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A personal view on Gangrene.
I might as well wrap up these Wiki posts with personal experiences!
First of all, no one really emphasizes the smell Gangrene has. It is terrible. My Grandmother had told me that she had some "sores" on her feet after dropping something heavy on her toes, but she didn't want to take her band 🤬 off to show me. A week later she did show me (at that point she had ace bandages on)...and I was not prepared for the black necrosis of her skin or the fact that there were larvae infested in it. Or the smells that it produced. Since she had waited so long to go to the doctor, the Gangrene in both of her legs had progressed so terribly that she ended up having to have both of her legs amputated. The progression of her wounds, to necrosis from dropping something on her feet, to the double amputation was bind blowing. From start to finish it was about a 4-5 week ordeal. At first she refused to believe that she needed her legs to be amputated but then she started going into septic shock and she nearly died before she agreed to it.

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A personal view on Lyme's disease.
5 years ago my friend, who lives in Maine, thought she had the flu. She was one of those people who never went to the hospital but after a month of feeling under the weather she finally went in. It seemed like as soon as she was diagnosed her signs and symptoms just continued to get worse and worse. She lost a lot of her hair (which doesn't typically happen) but ultimately, and what she still struggles with the most is the arthritis (that continues to get worse). After watching everything she's been though, I feel like there isn't enough publicity on the dangers of contracting Lyme disease, especially in the states where ticks are looking to hitch a ride to get some lunch while you're just walking through the grass to mailbox. This article highlights the dangers of Lyme disease and brings attention to the fact that it is a serious and rapidly growing issue.

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Abstract

Since its identification nearly 30 years ago, Lyme disease has continued to spread, and there have been increasing numbers of cases in the northeastern and north central US. The Lyme disease agent, Borrelia burgdorferi, causes infection by migration through tissues, adhesion to host cells, and evasion of immune clearance. Both innate and adaptive immune responses, especially macrophage- and antibody-mediated killing, are required for optimal control of the infection and spirochetal eradication. Ecological conditions favorable to the disease, and the challenge of prevention, predict that Lyme disease will be a continuing public health concern.

In the late 20th century, Lyme disease, or Lyme borreliosis, was recognized as an important emerging infection ( 1). It is now the most commonly reported arthropod-borne illness in the US and Europe and is also found in Asia ( 2). Since surveillance for Lyme disease was begun in the US by the Centers for Disease Control and Prevention, the number of reported cases has increased steadily, and in the year 2000, more than 18,000 cases were reported ( 3).

Lyme disease was recognized as a separate entity in 1976 because of geographic clustering of children in the Lyme, Connecticut, area who were thought to have juvenile rheumatoid arthritis (4, S1 ). It then became apparent that Lyme arthritis was a late manifestation of an apparently tick-transmitted, multisystem disease, of which some manifestations had been recognized previously in Europe and America (S2-S6 ). In 1981, Burgdorfer and colleagues discovered a previously unidentified spirochetal bacterium, called Borrelia burgdorferi, in a nymphal Ixodes scapularis (also called Ixodes dammini) tick (S7 ). This spirochete was then cultured from patients with early Lyme disease, and patients' immune responses were linked conclusively with that organism, proving the spirochetal etiology of the infection (S8, S9).

Based on genotyping of isolates from ticks, animals, and humans, the formerly designated B. burgdorferi has now been subdivided into multiple Borrelia species, including three that cause human infection. In the US, the sole cause is B. burgdorferi (S10 ). Although all three species are found in Europe, most of the disease there is due to Borrelia afzelii or Borrelia garinii, and only these two species seem to be responsible for the illness in Asia (S11, S12 ). During the 20th century, conditions evolved in the northeastern US that were especially favorable for enzootic B. burgdorferi infection ( 5). In this setting, Lyme disease continues to flourish and spread.

Biology of B. burgdorferi

The agents of Lyme borreliosis belong to the eubacterial phylum of spirochetes, which are vigorously motile, corkscrew-shaped bacteria (Figure ). The spirochetal cell wall consists of a cytoplasmic membrane surrounded by peptidoglycan and flagella and then by a loosely associated outer membrane. The B. burgdorferi (strain B31) genome has been completely sequenced. It has a small linear chromosome that is just under one megabase ( 6), and nine circular and 12 linear plasmids that constitute 40% of its DNA ( 7). Some of these plasmids are indispensable and could be thought of as mini-chromosomes. Although it has been difficult to manipulate the B. burgdorferi genome, progress has recently been made using modified selectable markers and shuttle vectors ( 8, S13-S18 ).

The most remarkable aspect of the B. burgdorferi genome is the large number of sequences encoding predicted or known lipoproteins, including outer-surface proteins (Osp's) A through F ( 6). Lipoproteins are found in the outer leaflet of the cytoplasmic membrane, and in both the inner and the outer leaflets of the outer membrane. Some of these proteins are differentially expressed, and one surface-exposed lipoprotein, called VlsE, undergoes extensive antigenic variation ( 9). In contrast, the genome encodes very few proteins with recognizable biosynthetic activity, and therefore, the organism depends on the host for most of its nutritional requirements. A very unusual feature of B. burgdorferi is that it does not require iron, at least for growth in vitro ( 10). This may allow the spirochete to circumvent the usual host defense of limiting the availability of iron. Finally, the B. burgdorferi genome encodes no recognizable toxins. Instead, this extracellular pathogen causes infection by migration through tissues, adhesion to host cells, and evasion of immune clearance.

Enzootic cycles of B. burgdorferi infection

The genus Borrelia currently includes three pathogenic species that cause Lyme borreliosis (S10-S12 ) and eight closely related species that rarely if ever cause human infection (S19-S25 ). These spirochetes live in nature in enzootic cycles involving ticks of the Ixodes ricinus complex (also called the Ixodes persulcatus complex) and a wide range of animal hosts (Table ) ( 11). These enzootic cycles have evolved somewhat differently in different locations (S26 ). The important vectors of the three pathogenic species of human Lyme borreliosis are the deer tick, I. scapularis, in the northeastern and north central US; Ixodes pacificus in the western US; the sheep tick, I. ricinus, in Europe; and the taiga tick, I. persulcatus, in Asia.

Table 1

In the northeastern US from Maine to Maryland and in the north central states of Wisconsin and Minnesota, a highly efficient, horizontal cycle of B. burgdorferi transmission occurs among larval and nymphal I. scapularis ticks and certain rodents, particularly white-footed mice and chipmunks ( 12, S27 ). This cycle results in high rates of infection among rodents and nymphal ticks and many new cases of human Lyme disease during the late spring and early summer months (Figure ). White-tailed deer, which are not involved in the life cycle of the spirochete, are the preferred host of adult I. scapularis, and they seem to be critical for the survival of the ticks (S28 ).

The vector ecology of B. burgdorferi is quite different on the West Coast in northern California, where the frequency of Lyme disease is low. There, two intersecting cycles are necessary for disease transmission, one involving the dusky-footed wood rat and Ixodes spinipalpis (also called Ixodes neotomae) ticks, which do not bite humans and which maintain the cycle in nature, and the other involving wood rats and I. pacificus ticks, which are less often infected but do bite humans (S29 ). Similarly, in Colorado, wood rats and I. spinipalpis ticks may be infected with Borrelia bissettii, one of the nonpathogenic species, in a cycle that is not known to cause human infection ( 13). In the southeastern US, nymphal I. scapularis feed primarily on lizards, which are resistant to B. burgdorferi infection because of complement-mediated killing of the spirochete ( 14). Therefore, Lyme disease is rare in that part of the country.

In Europe, there is still debate about the preferred animal hosts of I. ricinus. These ticks feed on more than 300 animal species, including large and small mammals, birds, and reptiles ( 15). In Asia, immature I. persulcatus commonly feed on voles, shrews, and birds, and adult ticks feed on virtually all larger animals, including hares, deer, and cattle ( 16). Because the Borrelia species differ in their resistance to complement-mediated killing, small rodents are important reservoirs for B. afzelii, B. bissettii, and Borrelia japonica, whereas birds are strongly associated with B. garinii, Borrelia valaisiana, and Borrelia turdi ( 17).

Emergence of human Lyme borreliosis

The earliest known American cases of Lyme disease occurred in Cape Cod in the 1960s (S30 ). However, B. burgdorferi DNA has been identified by PCR in museum specimens of ticks and mice from Long Island dating from the late 19th and early 20th centuries (S31 ), and the infection has probably been present in North America for millennia ( 2). During the European colonization of North America, woodland in New England was cleared for farming, and deer were hunted almost to extinction ( 5). However, during the 20th century, conditions improved in the northeastern US for the ecology of Lyme disease. As farmland reverted to woodland, deer proliferated, white-footed mice were plentiful, and the deer tick thrived. Soil moisture and land cover, as found near rivers and along the coast, were favorable for tick survival ( 18). Finally, these areas became heavily populated with both humans and deer, as more rural wooded areas became wooded suburbs in which deer were without predators and hunting was prohibited.

During the past 40 years, the infection has continued to spread in the northeastern US ( 19); it has caused focal outbreaks in some coastal areas (S30, S32, S33 ), and it now affects suburban locations near Boston, New York, Philadelphia, and Baltimore, the most heavily populated parts of the country (S34 ). In the year 2000, the overall incidence of reported cases in Connecticut, the state with the highest reported frequency of Lyme disease, was 111 per 100,000 residents ( 3). However, most of the cases still clustered in foci, particularly in two counties in the southeastern part of the state where the original epidemiologic investigation took place in the town of Lyme (S1 ). In a large, two-year vaccine trial, such high-risk areas had a yearly incidence of the disease of greater than 1 per 100 participants, and the frequency of seropositivity to B. burgdorferi at study entry was as high as 5 per 100 participants ( 20).

As in America, the European agents of Lyme borreliosis have probably been present there for many thousands of years. They are now known to be widely established in Europe's remaining forested areas ( 15). The highest reported frequencies of the disease are in middle Europe, particularly in Germany, Austria, Slovenia, and Sweden ( 2). In 1995, the yearly incidence of the disease in Slovenia and Austria was estimated to be 120-130 cases per 100,000 residents ( 2), similar to the frequency in Connecticut.

Clinical manifestations and disease pathogenesis

To maintain its complex enzootic cycle, B. burgdorferi must adapt to markedly different environments, the tick and the mammalian or avian host. The spirochete survives in a dormant state in the nymphal tick midgut during the fall, winter, and early spring, where it expresses primarily OspA ( 21). When the tick feeds in the late spring or early summer, the expression of a number of spirochetal proteins is altered (S35 ). For example, OspA is downregulated, and OspC is upregulated ( 21). OspC expression is required for infection of the mammalian host ( 22, 23). In addition, the spirochete binds mammalian plasminogen and its activators, present in the blood meal, which facilitates spreading of the organism within the tick ( 24). Within the salivary gland, OspC expression predominates, but some organisms express only OspE and OspF; OspA and OspB are absent ( 25).

After transmission of the spirochete, human Lyme disease generally occurs in stages, with remissions and exacerbations and different clinical manifestations at each stage ( 4). Early infection consists of stage 1, localized infection of the skin, followed within days or weeks by stage 2, disseminated infection, and months to years later by stage 3, persistent infection. However, the infection is variable; some patients have only localized infection of the skin, while others have only later manifestations of the illness, such as arthritis. Moreover, there are regional variations, primarily between the illness found in America and that found in Europe and Asia ( 1).

Localized infection

After an incubation period of 3-32 days, a slowly expanding skin lesion, called erythema migrans (EM), forms at the site of the tick bite in 70-80% of cases ( 26, 27). In the US, the skin lesion is frequently accompanied by flu-like symptoms, such as malaise and fatigue, headache, arthralgias, myalgias, and fever, and by signs that suggest dissemination of the spirochete ( 28). In about 18% of cases ( 27), these symptoms are the presenting manifestation of the illness ( 29). In contrast, EM in Europe is more often an indolent, localized infection, and spirochetal dissemination is less common ( 30).

In addition to the Lyme disease agent, I. scapularis ticks in the US and I. ricinus ticks in Europe may transmit Babesia microti (a red-blood-cell parasite) or Anaplasma phagocytophilum (formerly referred to as "the agent of human granulocytic ehrlichiosis") ( 31- 33). In a recent prospective study in the US, 4% of patients with culture-proven EM had coinfection with one of these other two tick-borne agents ( 34). Although these two infections are usually asymptomatic, coinfection may lead to more severe, acute flu-like illness ( 35).

