichenowi from chimpanzees to humans may be possible (or vice versa). The fact that this transmission has not happened repeatedly may reflect the difficulty in changing the sialic acid binding specificity of the parasite-binding proteins. In this regard, it is interesting that a major barrier limiting cross-transmission of avian influenza into humans (and vice versa) is due to differences in sialic acid linkage binding specificity.

The origin of malignant malaria. 2009 PNAS USA August 3, 2009
Plasmodium falciparum, the causative agent of malignant malaria, is among the most severe human infectious diseases. The closest known relative of P. falciparum is a chimpanzee parasite, Plasmodium reichenowi, of which one single isolate was previously known. The co-speciation hypothesis suggests that both parasites evolved separately from a common ancestor over the last 5–7 million years, in parallel with the divergence of their hosts, the hominin and chimpanzee lineages. Genetic analysis of eight new isolates of P. reichenowi, from wild and wild-born captive chimpanzees in Cameroon and Cote d’Ivoire, shows that P. reichenowi is a geographically widespread and genetically diverse chimpanzee parasite. The genetic lineage comprising the totality of global P. falciparum is fully included within the much broader genetic diversity of P. reichenowi. This finding is inconsistent with the co-speciation hypothesis. Phylogenetic analysis indicates that all extant P. falciparum populations originated from P. reichenowi, likely by a single host transfer, which may have occurred as early as 2–3 million years ago, or as recently as 10,000 years ago. The evolutionary history of this relationship may be explained by two critical genetic mutations. First, inactivation of the CMAH gene in the human lineage rendered human ancestors unable to generate the sialic acid Neu5Gc from its precursor Neu5Ac, and likely made humans resistant to P. reichenowi. More recently, mutations in the dominant invasion receptor EBA 175 in the P. falciparum lineage provided the parasite with preference for the overabundant Neu5Ac precursor, accounting for its extreme human pathogenicity.

Related:

• Evolving protection against malaria
• Evolution-Proof Insecticides Against Malaria
• Malaria, mosquitoes and the legacy of Ronald Ross
• Nature Collections – Malaria

On Sunday BBC World Service emailed me to ask about the outbreak of pneumonic plague in China (latest news). Unfortunately, I didn’t get the email until today, but for BBC World Service (and everyone else), here are:

10 Things You Should Know About Pneumonic Plague

1. Plague is caused by the Gram-negative bacterium Yersinia pestis.
2. Most forms of plague, such as bubonic plague, are transmitted from the animal host (usually a rodent) by insect vectors such as fleas.
3. In bubonic plague, patients develop swollen, tender lymph glands (called buboes) and fever, headache, chills, and weakness. Bubonic plague does not spread from person to person.
4. Pneumonic plague is the least common but most dangerous and fatal form of the disease.
5. Pneumonic plague is transmitted directly from one person to another by aerosols.
6. Infected people usually get “flu-like” symptoms after an incubation period of 3 to 7 days, with fever, chills, head and body-aches, vomiting and nausea.
7. Yersinia pestis infections are relatively easily treated with antibiotics.
8. Peumonic plague is very virulent, so treatment needs to start early to prevent serious illness or death – within hours of symptoms starting.
9. Although you might think of plague is a disease of the middle ages, it hasn’t gone away – it still occurs in many countries in Africa, the former Soviet Union, the Americas, and Asia. Previous outbreaks of pneumonic plague have occurred in Africa, India, and elsewhere. African countries accounted for nearly 90% of the 28,530 plague cases reported to the World Health Organization from 1994-2003 (Bubonic and pneumonic plague – Uganda, 2006. MMWR 2009 58(28): 778-781).
10. A safe and effective pneumonic plague vaccine would prevent future outbreaks and thwart the use of Y. pestis as an agent of terror. Unfortunately, over 100 years of research have yet to generate a safe and effective pneumonic plague vaccine (Current challenges in the development of vaccines for pneumonic plague. Expert Rev Vaccines. 2008 7(2): 209-221).
11. Should I be worried about this outbreak?
    No, not particularly. This outbreak is in an isolated region and the Chinese authorities have taken appropriate steps to contain it. I would have been much more worried if it had occurred in a metropolitan region such as Beijing or Shanghai.

Related:

• How plague bacterium Yersinia pestis damages eukaryotic cells
• Plague: From the 14th to the 21st century and still going strong
• Ancient Plague
• Plague. Br Med Bull. 1998 54(3): 625-633
• Epidemiologic determinants for modeling pneumonic plague outbreaks. Emerg Infect Dis. 2004 10(4): 608-614
• Immune defense against pneumonic plague. Immunol Rev. 2008 225: 256-271

Viruses are major targets of the immune system. A variety of virus pathogen-associated molecular patterns (PAMPs), such as the high repetition of capsomers and/or peplomers on virion surface, the production of unique RNA replication intermediates and genome modifications, and others, are recognized as markers of viral invasion by responsive molecules on immune effector cells. The integration of stimuli delivered by different virus PAMPs leads to inflammation and immune activation which, in turn, are key components of both pathogenesis and recovery from viral infection.

Dendritic cells (DCs) possess properties and abilities enabling them to act as unique immune “live adjuvants”. Like no other antigen-presenting cell, they can perform multiple immunogenic tasks, including i) priming of naive T cells by the expression of special costimulatory surface molecules; ii) cross-presentation, that is, presentation of exogenous antigens in the context of MHC class I molecules to CD8+ T lymphocytes, in addition to presentation of MHC class II-restricted peptides; and iii) polarizing naive T cells to various Th phenotypes. DC activity is normally triggered by pathogens via a variety of receptor molecules and includes the release of distinct interleukins (ILs) directed at regulating T cell differentiation.

Influence of Dendritic Cells on Viral Pathogenicity. 2009 PLoS Pathog 5(7): e1000384 doi:10.1371/journal.ppat.1000384
Although most viral infections cause minor, if any, symptoms, a certain number result in serious illness. Viral disease symptoms result both from direct viral replication within host cells and from indirect immunopathological consequences. Dendritic cells (DCs) are key determinants of viral disease outcome; they activate immune responses during viral infection and direct T cells toward distinct T helper type responses. Certain viruses are able to skew cytokine secretion by DCs inducing and/or downregulating the immune system with the aim of facilitating and prolonging release of progeny. Thus, the interaction of DCs with viruses most often results in the absence of disease or complete recovery when natural functions of DCs prevail, but may lead to chronic illness or death when these functions are outmanoeuvred by viruses in the exploitation of DCs.

Related:

• Toll-Like Receptors