In most patients, immune cells first encounter B. burgdorferi at the site of the tick bite. Depending on the Borrelia species and the host, complement-mediated lysis of the organism may be the first line of host defense (Figure ) ( 36). On histologic examination, the resulting EM skin lesions consist of mild to marked perivascular infiltrates of lymphocytes, DCs, macrophages, and small numbers of plasma cells ( 37). As a part of the innate immune response, macrophages engulf and kill spirochetes ( 38- 41). Inflammatory cells within the lesion produce primarily proinflammatory cytokines, including TNF-α and IFN-γ ( 37, 42). B. burgdorferi-stimulated PBMCs from patients with EM produce Th1 proinflammatory cytokines, especially IFN-γ ( 43). Within days after disease onset, most patients have an IgM antibody response to OspC or the 41-kDa flagellar protein of the spirochete ( 44). Thus, both innate and adaptive cellular elements are mobilized to fight the infection.

Disseminated infection

Within days to weeks after disease onset, B. burgdorferi often disseminates widely. During this period, the spirochete has been recovered from blood and cerebrospinal fluid (S7, S36, S37 ), and it has been seen in small numbers in specimens of myocardium, retina, muscle, bone, spleen, liver, meninges, and brain ( 45). Possible clinical manifestations include secondary annular skin lesions, acute lymphocytic meningitis, cranial neuropathy, radiculoneuritis, atrioventricular nodal block, migratory musculoskeletal pain in joints, bursae, tendon, muscle, or bone, and, rarely, eye manifestations (reviewed in ref. 4). Less often, spirochetal dissemination is asymptomatic.

To disseminate, B. burgdorferi binds certain host proteins and adheres to integrins, proteoglycans, or glycoproteins on host cells or tissue matrices. As in the tick, spreading of the spirochete through tissue matrices may be facilitated by the binding of plasminogen and its activators to the surface of the organism ( 24). A 47-kDa spirochetal protein (BBK32) binds fibronectin, an ECM protein ( 46). The sequences of OspC vary considerably among strains, and only a few sequences are associated with disseminated infection ( 47), probably because they bind as-yet unidentified host structures. A 66-kDa outer-surface protein of the spirochete binds the fibrinogen receptor (α IIbβ ₃) and the vitronectin receptor (α vβ ₃) ( 48), which may allow the organism to establish an initial foothold and disseminate in the vasculature. A 26-kDa Borrelia glycosaminoglycan-binding (GAG-binding) protein, Bgp, binds to the GAG side chains of heparan sulfate on endothelial cells, and to both heparan sulfate and dermatan sulfate on neuronal cells ( 49, 50). Finally, spirochetal decorin-binding proteins A and B (DbpA and DbpB) bind decorin, a proteoglycan that associates with collagen ( 51). This may explain the alignment of spirochetes with collagen fibrils in the ECM of the heart, nervous system, or joints ( 45).

Despite an active immune response, B. burgdorferi may survive during dissemination by changing or minimizing antigenic expression of surface proteins and by inhibiting certain critical host immune responses. Two linear plasmids (lp's) seem to be essential, including lp25, which encodes a nicotinamidase ( 52), and lp28-1, which encodes the VlsE lipoprotein ( 53), the protein that undergoes antigenic variation. In addition, the spirochete has a number of families of highly homologous, differentially expressed lipoproteins, including the OspE/F paralogs, which further contribute to antigenic diversity ( 54). B. burgdorferi may downregulate lipoproteins because of host immune pressure ( 54, 55). For example, in a mouse model, the development of antibody to OspC, a prominent early response, induces downregulation of OspC; and therefore, this antibody response does not completely clear the infection ( 56). Finally, B. afzelii and, to a lesser degree, B. burgdorferi have complement regulator-acquiring surface proteins that bind complement factor H and factor H-like protein 1 ( 57). These complement factors inactivate C3b, which protects the organism from complement-mediated killing ( 57, S38-S41 ). In contrast, B. garinii is efficiently killed by complement (S42 ).

As shown definitively in mouse models, both innate and adaptive immune responses are required for optimal control of disseminated infection (Figure ). B. burgdorferi lipoproteins, which are B cell mitogens (S39 ), stimulate adaptive T cell-independent B cell responses ( 58, S43, S44 ). For example, antibody responses to OspC kill spirochetes ( 59). In addition, humoral immune responses to nonlipidated spirochetal proteins, which are more likely to be T cell-dependent, aid in spirochetal killing ( 60, 61). The primary role of B. burgdorferi-specific Th1 cells is to prime these T cell-dependent B cell responses ( 62). The combination of these responses leads to the production of antibodies against many components of the organism ( 63, 64), which promote spirochetal killing by complement fixation and opsonization (S45 ). Within several weeks to months, these antibody responses, in conjunction with innate immune mechanisms, control widely disseminated infection even without antibiotic treatment, and generalized symptoms resolve.

Persistent infection

After weeks of disseminated infection, the Lyme disease agents may still survive in localized niches for several years. By this time, systemic symptoms are minimal or absent altogether. Although each of the three pathogenic species may spread to the joints, nervous system, or other skin sites, they seem to vary in the frequency of dissemination to these sites and in their ability to persist there. B. burgdorferi, the sole cause of the infection in the US, seems to be the most arthritogenic. Months after the onset of illness, about 60% of untreated patients with this infection experience intermittent attacks of arthritis, primarily of the large joints, especially the knee ( 65).

As shown in a mouse model, neutrophil extravasation into the infected joint is a key initial step in the development of joint inflammation ( 66). In the human infection, CD4+ Th cells are of the proinflammatory Th1 subset (S46, S47 ), and B. burgdorferi-specific CD8+ T cells are found as well (S48 ). Within the joint, B. burgdorferi-specific γδ T cells may aid in the regulation of these inflammatory responses (S49, S50 ). Compared with other inbred strains of mice, C57BL/6 mice are protected from severe arthritis by IL-6 and IL-10, despite large numbers of spirochetes in the joint ( 67, 68). It is unknown, however, whether certain human patients control joint inflammation in this way. Patients with Lyme arthritis have very high antibody responses to many spirochetal proteins, suggestive of hyperimmunization due to recurrent waves of spirochetal growth ( 63, 64). Even without antibiotic treatment, the number of patients who continue to have attacks of arthritis decreases by about 10-20% each year, and few patients have had attacks for longer than 5 years ( 65). Thus, these immune mechanisms seem to succeed eventually in eradicating B. burgdorferi from the joint.

In Europe and Asia, B. afzelii may persist in the skin for decades, resulting in acrodermatitis chronica atrophicans, a skin condition that occurs primarily on sun-exposed surfaces of distal extremities in elderly women (S51 ). Compared with EM lesions, infiltrates of T cells and macrophages in acrodermatitis lesions had a restricted cytokine profile, lacking IFN-γ production ( 37). Consistent with this finding, ultraviolet B irradiation of B. burgdorferi-infected C3H mice decreased the Th1 response ( 69). Thus, spirochetal persistence in acrodermatitis skin lesions may involve both spirochetal factors and an ineffective local immune response.

B. garinii, which is also found only in Europe and Asia, appears to be the most neurotropic of the three Borrelia species. It may cause an exceptionally wide range of neurologic abnormalities ( 70), including borrelial encephalomyelitis (S52 ), a multiple sclerosis-like illness. In the US, a rare, late neurologic syndrome has been described, called Lyme encephalopathy or polyneuropathy, which is manifested primarily by subtle cognitive disturbances, spinal radicular pain, or distal paresthesias ( 71, S53 ). With each of these three late neurologic complications, the possible duration of spirochetal persistence and the pathogenetic mechanisms are unknown.

Putative postinfectious syndromes

Treatment-resistant Lyme arthritis.

About 10% of patients with Lyme arthritis have persistent joint inflammation for months or even several years after standard courses of antibiotic treatment ( 72), a complication rarely noted in Europe (S54 ). Although B. burgdorferi DNA can often be detected by PCR in the joint fluid of these patients prior to antibiotic treatment ( 73, S55 ), PCR results are usually negative after antibiotic treatment ( 73), suggesting that joint swelling may persist after complete or nearly complete eradication of the spirochete from the joint with antibiotic therapy.

To explain this course, it has been hypothesized that these patients may have persistent infection or infection-induced autoimmunity ( 74). In support of the persistent-infection hypothesis, ex vivo-infected synovial cells contained B. burgdorferi in the cytosol ( 75), a site that might be protected from antibiotics. However, spirochetes have not been seen in intracellular locations in situ in human or mouse synovia ( 45). Moreover, PCR results for B. burgdorferi DNA were negative in synovial tissue in all 26 patients with treatment-resistant arthritis who underwent arthroscopic synovectomy a median of 7 months after the completion of antibiotic therapy ( 76). This methodology may be insufficient to identify rare spirochetes and would not detect retained spirochetal antigens.

In support of the autoimmunity hypothesis, treatment-resistant Lyme arthritis is associated with HLA-DRB1*0401, 0101, and other related alleles ( 77), and with cellular and humoral immune responses to OspA of B. burgdorferi ( 78, S56-S58 ). In an epitope-mapping study, 15 of 16 treatment-resistant patients had T cell reactivity with the OspA ₁₆₅₋₁₇₃ epitope, the immunodominant epitope presented by the DRB1*0401 or 0101 molecule, compared with only one of five treatment-responsive patients ( 78). One homolog of this epitope, human lymphocyte function-associated antigen 1α L332-340 (LFA-1α L332-340), acted as a weak, partial agonist for OspA ₁₆₅₋₁₇₃-reactive T cells in DRB1*0401-positive patients ( 79, 80), but the LFA-1 peptide did not bind the 0101 molecule ( 77), which suggests that the LFA-1 peptide is unlikely to be a relevant autoantigen. Although the pathogenesis of this syndrome is incompletely delineated, future technologies may allow the identification of spirochetal components or a relevant autoantigen, or both, in the synovia of these patients.

Post-Lyme disease syndrome.

A small percentage of patients with well-documented Lyme disease may develop disabling musculoskeletal pain, neurocognitive symptoms, or fatigue along with or soon after symptoms of the infection (S59-S62 ). This post-Lyme disease syndrome, or chronic Lyme disease (the terms are used interchangeably), which is similar to chronic fatigue syndrome or fibromyalgia, persists for months or years after standard antibiotic treatment of the infection. In a study of such patients who then received intravenous ceftriaxone for 30 days followed by oral doxycycline for 60 days, or intravenous or oral placebo preparations for the same duration, no significant differences were found between the groups in the percentage of patients who said that their symptoms had improved, gotten worse, or stayed the same ( 81). Therefore, it is hypothesized that B. burgdorferi may trigger immunologic or neurohormonal processes in the brain that cause persistent pain, neurocognitive, or fatigue symptoms, despite spirochetal killing with antibiotic therapy ( 82). Among B. burgdorferi-infected patients, a prior history of depression or anxiety seems to be a risk factor for the development of chronic Lyme disease ( 83).

A counterculture has emerged regarding chronic Lyme disease ( 84). In contrast with the findings of evidence-based medicine, some people believe that the tests for Lyme disease are often inaccurately negative, and that antibiotic therapy is necessary for months or years to suppress the symptoms of this often incurable illness. A number of investigators at academic medical centers have reported series of patients referred for chronic Lyme disease in which the majority of patients had pain or fatigue syndromes with little or no evidence of past or present B. burgdorferi infection ( 85- 87). Prolonged antibiotic therapy may be harmful. In studies of patients with unsubstantiated Lyme disease, minor side effects were common ( 86), prolonged ceftriaxone therapy sometimes resulted in biliary complications ( 88), and in one reported case, the prolonged administration of cefotaxime resulted in death ( 89). Furthermore, prolonged use of antibiotics was recently associated with an increased risk of breast cancer ( 90). Although antibiotic use may not be causally related to cancer, this observation reinforces the advisability of prudent use of antibiotics.

Diagnosis and treatment

Algorithms for the diagnosis and treatment of early or late Lyme disease are presented in Figures and . Except in those with active EM, the diagnosis is usually based on the recognition of a characteristic clinical picture (S63 ) and a positive antibody response to B. burgdorferi by whole-cell sonicate ELISA and Western blot, interpreted according to the criteria of the Centers for Disease Control and Prevention (S64 ). Evidence-based treatment recommendations are incorporated from those presented by the Infectious Disease Society of America ( 91).

Every summer, the lay public and physicians in endemic areas deal with the early events surrounding Lyme disease, including tick bites, early infection, and coinfection (Figure ). Since 24-72 hours of tick attachment is necessary before transmission of the spirochete occurs, removal of the tick within 24 hours of attachment is usually sufficient to prevent Lyme disease ( 54, S65, S66 ). If an engorged nymphal I. scapularis tick is found, a single, 200-mg dose of doxycycline usually prevents the infection ( 92). Serologic tests are insensitive during the first 1 or 2 weeks of infection and depend largely on detection of a positive IgM response, which may still represent a false-positive response ( 63, S67 ). Because of these limitations, treatment is recommended for 10 to 20 days, without serologic testing, for presumed EM, most commonly with doxycycline in adults or amoxicillin in children ( 93, S68 ). If serologic testing is done, both acute and convalescent samples should be obtained, since most patients have a positive IgM or IgG response by convalescence at the conclusion of antibiotic treatment, and the demonstration of seroconversion provides better serologic support for the diagnosis. Reinfection may occur in patients who are treated with antibiotics early in the illness ( 94).

Flu-like illness during summer is a more difficult issue, since most cases are not caused by B. burgdorferi infection. However, if a patient from a highly endemic area has a febrile illness with headache and joint or muscle pain, without respiratory or gastrointestinal symptoms, in the weeks surrounding the summer solstice, antibiotic treatment may be indicated (Figure ). For such patients, a second-generation serologic test, an IgG ELISA that uses a peptide in the sixth invariant region of the VlsE lipoprotein of B. burgdorferi, may be valuable, since this test typically becomes positive before five IgG bands are present on Western blot ( 29, 95). Although both babesiosis and anaplasmosis are usually asymptomatic, coinfection should be considered in a patient with more severe flu-like symptoms, including high fever, particularly if the patient is very young or old or asplenic (Figure ). Fortunately, Lyme disease and anaplasmosis can both be treated with doxycycline. For severe cases of babesiosis, intravenous clindamycin and oral quinine, or oral atovaquone and azithromycin, may be effective (S69 ).

By the time that organ-system involvement is present in Lyme disease, which is at least several weeks after the onset of infection, almost all patients have a positive IgG response to B. burgdorferi ( 63) (Figure ). Objective neurologic abnormalities require treatment with intravenous antibiotic therapy, usually intravenous ceftriaxone (S70 ), with the possible exception of facial palsy alone, without other neurologic manifestations. Lyme arthritis may be treated with either oral or intravenous therapy ( 72, S70 ), but oral therapy is easier to administer, is associated with fewer side effects, and is considerably less expensive (S71 ). Reinfection has not been reported in patients with the expanded immune response associated with Lyme arthritis.

After antibiotic treatment, antibody titers fall slowly, but IgG and even IgM responses may persist for years ( 96), as may the IgG response to the VlsE peptide ( 97). Moreover, asymptomatic IgG seroconversion to B. burgdorferi occurs in about 7% of patients in the US ( 98). If patients with asymptomatic seroconversion or past infection have symptoms caused by another illness, the danger is to attribute them incorrectly to Lyme disease, and therefore, the clinical picture must always be considered with the serologic result.

If patients with Lyme arthritis have persistent joint inflammation after 2 months of oral antibiotics or 1 month of intravenous antibiotics and the results of PCR testing are negative, we treat them with nonsteroidal anti-inflammatory agents, disease-modifying antirheumatic drugs, or arthroscopic synovectomy. In those with post-Lyme disease syndrome, we follow the guidelines for treating chronic fatigue syndrome or fibromyalgia ( 82).

Prevention

Ecological conditions favorable to Lyme disease, the steady increase in the number of cases, and the challenge of prevention predict that the infection will be a continuing public health concern. Personal protection measures, including protective clothing, repellents or acaricides, tick checks, and landscape modifications in or near residential areas, may be helpful ( 99). However, these measures are difficult to perform regularly throughout the summer. Attempts to control the infection on a larger scale by the eradication of deer or widespread use of acaricides, which may be effective, have had limited public acceptance ( 99). New methods of tick control, including host-targeted acaricides against rodents and deer, are being developed and may provide help in the future.

In the 1990s, recombinant OspA vaccines were developed and shown to be safe and effective for the prevention of Lyme disease in the US ( 20, S72, S73 ). Although one of the vaccines was licensed commercially, its acceptance by the public and by physicians was also limited, and it was withdrawn by the manufacturer in 2002 ( 100). Some of the reasons why its acceptance was limited included the low risk of Lyme disease in most parts of the country, the need for booster injections every year or every other year, and the relatively high cost of this preventive approach compared with antibiotic treatment of early infection (S74, S75 ). In addition, there was a theoretical, though never proven, concern that in rare cases, vaccination might trigger autoimmune arthritis.

For now, control of Lyme disease depends primarily on public and physician education about personal protection measures, signs and symptoms of the disease, and appropriate antibiotic therapy ( 99). However, if the risk of the infection continues to increase or if public perceptions change, vaccine development may again become a priority. Experience gained in the last ten years has proven the feasibility of vaccination for the prevention of this complex, tick-transmitted infection.

Acknowledgments

This work was supported in part by a grant from the NIH (AR20358), a Centers for Disease Control and Prevention Cooperative Agreement (CCU110291), the English, Bonter, Mitchell Foundation, the Lyme/Arthritis Research Fund, and the Eshe Fund.

Due to space constraints, a number of important references could not be included in this article. Interested readers can find a supplementary reading list at http://www.jci.org/cgi/content/full/113/8/1093/DC1.

Footnotes

Nonstandard abbreviations used: outer-surface protein (Osp); erythema migrans (EM); linear plasmid (lp); lymphocyte function-associated antigen 1 (LFA-1).

Conflict of interest: The authors have declared that no conflict of interest exists.

References

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Since its identification nearly 30 years ago, Lyme disease has continued to spread, and there have been increasing numbers of cases in the northeastern and north central US. The Lyme disease agent, Borrelia burgdorferi, causes infection by migration through ...

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Stopping the progression of periodontal disease

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Stopping the progression of periodontal disease

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In chapter 25 we discussed microbial diseases of the digestive system including infection of the gums, or gingivitis. This article discusses in more detail the causative organisms of gingivitis as well as how the disease progresses and how to prevent it.https://www.ncbi.nlm.nih.gov/books/NBK8259/

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A new facility located in a congested community with high tuberculosis rates brings basic science and cutting edge techniques into the heart of disease circulation.

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A new facility located in a congested community with high tuberculosis rates brings basic science and cutting edge techniques into the heart of disease circulation.

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In Masiphumelele, an informal settlement of tin shacks, squat brick buildings, and narrow lanes south of Cape Town, 23,000 people go to school, run businesses, sleep, and socialize cheek by jowl. As a result, communicable diseases are rife—especially tuberculosis (TB), which infects around 80 percent of residents by the time they reach adulthood.

A new research facility opened here this month aims to curb TB by studying how it is transmitted in the local community. The R10 million ($700,000 USD) Aerobiology TB Research Facility will allow microbiologists from the University of Cape Town (UCT) to study Mycobacterium tuberculosis captured from the exhaled air of local TB patients.

It will do so using locally developed technology. On the ground floor of the two-story building, TB patients will enter into a “clean box” about the size of a phone booth and spend some time in there. The air in the box—about 300 liters—will be vacuumed up and run through sterile water, locking any particulate matter including bacteria in a 5-milliliter tube. Scientists will then scour the samples for TB bugs.

For now, it’s not the easiest or cheapest way to identify TB infection. But in time, the scientists hope to scale it up into a high-throughput diagnostic tool to help identify so-called “super-spreaders” in the community. They also want to identify the locations in the community where TB is spread, which would help target TB prevention services. “We want to find everyone who is transmitting in the neighborhood,” says Robin Wood, director of UCT’s Desmond Tutu HIV Centre and one of the brains behind the new site.

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In Masiphumelele, an informal settlement of tin shacks, squat brick buildings, and narrow lanes south of Cape Town, 23,000 people go to school, run businesses, sleep, and socialize cheek by jowl. As a result, communicable diseases are rife-especially tuberculosis (TB), which infects around 80 percent of residents by the time they reach adulthood.

A new research facility opened here this month aims to curb TB by studying how it is transmitted in the local community. The R10 million ($700,000 USD) Aerobiology TB Research Facility will allow microbiologists from the University of Cape Town (UCT) to study Mycobacterium tuberculosis captured from the exhaled air of local TB patients.

It will do so using locally developed technology. On the ground floor of the two-story building, TB patients will enter into a "clean box" about the size of a phone booth and spend some time in there. The air in the box-about 300 liters-will be vacuumed up and run through sterile water, locking any particulate matter including bacteria in a 5-milliliter tube. Scientists will then scour the samples for TB bugs.

For now, it's not the easiest or cheapest way to identify TB infection. But in time, the scientists hope to scale it up into a high-throughput diagnostic tool to help identify so-called "super-spreaders" in the community. They also want to identify the locations in the community where TB is spread, which would help target TB prevention services. "We want to find everyone who is transmitting in the neighborhood," says Robin Wood, director of UCT's Desmond Tutu HIV Centre and one of the brains behind the new site.

As basic scientists we don't do a lot of social research, we don't understand the social factors. But when you bring all of it together in one place, it becomes really powerful.

Spotting super-spreaders will be easier said than done. To do that, the technology will have to be able to screen dozens of patients per day in Masiphumelele alone, returning findings quickly and without inconveniencing patients. This will require advanced automation of the sample processing, whereas microscopists currently have to inspect thousands of nanowells one-by-one to detect bugs in one sample. Research is also needed into whether the amount of TB a person exudes determines how infectious he or she is, or whether it's specific strains of TB that drive infection.

Further afield, the challenge will be multiplied thousandfold. The city of Cape Town has more individuals living with TB than the United States, the United Kingdom, Germany, and France put together, Wood says, and the bacterium infects twice as many people in Cape Town as it did 100 years ago. Childhood infection rates are particularly high. By the age of five, 20 percent of children in Masiphumelele are infected with TB, and by the time they have reached high school that proportion rises to 50 percent.

Infection rates are so high here partly because HIV has rendered millions of South Africans susceptible to TB. But Wood thinks HIV alone doesn't explain the elevated infection rates in places like Masiphumelele. Rather, he thinks there is a large reservoir of infected individuals who aren't reached by treatment programs, which focus on active disease. "You'll never stop the disease unless you stop people getting it," he says.

This is where the clean-room sampling technology comes in. Unlike TB tests where patients are asked to cough, samples from the clean box are passive-patients may cough if they need to (and these are documented), but they are not prompted to. This will allow the scientists to determine whether coughing transmits TB better than just breathing the same air as somebody who is infected.

The technology is still in its infancy, and for the next few years, microbiologists from UCT plan to perfect the clean box collecting mechanism. Digby Warner from UCT's Institute of Infectious Disease and Molecular Medicine who leads the microbiology work says it's exhilarating to work on TB obtained from patients. Working on lab strains is "like seeing lions in the zoo," he says. But studying TB from people infected naturally is "like seeing the organism in the wild."

For others on the team, the center's location provides a welcome human connection with the disease they study. Anastasia Koch, who will study the genomic fingerprints of M. tuberculosis extracted from the samples, says she knows of no other location in the world where such high-tech equipment is located in such close proximity to the affected community. "That changes the way you think about the research," she says. "As you drive into 'Masi' you think about how transmission happens socially. As basic scientists we don't do a lot of social research, we don't understand the social factors. But when you bring all of it together in one place, it becomes really powerful."

The next step for the microbiology team is to ensure that what they are seeing in the samples is, in fact, M. tuberculosis. To do that, they have to isolate single cells and study them-something the team hasn't been able to do just yet. "We have a lot of circumstantial evidence that what we're seeing in our slides is TB. It looks like TB, we can culture TB from it, and it stains like TB," Warner says. But there's a lot of "gunk" in the slides, including other bacteria, he says, and it's vital for the sake of future automation that the TB identification is above reproach. "The challenge over the next few years is to get to a point where we can capture the organism off the slide, and either grow it up in culture or get a lipid or protein signal to confirm that what we have seen is definitely TB."

For this next stage, Warner and his colleagues are teaming up with colleagues at MIT and Imperial College London. They will use a new fluorescent probe developed by MIT to see if it is better at selectively labeling M. tuberculosis than the TB-highlighting probe the Cape Town team currently uses, called DMN-trehalose, and work on ways to extract the highlighted bacteria from the samples for further analysis.

But Wood's method of studying transmission is not without its detractors. Not all TB particles detected in exhaled air are able to cause infection, says Edward Nardell of Harvard Medical School, and counting microbes in the air could therefore overestimate the infectiousness of patients. Nardell is part of a group that since 2005 has been studying TB transmission in another part of South Africa by venting air from tuberculosis patient rooms through guinea pig cages to find how many animals catch the disease. "This measures actual infection, the event of interest," he says. "Sometimes old methods remain the best."

Eric Rubin, a microbiologist at Harvard T.H. Chan School of Public Health, says the work Wood is undertaking is "unusual and difficult." But he says that while the transmission work on guinea pigs has yielded interesting and clinically translatable results, "Robin's work is different as he is interested in underlying molecular mechanisms."

Others are more unequivocally supportive. "Having such a dedicated unit unravelling how TB is specifically conveyed from an infected person to a susceptible person is a step change," says Derrick Crook, an infectious disease microbiology specialist at the University of Oxford. "The benefit is that the factors that promote or prevent this can now be disentangled. Doing it where such spread is happening gives the researchers the best possible chance of sorting this out."

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Lab in South African "Township" to Sample TB from Breathed Air

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In Masiphumelele, an informal settlement of tin shacks, squat brick buildings, and narrow lanes south of Cape Town, 23,000 people go to school, run businesses, sleep, and socialize cheek by jowl. As a result, communicable diseases are rife-especially tuberculosis (TB), which infects around 80 percent of residents by the time they reach adulthood.

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Does Herpes Cause Alzheimer's? ... WIKI 8 -- Tyler Bueno

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Does Herpes Cause Alzheimer's? ... WIKI 8 -- Tyler Bueno

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The herpes virus is dubbed 'the gift that keeps on giving.' They remain in the brain as lifelong neurons and immune cells. But did you know it can also be taking our memories as well? Decades of research states that there is a quite scary correlation between Alzheimer's and herpes. Professor Itzhaki says that, "HSV1 could account for 50% of Alzheimer's cases." "They also incentivize development of an HSV1 vaccine, which would likely be the most effective treatment." There has been a growing use worldwide of HPV vaccination to prevent cervical cancer -- another virus-disease link which emerged in a similar process of research.

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What causes Alzheimer's disease? The answer could be right under our noses, says leading expert Professor Ruth Itzhaki. Her latest paper presents a lifetime of research evidence that the herpes virus responsible for cold sores can also cause Alzheimer's -- and new data which show antiviral drugs drastically reduce risk of senile dementia in patients with severe herpes infections. The review in Frontiers in Ageing Neuroscience raises the tantalizing prospect of a simple, effective preventive treatment for one of humanity's costliest disorders.
The HSV1 theory of Alzheimer's disease
Herpes viruses are the dreaded 'gift that keeps on giving'. They remain lifelong in our neurons and immune cells, reactivating and resurfacing in characteristic blisters when we're run down by stress or illness. Most people are infected by Herpes Simplex Virus 1 (HSV1) by the time they reach old age.

But what happens to infected neurons in our brain during this reactivation?

"HSV1 could account for 50% or more of Alzheimer's disease cases," says Professor Itzhaki, who has spent over 25 years at the University of Manchester investigating a potential link.

HSV1 is better known as the cause of cold sores. Itzhaki has shown previously that cold sores occur more frequently in carriers of APOE-ε4 -- a gene variant that confers increased risk of Alzheimer's.

"Our theory is that in APOE-ε4 carriers, reactivation is more frequent or more harmful in HSV1-infected brain cells, which as a result accumulate damage that culminates in development of Alzheimer's."
Proving the theory
Few countries collect the population data required to test this theory -- for example, to find out whether antiviral treatments reduce dementia risk.

In Taiwan however, researchers have done just that. There, 99.9% of the population is enrolled in a National Health Insurance Research Database, which is being extensively mined for information on microbial infections and disease. In 2017-2018 three studies were published describing Taiwanese data on the development of senile dementia -- of which Alzheimer's is the main cause -- and the treatment of patients with marked overt signs of infection with HSV or varicella zoster virus (VZV, the chickenpox virus).

"The striking results include evidence that the risk of senile dementia is much greater in those who are infected with HSV, and that anti-herpes antiviral treatment causes a dramatic decrease in number of those subjects severely affected by HSV1 who later develop dementia."

Previous findings from Itzhaki's own research group provide a mechanistic link which supports these epidemiological findings. They found that HSV1 causes protein deposits characteristic of Alzheimer's: 'plaques' between neurons, and 'tangles' inside of them.

"Viral DNA is located very specifically within plaques in postmortem brain tissue from Alzheimer's sufferers. The main proteins of both plaques and tangles accumulate also in HSV1-infected cell cultures -- and antiviral drugs can prevent this."
Towards a cure
"It should be stressed that the results of these Taiwanese studies apply only to severe HSV1 (or VZV) infections, which are rare," admits Itzhaki. "Ideally, we would study dementia rates amongst people who have suffered mild HSV1 infection, including herpes labialis (cold sores) or mild genital herpes, but these are far less likely to be documented."

Although further work is needed to confirm and define a causal link between HSV1 infection and Alzheimer's, Itzhaki is enthusiastic about the treatment prospects.

"Considering that over 150 publications strongly support an HSV1 role in Alzheimer's, these Taiwan findings greatly justify usage of antiherpes antivirals -- which are safe and well-tolerated -- to treat Alzheimer's disease.

"They also incentivize development of an HSV1 vaccine, which would likely be the most effective treatment."

This echoes the growing use worldwide of human papillomavirus (HPV) vaccination to prevent cervical cancer -- another virus-disease link which emerged in a similar process of research.

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alzheimer's research; herpes; healthy aging; viruses; alzheimer's; dementia; disorders and syndromes; caregiving

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Herpes is the dreaded 'gift that keeps on giving'. But could it also be taking our memories? Decades of research show a striking correlation between Alzheimer's disease risk and infection with Herpes Simplex Virus 1 (HSV1) in people carrying a specific gene.

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In 1855, a German bacteriologist by the name of Theodor Escherich discovered E. Coli in the human colon, a severe and harm producing bacteria that causes enterohemorrhagic.  ((http://www.fda.gov/For Consumers/Consumer updates/ucm049070.htm). Enterohemorrhagic is the bacteria’s ability to damage the intestine and cause of bloody diarrhea, as well as, brain, and kidney damage.  E-Coli 0157: H7 is a bacterium mainly found in the feces of the beef and dairy of cattle, pigs, and poultry.  The contaminated feces from animals may be transferred to vegetable and fruit.  Escherichia coli (E. Coli) is the most widespread infecting organism in the family of gram-negative bacteria know as Enterobacteriaceae.  Escherichia coli 0157: H7 is a stereotype species of bacteria.  Shiga is one type of E. coli producing disease known to cause foodborne illness, through consumption of contaminated and undercooked food, including unpasteurized milk and undercooked ground beef.  Escherichia coli occurs when bacterial fimbriae attach to the enterocyte (causing an infection of the ileum and colon).  The bacterial translocated intimin receptor (Tir), migrated to the enterocyte, which binds to the Tir, releasing the Shiga toxin by the bacteria.  The Shiga toxins bind to the receptor Gb3/Gb4, and the virus internalizes inside the cell.  Shiga toxins stop protein synthesis, which leads to cell damage, bloody diarrhea, and death. Shiga toxins enter circulation and cause damage to the red blood cells, platelets, kidney, and brain, and can lead to possible death. (Meyer, Ralph R, 2015, p 396, 398, 3p) A regulatory representative made a change regarding meat and food preparation but despite the improvements, there continue to be outbreaks of the harmful and deadly bacteria of E-Coli.  The FDA (Food and Drug Administration) inspects the food manufacturing facility and determines the potential risk for E. Coli contamination.  The public health officials learn of potential E. coli contamination in any food product.   the food is contaminated, the FDA issues a recall and reports that there is an E. coli epidemic associated with a particular food source.  The contaminated food is removed from the marketplace, and an announcement of the recall is made on television.  The food source is labeled and removed from the market to prevent further E. Coli outbreaks.  (http://www.fda.gov/For Consumers/Consumer updates/ucm049070.htm). 

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In 1855, a German bacteriologist by the name of Theodor Escherich discovered E. Coli in the human colon, a severe and harm producing bacteria that causes enterohemorrhagic.  ((http://www.fda.gov/For Consumers/Consumer updates/ucm049070.htm). Enterohemorrhagic is the bacteria’s ability to damage the intestine and cause of bloody diarrhea, as well as, brain, and kidney damage.  E-Coli 0157: H7 is a bacterium mainly found in the feces of the beef and dairy of cattle, pigs, and poultry.  The contaminated feces from animals may be transferred to vegetable and fruit.  Escherichia coli (E. Coli) is the most widespread infecting organism in the family of gram-negative bacteria know as Enterobacteriaceae.  Escherichia coli 0157: H7 is a stereotype species of bacteria.  Shiga is one type of E. coli producing disease known to cause foodborne illness, through consumption of contaminated and undercooked food, including unpasteurized milk and undercooked ground beef.  Escherichia coli occurs when bacterial fimbriae attach to the enterocyte (causing an infection of the ileum and colon).  The bacterial translocated intimin receptor (Tir), migrated to the enterocyte, which binds to the Tir, releasing the Shiga toxin by the bacteria.  The Shiga toxins bind to the receptor Gb3/Gb4, and the virus internalizes inside the cell.  Shiga toxins stop protein synthesis, which leads to cell damage, bloody diarrhea, and death. Shiga toxins enter circulation and cause damage to the red blood cells, platelets, kidney, and brain, and can lead to possible death. (Meyer, Ralph R, 2015, p 396, 398, 3p) A regulatory representative made a change regarding meat and food preparation but despite the improvements, there continue to be outbreaks of the harmful and deadly bacteria of E-Coli.  The FDA (Food and Drug Administration) inspects the food manufacturing facility and determines the potential risk for E. Coli contamination.  The public health officials learn of potential E. coli contamination in any food product.   the food is contaminated, the FDA issues a recall and reports that there is an E. coli epidemic associated with a particular food source.  The contaminated food is removed from the marketplace, and an announcement of the recall is made on television.  The food source is labeled and removed from the market to prevent further E. Coli outbreaks.  (http://www.fda.gov/For Consumers/Consumer updates/ucm049070.htm). 

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Why “Chickenpox Parties” Are a Terrible Idea—in Case It’s Not Obvious .. WIKI 7 -- Tyler Bueno

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Why “Chickenpox Parties” Are a Terrible Idea—in Case It’s Not Obvious .. WIKI 7 -- Tyler Bueno

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It was previously reported that the Kentucky governor, Matt Bevin, stated that he exposed his nine unvaccinated kids to a chicken pox party. Without the proper vaccine, chicken pox can do horrendous things to the body. That itchy disease can cause brain inflammation, hemorrhaging, blood stream infections, and dehydration. If a pregnant woman is exposed to chicken pox, there is a small chance that it can lead to birth defects. If people keep sending their unvaccinated children to chicken pox parties, then the virus will circulate. Chicken pox is a preventable disease to vaccinate.

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Kentucky Governor Matt Bevin made headlines Tuesday after revealing in a radio interview that he had purposefully exposed his nine unvaccinated children to chickenpox, drawing swift condemnation from health experts.

In case anyone needs a refresher on why you shouldn't deprive children of safe, potentially lifesaving vaccines or purposefully expose them to serious, potentially life-threatening infections, here's a quick rundown.

Chickenpox is nothing to mess with

Though most children who get the itchy, highly contagious viral disease go on to recover after a week or so of misery, chickenpox can cause severe complications and even death in some. Complications include nasty skin infections, pneumonia, brain inflammation, hemorrhaging, blood stream infections, and dehydration.

If the infection strikes early in a pregnancy, there's a small chance it could cause birth defects, including abnormally formed limbs, brain, eyes, and skull, as well as intellectual disabilities. If it strikes just before birth, a newborn has a 30 percent chance of getting a severe form of the disease, which can be fatal.

In addition to newborns, people who have an increased risk of severe complications from chickenpox include teens, adults, pregnant women, and people who have a weakened immune system, such as cancer patients on chemotherapy, transplant patients, and those with HIV/AIDS.

But even healthy children may develop complications. There is no way to determine in advance the severity of the infection.

And the fight's not over after chickenpox. Then there's shingles

The same virus that causes chickenpox causes shingles, or zoster. After chickenpox subsides, the virus, varicella-zoster virus (VZV), goes dormant. It hides out in dorsal root ganglia, which are nerves that transmit signals to the spinal cord. VZV can react at any point later in life to cause shingles, which commonly manifests as an incredibly painful, sometimes itchy rash on the trunk of the body.

Shingles is also nothing to mess with, as Ars' own Managing Editor Eric Bangeman can attest. He battled with the resurgence in the fall of 2015 and described it as "several days of acute misery sandwiched by a couple of weeks of feeling crappy."

Shingles also has the potential to cause complications. The most common-occurring in around 13 percent or more of shingles cases-is postherpetic neuralgia (PHN), which is persistent pain for weeks, months, or even years in the area of the rash after the rash disappears. There's also the possibility that shingles could lead to bacterial superinfections on the rash and issues with the eyes that can lead to vision loss, as well as inflammation of the brain or liver, and nerve palsies.

Of course, nearly all of this can be avoided because...

There are vaccines for this

The chickenpox vaccine-aka varicella vaccine-debuted in the US in 1995. It's safe and highly effective. Two doses of it is up to 98 percent effective at preventing all forms of chickenpox. In the rare cases when a vaccinated person still gets chickenpox, the disease is very mild. The vaccine is 100 percent effective at preventing severe forms of the illness.

In the years before the vaccine was available, there were an average of 4 million cases of chickenpox each year in the United States. This led to an average of 10,500 to 13,000 hospitalizations and 100 to 150 deaths each year, according to the Centers for Disease Control and Prevention. With the availability of the vaccine, cases of chickenpox in 31 monitored states fell 79 percent between 2000 and 2010. Deaths from the disease fell 87 percent between four-year periods before and after the vaccine arrived.

The vaccine contains a live but weakened VZV, which causes a latent infection. This can reactivate later in life to cause shingles. However, in a recent study, children who had been vaccinated for chickenpox had a 79 percent lower chance of getting shingles than those who had gotten chickenpox.

Also, there are now two vaccines to prevent shingles in older adults. The current preferred vaccine is the recombinant zoster vaccine Shingrix, which is more than 90 percent effective at preventing shingles after two doses.

This should make "chickenpox parties" obsolete, if not just dangerous

In the past, some parents may have thought it was a good idea to expose their children to chickenpox on purpose to ensure that they got the disease before they were older, when it is more likely to lead to complications. However, as noted earlier, chickenpox can be severe even in healthy children, and it's impossible to tell in advance how severe each case will become. Moreover, with the advent of safe and effective vaccines, there's no reason to subject children to preventable infectious disease that-even in mild cases-causes hundreds of agonizing, itchy blisters along with fever, malaise, and headache.

But it's not just about your kid

Vaccination protects vulnerable people, including those with who can't get vaccines due to medical conditions or those who are immunocompromised. Even if the kids at the parties go on to have mild cases and fully recover-as was the case for Gov. Bevin's children-the parties can keep the virus circulating.

The dangers of allowing chickenpox to keep spreading hit home for Italian politician Massimiliano Fedriga, who came down with the disease last week after opposing legislation that mandated the immunization in school children.

Prominent Italian microbiologist Roberto Burioni responded in a Facebook post, noting that the situation was unfortunate for Fedriga but could have been even more tragic if, for instance, the virus had spread to a fetus or a child undergoing a transplant.

"The only way we have to avoid these tragedies (because they are tragedies) is to vaccinate us all to prevent the circulation of this dangerous virus, which could have hit a much more vulnerable person," he wrote.

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Why "chickenpox parties" are a terrible idea-in case it's not obvious

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Kentucky Governor Matt Bevin made headlines Tuesday after revealing in a radio interview that he had purposefully exposed his nine unvaccinated children to chickenpox, drawing swift condemnation from health experts. In case anyone needs a refresher on why you shouldn't deprive children of safe, potentially lifesaving vaccines or purposefully expose them to serious, potentially life-threatening infections, here's a quick rundown.

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At first site most people, like me, are grossed out by tape worms. But there are some people who use tape worms for quick weight loss. This Iowa women sparked an internet debate over ingesting tape worms. This is apparently becoming a trend in Hong Kong, even against doctor recommendations.

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An Iowa woman recently discovered something worse than being overweight: swallowing a parasitic worm in order to drop a few pounds.

The woman went to her doctor and admitted she'd bought a tapeworm off the Internet and swallowed it, says Dr. Patricia Quinlisk, the medical director of the Iowa Department of Public Health. The woman's doctor, understandably, wasn't sure of what to do in such a situation, and so he contacted the state's public health department for advice. This week, Quinlisk relayed a warning and treatment advice in her weekly email to state public health workers.

"Ingesting tapeworms is extremely risky and can cause a wide range of undesirable side effects, including rare deaths," Quinlisk wrote in the email, as the Des Moines Register reported Friday. "Those desiring to lose weight are advised to stick with proven weight loss methods - consuming fewer calories and increasing physical activity."

There are a few different kinds of tapeworms, but it's the beef tapeworm, or Taenia saginata, that is usually used in these sorts of quick weight-loss schemes, Quinlisk says. In the late 19th and early 20th centuries, advertisements touted "easy to swallow," "sanitized tape worms" as a weapon against fat - "the ENEMY that is shortening your life," as one vintage ad recently showcased by the National Women's History Museum's website reads.

More recently, reports surfaced that dieters in Hong Kong were swallowing tapeworms to lose weight. And in 2009, Tyra Banks did an episode of her talk show in which she interviewed women who said they would be willing to swallow a tapeworm if it really meant they could easily drop a few pounds.

Today

Quinlisk says that the capsules sold in the past by snake oil hucksters, and online today, likely contain the microscopic head of a Taenia saginata.

"When people would order from snake oil medicine kinds of people a weight loss pill, it would be the head of a Taenia saginata ... and it would develop into a 30-foot-long tapeworm in your body," Quinlisk says. "The worm would get into your gut - it's got little hooks on the head - and it would grab onto your intestine and start growing."

And, technically, this parasitic infection, called taeniasis, does cause weight loss.

"Tapeworms will cause you to lose weight because you have this huge worm in your intestines eating your food," Quinlisk says.

At a dangerous, disgusting cost. The Centers for Disease Control and Prevention include "weight loss" and "loss of appetite" in its list of the symptoms of taeniasis - a list also including abdominal pain and upset stomach. Quinlisk adds that this could kill you.

Also from the CDC: "The most visible sign of taeniasis is the active passing of proglottids (tapeworm segments) through the anus and in the feces. In rare cases, tapeworm segments become lodged in the appendix, or the bile and pancreatic ducts."

To get the parasite out of a person's body, doctors will usually prescribe an anti-worm medication like praziquantel or niclosamide, which force all the muscles in the worm's body to contract, killing it. The tapeworm will then harmlessly pass through the intestines and out of the body.

Years ago, Quinlisk volunteered for the Peace Corps and spent time in Nepal, where she would see people suffering from tapeworms they swallowed while eating undercooked, infested meat. The tapeworms made these Nepalese Quinlisk saw very ill, robbing them of many nutrients their food would have otherwise provided for them.

"I can't imagine anybody doing this on purpose," she says.

Diet historian Susan Yager, "just cannot believe" people would use tapeworms to shed pounds. Yager, who studied the history of diets in America for her 2010 book, "The Hundred Year Diet: America's Voracious Appetite for Losing Weight," says if people used tapeworms as a weight loss method, either now or 100 years ago, it's likely a very small number. The CDC, for example, says that the number of new tapeworm cases is probably fewer than 1,000 - and many of those cases may be from undercooked beef or pork.

Today

"Probably, some people have done it. I have no question in my mind that people have done everything in the world to try to lose weight," Yager says. "But I don't think it was ever widespread."

The only other diet that even halfway compares to the over-the-top nature of the tapeworm diet, Yager says, might be the hCG diet, in which dieters inject themselves with a hormone found in the urine of pregnant women. The hCG diet was popular in the 1960s and '70s and experienced a resurgence in recent years.

Then there's "absolute fasting." Proponents of this one say you can live your life in exactly the way you always have; you just don't get to eat any more, ever again, Yager says.

It's easy to make light of extreme dieting strategies, but if a person is so desperate to lose weight they're tempted to try something as horrific as inviting a 30-foot parasitic worm to take up residence inside their intestines -- well, that could be a sign that there's a bigger issue happening here, says New York City registered dietitian Elisa Zied.

iVillage: Fad diets you shouldn't try

"I think that's a red flag -- that they would be willing to sacrifice their health in order to lose weight," says Zied, who urges anyone considering an extreme weight-loss plan to contact someone with a background in science, like a dietitian or nutritionist, or, as a first step, to visit a reputable website like eatright.org.

"If you get to the point of desperation where you will try anything, you need to just get back to the basics and really think about what's going on in your life, and how you're eating and how you're being physically active," she says.

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Iowa woman tries 'tapeworm diet', prompts doctor warning

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An Iowa woman recently discovered something worse than being overweight: swallowing a parasitic worm in order to drop a few pounds. The woman went to her doctor and admitted she'd bought a tapeworm off the Internet and swallowed it, says Dr. Patricia Quinlisk, the medical director of the Iowa Department of Public Health.

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You are born with PCOS, thanks to your mom.
Although I already posted my last 2 wiki posts I wanted to share this info as PCOS has affected a number if us.
Interesting article about new research on PCOS leading to the clinical development of the first drug designed to battle polysystolic ovary syndrome.
-With plans to trial the drug in humans, the next tests are planned to take place later in the year.

“It could be an attractive strategy to restore ovulation and eventually increase the pregnancy rate in these women,” said Giacobini, reports New Scientist.

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Polycystic ovary syndrome (PCOS) is a condition that affects roughly one in five women - and now, scientists think they know why. (Just in time for National Women's Health Week.)

A study published in Nature Medicine found a link between hormonal imbalance in the womb and PCOS, specifically prenatal exposure to a growth factor called anti-Müllerian hormone (AMH).

The team, led by Paolo Giacobini at the French National Institute of Health and Medical Research, realized levels of AMH were 30 percent higher in pregnant women with PCOS than those without. Because there is a hereditary component to the condition, they decided to test whether or not women with this hormonal imbalance give birth to daughters with PCOS.

"It's a radical new way of thinking about polycystic ovary syndrome and opens up a whole range of opportunities for further investigation," explained Robert Norman from the University of Adelaide, Australia, reports New Scientist.

For the study, the researchers injected pregnant mice with AMH so that they had a higher than normal concentration of the hormone. Indeed, they gave birth to daughters who later developed PCOS-like tendencies. These included problems with fertility, delayed puberty, and erratic ovulation.

According to the researchers, the added AMH appeared to prompt the overstimulation of a particular set of brain cells called GnRH neurons, which are responsible for managing the body's testosterone levels. Hence, the offspring displayed higher levels of testosterone. The result: a " masculinization of the exposed female fetus" and a " PCOS-like reproductive and neuroendocrine phenotype" by the time they reached maturity.

But, excitingly, the team weren't just able to determine the cause of PCOS, they were able to reverse it (in mice, anyway). To do so, the researchers dosed the polycystic mice with an IVF drug called cetrorelix, which made the symptoms to go away.

This could be great news for the millions of women with the condition, often characterized by excessive hair growth, hair loss, acne, and obesity, though symptoms can vary from patient to patient. It is also the most common cause of infertility.

Next up, the team is planning to trial the drug in humans. Tests are planned to take place later in the year.

"It could be an attractive strategy to restore ovulation and eventually increase the pregnancy rate in these women," said Giacobini, reports New Scientist.

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Scientists Finally Think They Know What Causes Polycystic Ovary Syndrome - And How To Cure It

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Polycystic ovary syndrome (PCOS) is a condition that affects roughly one in five women - and now, scientists think they know why. (Just in time for National Women's Health Week.) A study published in Nature Medicine found a link between hormonal imbalance in the womb and PCOS, specifically prenatal exposure to a growth factor called anti-Müllerian hormone (AMH).

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In class we have been discussing Hepatitis and how it can affect the body systemically. We somewhat touched on what we can do to protect ourselves from it. I thought that this article was interesting because researchers have found a way to give an oral vaccine for Hepatitis B. Small children are most at risk for being infected, and many people in the world are not vaccinated against Hepatitis B. The researchers say that eliminating the use of the needle itself allows children to not have to deal with being poked. They also said that it eliminates the needs of using a sharps container and needing to use sterilized needles. I thought that this was a good idea because it can help eliminate the risk of infection through exposure to others' bodily fluids. The researchers also brought to the attention of readers that oral vaccinations are less expensive than administered injections. They also found that the vaccine is clumping while administered and this is making it less effective. While I think that this is a really exciting way to administer medications, I still believe that scientists have a long way to go on making more vaccinations to be orally administered.

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A team of researchers found that oral administration of Hepatitis B vaccine protects children against dangerous viruses and have also delivered a 'recipe' called virologists to improve the vaccine drops.

The study was published in Scientific Reports.

Millions of people are infected with hepatitis B every year and particularly small children are at risk. Due to the high cost and the stable environmental conditions required for vaccine storage, many people in developing countries are not vaccinated against this dangerous virus.

"Getting rid of needles being poked into the arms of little children is an advantage in itself. It also eliminates any need to sterilize needles and possible side effects such as swelling and infection. And, unlike the vaccine in use today, this type of vaccine needn't be refrigerated. As such, costs will be reduced and the vaccine's administration will be eased," explained Martin K. Rasmussen, one of the main authors.

As such, researchers have been working to produce a drop or powdered form of the oral vaccine. Oral vaccinations are cheaper and more easily administered than injections. However, developing a sufficiently effective oral hepatitis B vaccine has so far eluded researchers.

"We have used a technology commonly used in solid-state physics to explore how the vaccine behaves within a particular type of encapsulation. This has yielded crucial information that would not otherwise have been achievable. When we scientists venture beyond our comfort zone and deploy each other's knowledge across disciplines, entirely new possibilities can emerge," said Heloisa Bordallo, one of the main authors.

A major challenge of making an oral vaccine is to encapsulate it in a material that can endure the harsh conditions of our digestive system, to protect the vaccine from being destroyed before it reaches its intended destination in the body.

The research team's collaborative partners in Brazil have long known that the silica-material SBA-15 is well-suited to encapsulate a hepatitis B vaccine. However, they did not know exactly how the material protected the vaccine. Nor were they certain about why their vaccine was not always completely effective.

This is where the team of physicists came into the picture. Using a special technique that combines X-ray and neutron imaging, researchers at the Niels Bohr Institute were able to produce 3D images of the inside of the SBA-15 silica.

It marked a crucial step in the use of this technique to develop pharmaceuticals. The imagery allows researchers to see how the vaccine behaves inside the silica, right down to the particle scale. Among other things, they were able to see that the vaccine had a tendency to clump within the silica, making it less effective.

"Now we know what makes the vaccine less effective, and how to optimise it. We know exactly how much vaccine should be put in the silica capsule for it to work best in the body and the clinical trials can be better interpreted," explained Bordallo.

(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)

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Oral vaccine of Hepatitis B will protect kids from dangerous viruses

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Read more about Oral vaccine of Hepatitis B will protect kids from dangerous viruses on Business Standard.

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Bacterial diseases of the Nervous System. Wiki 8 

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Bacterial diseases of the Nervous System. Wiki 8 

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Discussing diseases of all kinds throughout chapters 24-26, the microbial diseases of the nervous system caught most of my attention. Most microbial diseases of the brain are considered extremely serious as they have an effect on critical functions of the brain. Meningiococccal meningitis in particular, caused by a gram negative diplococcus is transmitted through the respiratory route inhabiting the nasopharynx. Patients often suffer signs and symptoms such as seizures, headaches, etc.

Haemophilus isa small, gram negative rod that affects young children (generally in the first few years of life), qualified as a nerve disorder. This generally involves potential mental issues, nerve damage. and in the most serious cases, permanent mental damage.

Leprosy, a disease we have studied both in class and in lab, is considered a disease that can destroy not only peripheral nerves but those of the skin as well. Acid fast bacillus is often involved (mycobacterium). This organism may be known as the Hansen's disease.

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Bacterial Diseases of the Nervous System

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Microbial diseases affecting the nervous system tend to be serious because of the critical functions performed by the brain, spinal cord, and peripheral and cra

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Salmonella as we learned is common illness caused by undercooked food and e coli. According the CDC the outbreak is in 10 states mostly in the south eastern part of the U.S. including Florida and Tennessee. The outbreak is mostly coming from restraunts who bought their meat from "Grant Park Packing in Franklin Park, Ill" the meat recalled on April 24th is estimated at over 53,000 pounds.
https://www.cdc.gov/ecoli/2019/o103-04-19/index.html

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Flu and Whooping Cough Vaccines Don’t Harm Babies

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Flu and Whooping Cough Vaccines Don’t Harm Babies

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Chapter 24 brings us to Microbial diseases of the respiratory system, and among some of the most heartbreaking cases, there is Pertussis; Whooping cough. This can wreak havoc on children and infants especially, and we see continued confirmation for way of vaccinations here. Maybe we don't exercise every single vaccine allowed, but it is the job of us that are going to be having children, to find out the latest and best information about protecting our little ones.

This article has some very solid evidence regarding the use of the T-dap vaccine, at least for a pregnant mom-to-be; absolutely terrible to have to watch your baby go through something so brutal, when it can be eradicated so safely it seems.

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Flu and Whooping Cough Vaccines Don't Harm Babies: Study

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Infants whose moms received the shots when they were pregnant were no more at risk of dying or being hospitalized than other babies.

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Tapeworms are one of the most common parasitic infections that targets humans. Usually when a human ingests undercooked meat it allows the tapeworm to make its way inside. Tapeworms are identified by the animals that they come from. The tapeworm lifecycle consists of three stages. It begins with the egg then larva, lastly it turns into an adult. If someone is infected with the worm and isn't sanitary for examples not washing their hands after the restroom, they can pass on the worm. The tapeworm eggs are passed through having bowel movements so when the hands touch prepared food it is then transmitted. Your doctor will diagnose the tapeworm via feces or through blood tests.

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Tapeworms are intestinal parasites that are shaped like a tape measure. A parasite is an animal or plant that lives inside another animal or plant.

A tapeworm cannot live freely on its own. It survives within the gut of animals, including humans.

Tapeworm eggs normally enter the human host from animals via food, especially raw or undercooked meat.

Humans can also become infected if there is contact with animal feces or contaminated water. When an infection is passed from an animal to a human, it is called zoonosis.

Anyone who has a tapeworm will need treatment to get rid of it. Treatment is 95 percent effective and can be completed in a few days.

Fast facts on tapeworms

Here are some key points about tapeworms. More detail and supporting information is in the main article.

Tapeworms are parasites that survive within another organism, known as the host.

They grow after the host ingests the eggs of the tapeworm.

Drinking contaminated water and eating contaminated food are the primary causes.

Oral medication is a common treatment.

Symptoms

Eggs of the tapeworm Taenia.
Most people who have a tapeworm experience no symptoms and are unaware of hosting one.

If signs and symptoms are present, they usually include tiredness, abdominal pain, weight loss, and diarrhea.

Symptoms may vary depending on the type of tapeworm, and they may include the following:

eggs, larvae, or segments from the tapeworm in stools

abdominal pain

vomiting

nausea

general weakness

inflammation of the intestine

diarrhea

weight loss

altered appetite

sleeping difficulties this may be as a result of other symptoms.

dizziness

convulsions in severe cases.

malnutrition

vitamin B12 deficiency in very rare cases

Complications

The risk of complications depends on several factors, including the type of tapeworm and whether or not the patient receives treatment:

Cysticercosis: If a human ingests pork tapeworm eggs there is a risk of larvae infection. The larvae can exit the intestine and infect tissues and organs elsewhere in the body, resulting in lesions or cysts.

Neurocysticercosis: This is a dangerous complication of pork tapeworm infection. The brain and nervous system are affected. The patient may have headaches, vision problems, seizures, meningitis, and confusion. In very severe cases the infection can be fatal.

Echinococcosis, or hydatid disease: The echinococcus tapeworm can cause an infection called echinococcosis. The larvae leave the gut and infect organs, most commonly the liver. The infection can result in large cysts, which place pressure on nearby blood vessels and affect circulation. In severe cases, surgery or liver transplantation is required.

Treatments

Treating tapeworm larvae infection is more complicated than treating an adult tapeworm infection.

While the adult tapeworm stays in the gut, the larvae may settle in other parts of the body. When a larvae infection finally produces symptoms, the infection may have been present for years. In some rare cases, larvae infection can be life-threatening.

Oral medications

Oral medications may be prescribed. The digestive system does not absorb these drugs well. They either dissolve or attack and kill the adult tapeworm.

A doctor may advise the patient to take a laxative to help the tapeworm come out in the stools. If the patient has a pork tapeworm infection, they may be given an anti-emetic medication, which prevents vomiting. Vomiting during a tapeworm infection can lead to reinfection by swallowing the tapeworm larvae,

The patient's stools will be checked several times 1 to 3 months after the course of medication. These medications, if procedures are followed properly, are 95 percent effective.

Anti-inflammatory medication

If the infection affects tissues outside the intestine, the patient may have to take a course of anti-inflammatory steroids to reduce swelling caused by the development of cysts.

Cyst surgery

If the patient has life-threatening cysts that have developed in vital organs, such as the lungs or liver, surgery may be required. The doctor may inject a cyst with medication, such as formalin, to destroy the larvae before removing the cyst.

Causes

The Taenia solium (pork tapeworm) Ingestion of eggs
Most people become infected after ingesting tapeworm eggs or larvae. The common methods of infection include:

Eggs get into humans via:

If a host, such as a pig, has a tapeworm inside, segments of the worm or its eggs may be present in the feces of the host. These drop onto the soil. Each segment may contain thousands of eggs.

A human can become infected by:
Eating infected meat or fish

drinking contaminated water

interacting with the animals and contaminated soil

consuming contaminated food

The eggs hatch into larvae and make their way into the gut or outside, and infect other parts of the body. This type of infection is most common with tapeworms that come from infected pigs, and much less common if the original host was cattle or fish.

If the meat or fish have larvae cysts and is undercooked or raw, the cysts can reach the intestine where they mature into adult tapeworms.

An adult tapeworm can:
Human-to-human transmission

live as long as 20 years

be up to 50 feet long

attach themselves to the walls of the intestine

pass through the human digestive system and end up in the toilet when stool is passed

Insect-to-human transmission
Fish tapeworm infection is more common in countries where the consumption of raw fish is common practice, such as Eastern Europe, Scandinavia, and Japan. Undercooked or raw freshwater fish such as salmon, are the most common sources.
Reinfecting yourself
The dwarf tapeworm can be transmitted from human to human. It is the only tapeworm that can go through its entire life cycle in one single host. Dwarf tapeworm infection is the most common tapeworm infection globally.
Ignoring risk factors for tapeworm infection
Fleas and some types of beetles may pick up the eggs by eating the droppings of infected rats or mice. These insects can infect humans. The insects are referred to as intermediate hosts and the tapeworm transitions from egg to the adult stage. This type of infection occurs with dwarf tapeworms and is much more common in areas where hygiene practices are poor.

During treatment, humans can reinfect themselves if they do not follow good hygiene practices. The eggs will be present in human stool. If the individual does not wash their hands after going to the toilet, there is a risk of reinfection.

Risk factors include:

Working with or exposure to animals: This is especially the case in areas where feces is not disposed of effectively.

General lack of hygiene: If you wash your hands infrequently, the risk of transferring infection into your mouth is greater.

Traveling to or living in certain parts of the world: In some countries, and parts of some countries where sanitation practices are poor, the risk of becoming infected with a tapeworm is much greater.

Consuming raw or undercooked meats and fish: Larvae and eggs present in meats and fish may infect people if eaten raw or undercooked. Experts say that sushi is safe if it has been frozen beforehand. The risk of contamination from fish mainly lies with freshwater fish.

Types

In human beings, tapeworm infection is most commonly caused by the following species:

pork tapeworm (Taenia solium)

beef tapeworm (Taenia saginata)

dwarf tapeworm (Hymenolepis nana)

fish tapeworm from raw freshwater fish (Diphyllobothrium latum)

dog tapeworm, more common in rural areas

The type of tapeworm will influence the area of the body that is infected and how severe the symptoms are.

Diagnosis

Any individual who suspects tapeworm infection or has the symptoms described above should see their doctor. Some patients may notice infection themselves by checking their stool for parts of the adult tapeworm. However, a doctor is still needed to check the stool by sending samples to a lab. The doctor may also examine the area around the patient's anus for signs of eggs or larvae.

The following diagnostic aids may be used, depending on the type of tapeworm larvae infection:

Blood tests: These aim to look for antibodies caused by infection.

Imaging scans: This could include a chest X-ray, ultrasound scan, CT scan, or MRI scan.

Organ tests: The doctor may want to check that the organs are functioning correctly.

Removal

Removing adult tapeworms from the body is easier than managing a larvae infection.

Taking a medicine that kills the tapeworm is normally enough to ensure that the body will remove the tapeworm in stools. Medicine is now advanced enough that surgery is often not necessary.

However, the drugs are highly toxic. If a tapeworm reaches the brain, surgery and medicine may be used together to remove the parasite.

Prevention

There are several effective methods of preventing tapeworm infection, including:

Good hygiene: Wash hands thoroughly with soap and water after using the bathroom and before eating.

Food precautions: In an area where tapeworms are common, make sure to wash and cook all fruits and vegetables with clean water.

Livestock: Properly dispose of animal and human feces. Minimize animal exposure to tapeworm eggs.

Meat: Cook meat to a temperature of at least 150 °Fahrenheit (66 °Celcius) thoroughly. This will kill larvae or eggs.

Meat and fish: Freeze fish and meat for at least 7 days. This will kill tapeworm eggs and larvae.

Raw foods: Do not consume raw or undercooked pork, beef, and fish.

Dogs: If you have a dog, make sure they are treated for tapeworms. Take special care with your personal hygiene. Make sure your dog only eats cooked meat and fish.

Kitchen hygiene: Make sure all work surfaces are regularly cleaned and disinfected.

Do not allow raw foods to touch other foods. Wash your hands after touching raw meat or fish. Experts say that smoking or drying meat or fish is not a reliable way to kill larvae or eggs.

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University of Illinois-Chicago, School of Medicine

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Tapeworms: Causes, symptoms, and treatments

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The tapeworm is a parasite that lives in the gut. Humans become infected when we eat food that contains tapeworm eggs or come into contact with contaminated water or animal feces. Treatment is 95 percent effective and can be completed in a few days. Learn about types, symptoms, complications, and prevention here.

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🤬 : An approach for targeting HIV reservoirs 

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🤬 : An approach for targeting HIV reservoirs 

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In chapter 26 we learn about microbial diseases of the urinary system. 🤬 affects the urinary system.  Current HIV treatments need to be taken for life by those infected as antiretroviral therapy is unable to eliminate viral reservoirs lurking in immune cells. Scientists have identified the characteristics of CD4 T lymphocytes that are preferentially infected by the virus. Thanks to metabolic activity inhibitors, the researchers have managed to destroy these infected cells, or 'reservoirs', ex vivo.

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AIDS: An approach for targeting HIV reservoirs

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Current HIV treatments need to be taken for life by those infected as antiretroviral therapy is unable to eliminate viral reservoirs lurking in immune cells. Scientists have identified the characteristics of CD4 T lymphocytes that are preferentially infected by the virus. Thanks to metabolic activity inhibitors, the researchers have managed to destroy these infected cells, or 'reservoirs', ex vivo.

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Walckenaer E, Poirel L, Leflon-Guibout V, et al. Genetic and Biochemical Characterization of the chromosomal class A β-lactamases of Raoultella (formerly Klebsiella) planticola and Raoutella ornithinolytica. Antimicrob Agents Chemother. 2004;48(1):305–312.

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Vital Signs: Epidemiology and Recent Trends in Methicillin-Resistant and in Methicillin-Susceptible Staphylococcus aureus Bloodstream Infections — United States

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Vital Signs: Epidemiology and Recent Trends in Methicillin-Resistant and in Methicillin-Susceptible Staphylococcus aureus Bloodstream Infections — United States

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Staphylococcus aureus is a major cause of community- and health care–associated infections (1), ranging from superficial skin and soft tissue infections (SSTI) to invasive infections, sepsis, and death. Methicillin-resistant S. aureus (MRSA) has long been recognized as a pathogen associated with health care settings; however, in the 1990s, community-associated MRSA infections, causing mostly SSTI, emerged in the United States (2). Substantial progress has been achieved in preventing MRSA bloodstream infections in U.S. health care facilities (3–5) after widespread introduction of enhanced infection control efforts in acute-care hospitals.

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Centers for Disease Control and Prevention

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On March 5, 2019, this report was posted online as an MMWR Early Release.

Athena P. Kourtis ¹; Kelly Hatfield ¹; James Baggs ¹; Yi Mu ¹; Isaac See ¹; Erin Epson ²; Joelle Nadle ³; Marion A. Kainer ⁴; Ghinwa Dumyati ⁵; Susan Petit ⁶; Susan M. Ray ⁷; Emerging Infections Program MRSA author group; David Ham ¹; Catherine Capers ¹; Heather Ewing ¹; Nicole Coffin ¹; L. Clifford McDonald ¹; John Jernigan ¹; Denise Cardo ¹ ( View author affiliations)

View suggested citation

Summary
What is already known about this topic?
Invasive methicillin-resistant Staphylococcus aureus (MRSA) infections have been declining in health care settings; however, the rate of decline has recently slowed.
What is added by this report?
Nearly 120,000 Staphylococcus aureus bloodstream infections and 20,000 associated deaths occurred in the United States in 2017. After years of progress, the rate of decline of MRSA bloodstream infections has slowed, whereas bloodstream infections caused by methicillin-susceptible S. aureus are increasing slightly in the community (3.9% annually, 2012-2017).
What are the implications for public health practice?
Adherence to CDC recommendations for preventing device- and procedure-associated infections and interrupting transmission, along with innovative, tailored interventions (including decolonization) are needed to further prevent S. aureus infections.

Abstract

Introduction: Staphylococcus aureus is one of the most common pathogens in health care facilities and in the community, and can cause invasive infections, sepsis, and death. Despite progress in preventing methicillin-resistant S. aureus (MRSA) infections in health care settings, assessment of the problem in both health care and community settings is needed. Further, the epidemiology of methicillin-susceptible S. aureus (MSSA) infections is not well described at the national level.

Methods: Data from the Emerging Infections Program (EIP) MRSA population surveillance (2005-2016) and from the Premier and Cerner Electronic Health Record databases (2012-2017) were analyzed to describe trends in incidence of hospital-onset and community-onset MRSA and MSSA bloodstream infections and to estimate the overall incidence of S. aureus bloodstream infections in the United States and associated in-hospital mortality.

Results: In 2017, an estimated 119,247 S. aureus bloodstream infections with 19,832 associated deaths occurred. During 2005-2012 rates of hospital-onset MRSA bloodstream infection decreased by 17.1% annually, but the decline slowed during 2013-2016. Community-onset MRSA declined less markedly (6.9% annually during 2005-2016), mostly related to declines in health care-associated infections. Hospital-onset MSSA has not significantly changed (p = 0.11), and community-onset MSSA infections have slightly increased (3.9% per year, p<0.0001) from 2012 to 2017.

Conclusions and Implications for Public Health Practice: Despite reductions in incidence of MRSA bloodstream infections since 2005, S. aureus infections account for significant morbidity and mortality in the United States. To reduce the incidence of these infections further, health care facilities should take steps to fully implement CDC recommendations for prevention of device- and procedure-associated infections and for interruption of transmission. New and novel prevention strategies are also needed.

Introduction

Staphylococcus aureus is a major cause of community- and health care-associated infections ( 1), ranging from superficial skin and soft tissue infections (SSTI) to invasive infections, sepsis, and death. Methicillin-resistant S. aureus (MRSA) has long been recognized as a pathogen associated with health care settings; however, in the 1990s, community-associated MRSA infections, causing mostly SSTI, emerged in the United States ( 2). Substantial progress has been achieved in preventing MRSA bloodstream infections in U.S. health care facilities ( 3- 5) after widespread introduction of enhanced infection control efforts in acute-care hospitals.

Although the rates of hospital-onset MRSA bloodstream infections have substantially decreased, evidence from the National Healthcare Safety Network (NHSN) and from the Emerging Infections Program (EIP) surveillance system suggests that the decline might have slowed in more recent years ( 4, 6); the United States is not on track to meet the 2020 goal of the Healthcare-Associated Infection National Action Plan of a 50% reduction in hospital-onset MRSA bloodstream infections from the 2015 baseline ( 7). Moreover, to protect patients, expanded efforts are needed to prevent methicillin-susceptible S. aureus (MSSA), which causes approximately half of all health care-associated S. aureus infections ( 8). There is little information on the current epidemiology of MSSA infections in the United States, and available data might not be nationally representative ( 9- 11).

A critical assessment of recent trends and incidence of both MRSA and MSSA invasive disease in the United States is crucial to informing public health policy and formulating a framework of approaches to further prevent S. aureus infections. In this report, recent data from the EIP population surveillance and two large electronic health record (EHR) data sets from over 400 U.S. acute care hospitals were used to update estimates of MRSA and MSSA bloodstream infections, and to estimate associated in-hospital mortality.

Methods

EIP population MRSA surveillance. MRSA bloodstream infection data were obtained from CDC's EIP active laboratory- and population-based surveillance for invasive MRSA in selected counties from six sites* reporting data continually from 2005 to 2016 (population in 2016 = 13 million). A case of MRSA bloodstream infection was defined as isolation of MRSA from a blood culture in a resident of the catchment area, who had not had a positive invasive culture from a normally sterile site in the preceding 30 days. Annual incidence was calculated per 100,000 census population and stratified according to patient epidemiologic exposure, determined through medical record review as 1) hospital-onset if the culture was obtained on or after the fourth day of an inpatient hospitalization; 2) health care-associated community-onset, if the culture was obtained from an outpatient or during the first 3 days of hospitalization in a patient with one of several significant prior health care exposures; and 3) community-associated, otherwise. Community-onset infections comprise health care-associated community-onset and community-associated infections. Further details about the surveillance program can be found elsewhere ( 3). Adjusted annual decreases were modeled using Poisson regression and accounting for changes in the overall population and dialysis population demographics. Postcensus bridged-race census files were used for EIP analyses.

EHR databases. The Premier Healthcare Database ( 12) and Cerner Health Facts EMR ( 13) data were used to identify S. aureus bloodstream infections among patients discharged from participating acute care hospitals reporting results of microbiologic cultures with antimicrobial susceptibility testing during January 1, 2012-December 31, 2017. A case was defined as the identification of S. aureus in a blood culture with reported antimicrobial sensitivity, without a positive S. aureus blood culture in the preceding 14 days. Community-onset and hospital-onset cases were defined as for EIP surveillance. Incidences of MSSA and MRSA were calculated as the number of community-onset cases per 1,000 hospital discharges and the number of hospital-onset cases per 10,000 patient-days. Trends in monthly incidence during 2012-2017 were assessed using generalized estimating equations to fit negative binomial regression models adjusted for seasonality and certain hospital characteristics and accounting for clustering and repeated measures. The outcome variable was the number of S. aureus bloodstream infections, and the predictor variable was a continuous time covariate. Adjusted rates are presented as relative annual trends. Deaths associated with S. aureus bloodstream infections were defined as deaths or discharges to hospice for patient hospitalizations with documented S. aureus bloodstream infections. Differences in annual mortality were assessed using generalized estimating equations binomial models adjusting for all the same characteristics as for incidence. Hospital characteristics were used in a raking-procedure to determine weights to extrapolate the number of discharges included in the sample to match the distribution of discharges for all hospitals from the American Hospital Association survey ( 14). Using these weights, national estimates of cases of S. aureus bloodstream infections and deaths associated with S. aureus bloodstream infections were extrapolated. All statistical analyses were performed using SAS (version 9.4; SAS Institute).

Results

Rates of hospital-onset and community-onset MRSA, EIP surveillance, 2005-2016. From 2005 to 2016, the incidence of hospital-onset and community-onset MRSA bloodstream infection declined 74% and 40%, respectively ( Figure 1). The decline in hospital-onset MRSA bloodstream infection rates has slowed in more recent years: adjusted rates decreased by 17.1% per year (p<0.001) during 2005-2012 but did not significantly change during 2013-2016 (p = 0.25). Adjusted community-onset MRSA bloodstream infection rates declined by 6.9% per year during 2005-2016 (p<0.001). Declines in rates of health care-associated community-onset infections accounted for most of the decline in community-onset MRSA bloodstream infections during 2005-2016 (Figure 1). Adjusted health care-associated community-onset bloodstream infection rates declined by 7.8% per year (p = 0.001), but community-associated bloodstream infections declined by only 2.5% per year (p = 0.001).

Rates of hospital-onset and community-onset MRSA and MSSA and associated mortality, EHR data, 2012-2017. From 2012 to 2017, 447 hospitals contributed data (average per year = 325). During this time, adjusted hospital-onset MRSA bloodstream infection rates declined 7.3% per year (p<0.0001) ( Figure 2), with no significant change in community-onset MRSA rates (p = 0.35). Hospital-onset MSSA rates did not change (p = 0.11), and community-onset MSSA rates significantly increased (3.9% per year, p<0.001) (Figure 2).

The overall unadjusted in-hospital mortality among patients with S. aureus bloodstream infections over the study period was 18%. No significant change was observed from 2012 to 2017, although significant differences were observed by epidemiologic classification: unadjusted MRSA and MSSA mortality rates were higher for hospital-onset cases (29% and 24%, respectively) than for community-onset cases (18% and 14%, respectively) (p<0.001).

Estimated morbidity of S. aureus bloodstream infections and in-hospital mortality, EHR data, United States, 2017. Overall, an estimated 119,247 cases of S. aureus bloodstream infections and 19,832 associated deaths occurred nationwide in 2017.

Conclusions and Comments

This study identified substantial reductions in hospital-onset MRSA bloodstream infection rates between 2005 and 2012; however, since 2012, the rate of decline has slowed. These trends are consistent with recent data from NHSN ( 4). Less marked declines were noted in rates of community-onset MRSA bloodstream infections compared with those of hospital-onset infections. The detailed epidemiologic information that EIP collects allowed subclassification of community-onset MRSA infections into those with prior health care exposure (health care-associated community-onset), which account for the majority of cases, and those without health care exposure (community-associated). Most of the reduction in MRSA bloodstream infection is attributable to reductions in health care-associated MRSA. Community-associated MRSA infection rates have changed little overall. Hospital-onset MSSA infection rates have not changed since 2012, whereas community-onset-MSSA infection rates might be increasing slightly.

The reasons for the declines in hospital-onset MRSA bloodstream infections might be attributable to a variety of infection control efforts, including improvements in preventing device- and procedure-associated infections ( 15- 17), as well as efforts to interrupt MRSA transmission in the hospital setting ( 5, 18). As has been reported previously ( 17), significant national reductions in central-line-associated bloodstream infections occurred during 2001-2009, particularly in those caused by S. aureus; these reductions have continued through more recent years ( 4). Meanwhile, evidence from the National Veterans Affairs system suggests that decreasing hospital transmission of MRSA likely also contributed to the observed reductions ( 19, 20).

National MRSA reductions primarily reflect declines in the incidence of infections caused by USA100 strains, which are predominantly transmitted in health care settings, and, to a lesser extent, USA300 strains, which are predominantly transmitted in the community ( 21). Historically, large shifts in S. aureus strain epidemiology have occurred ( 22). Whereas the reasons for some of these shifts might be related to strain virulence and fitness, health care-related interventions are likely to have played a role in the decrease in USA100.

The recent slowing in the reduction in hospital-onset MRSA bloodstream infections and the limited decline in community-associated MRSA and in MSSA infections point to the need for an updated S. aureus prevention framework, including greater use of evidence-based practices that can reduce transmission and prevent device- and procedure-associated infections, as well as new and novel approaches. These include strategies to suppress S. aureus colonization in patients during periods of high risk for invasive S. aureus infection, such as when invasive devices are in place, during admission to high-risk hospital units, or perioperatively for certain high-risk surgical procedures. The experience with MRSA suggests that the postdischarge period might also be important for targeting innovative prevention efforts: EIP data suggest that the majority of all MRSA bloodstream infections are health care-associated community-onset, and most occur in the 3 months after hospital discharge ( 3). A recent study suggests that prescribing serial decolonization protocols at the time of hospital discharge could significantly reduce postdischarge S. aureus infections ( 23). Suppression of S. aureus colonization might play an important role in decreasing transmission, but data to recommend this approach as a replacement for currently recommended strategies to prevent transmission, such as contact precautions, are insufficient ( 24). All hospitals should have strategies in place for preventing S. aureus infections; however, the prevention impact might be greatest in those with a particularly high S. aureus incidence. A recent review of NHSN data indicated that a relatively small number of hospitals (approximately 200) account for slightly over half of the hospital-onset MRSA incidence in excess of the 2020 goals and could be prioritized for prevention to reduce MRSA bloodstream infections nationally (NHSN, unpublished data).

Community-associated MRSA infections provide a reservoir that contributes to health care-associated disease incidence and fuels transmission both outside and within health care settings. USA300 strains, for example, emerged in the community and spread to health care settings ( 25). Community-associated S. aureus infections are not declining, and the ongoing opioid epidemic might be contributing to this trend. Emerging evidence suggests a 16-fold risk for invasive MRSA infection among persons who inject drugs; 9.2% of invasive MRSA cases in 2016 occurred in persons who inject drugs ( 26). Prevention of opioid misuse, increasing access and linkage to medication-assisted treatment for persons with opioid use disorder ( 27), ensuring access to sterile injecting equipment, improving education about safer injection practices and how to recognize early signs of infection, and linking those with an infection to care are needed. Additionally, community-associated S. aureus infections are known to disproportionately affect persons in lower socioeconomic strata ( 28); this has implications for the formulation of approaches to enhance prevention. The observed increases in rates of community-onset MSSA infections highlight the need to systematically study the epidemiology of MSSA and develop innovative, evidence-based prevention strategies for this setting. Research for a vaccine or for novel ways to decrease S. aureus bioburden should continue.

The incidence of S. aureus bloodstream infections and associated deaths is substantial and consistent with estimates using Nationwide Inpatient Sample data ( 29). Mortality was unchanged over the time studied and comparable to what was achieved in the VA hospital system through implementation of improved clinical management of infection ( 28). Appropriate and timely diagnosis and antimicrobial susceptibility-guided treatment of S. aureus infections remain key to reducing poor outcomes and preventing sepsis and death ( 29).

The findings in this report are subject to at least two limitations. First, the lack of detailed epidemiologic information on previous health care exposures captured in EHR precluded subclassification of community-onset infections into those with and without previous health care exposures. Second, possible variability in clinical or data capture practices across different hospitals might affect the validity of EHR data and trends.

Strengths of this study include the use of multiple data sources; the detailed epidemiologic information provided in the population-based EIP surveillance; the inclusion of two widely used EHR systems representing a large number of U.S. acute-care hospitals; and the use of weights to derive national estimates. As has been previously shown with another infection-related condition (sepsis), clinical criteria using EHR data are immune to temporal variations in coding practices that can be significant ( 30), whereas death-certificate data are an insensitive measure of sepsis-related mortality ( 31).

S. aureus infections account for substantial morbidity in the United States. Despite significant reductions in health care-associated MRSA infections, progress is slowing. MSSA infections have not decreased as much in hospitals and might be increasing in the community. Adherence to CDC recommendations ( 32) for preventing device- and procedure-associated infections and interrupting transmission, along with innovative interventions tailored to the needs of health care facilities (including decolonization) are needed to further prevent S. aureus infections.

Corresponding author: Athena P. Kourtis, apk3@dc.gov, 770-488-5216.

¹Division of Healthcare Quality Promotion, National Center for Emerging and Zoonotic Infectious Diseases, CDC; ²California Department of Health; ³California Emerging Infections Program, Oakland, California; ⁴Tennessee Emerging Infections Program, Nashville, Tennessee; ⁵New York-Rochester Emerging Infections Program, University of Rochester Medical Center, Rochester, New York; ⁶Connecticut Emerging Infections Program, New Haven, Connecticut; ⁷ Georgia Emerging Infections Program, Atlanta Georgia.

References

1. Dantes R, Mu Y, Belflower R, et al. ; Emerging Infections Program-Active Bacterial Core Surveillance MRSA Surveillance Investigators. National burden of invasive methicillin-resistant Staphylococcus aureus infections, United States, 2011. JAMA Intern Med 2013;173:1970-8.

2. CDC. Data summary of HAIs in the US: assessing progress 2006-2016. Atlanta, GA: US Department of Health and Human Services, CDC; 2017. https://www.cdc.gov/hai/data/archive/data-summary-assessing-progress.html

3. CDC. 2016 national and state healthcare associated infections progress report. Atlanta, GA: US Department of Health and Human Services, CDC; 2017. https://www.cdc.gov/hai/data/portal/progress-report.html

4. US Department of Health and Human Services. National action plan to reduce health care-associated infections Washington, DC: US Department of Health and Human Services; 2010.

5. Premier Applied Sciences. Premier healthcare database white paper: data that informs and performs. Charlotte, NC: Premier Applies Sciences; 2018.

6. American Hospital Association. AHA annual survey database Chicago, IL: American Hospital Association; 2017.

7. CDC. Reduction in central line-associated bloodstream infections among patients in intensive care units-Pennsylvania, April 2001-March 2005. MMWR Morb Mortal Wkly Rep 2005;54:1013-6.

8. CDC. Vital signs: central line-associated blood stream infections-United States, 2001, 2008, and 2009. MMWR Morb Mortal Wkly Rep 2011;60:243-8.

9. Perlin JB, Hickok JD, Septimus EJ, Moody JA, Englebright JD, Bracken RM. A bundled approach to reduce methicillin-resistant Staphylococcus aureus infections in a system of community hospitals. J Healthc Qual 2013;35:57-68.

10. Jones M, Jernigan JA, Evans M, et al. Vital signs: trends in Staphylococcus aureus infections in Veterans Affairs medical centers-United States, 2005-2017. MMWR Morb Mortal Wkly Rep 2019;68(9).

11. See I, Albrecht V, Mu Y, et al. Changes in incidence and strains of methicillin-resistant Staphylococcus aureus bloodstream infections, 2005-2013 [abstract]. ID Week; Oct 26-30, 2016; New Orleans, LA.

12. Huang SS, Singh R, McKinnell JA, et al. Decolonization to reduce postdischarge infection risk among MRSA carriers. N Engl J Med 2019;380:638-50.

13. CDC. Methicillin-resistant Staphylococcus aureus (MRSA). Information for inpatient clinicians and administrators. Atlanta, GA: US Department of Health and Human Services, CDC; 2016. https://www.cdc.gov/mrsa/healthcare/clinicians/index.html

14. Klein EY, Jiang W, Mojica N, et al. National costs associated with methicillin-susceptible and methicillin-resistant Staphylococcus aureus hospitalizations in the United States, 2010-2014. Clin Infect Dis 2019;68:22-8.

15. CDC. Healthcare Infection Control Practices Advisory Committee (HICPAC). Guidance documents. Atlanta, GA: US Department of Health and Human Services, CDC; 2018. https://www.cdc.gov/hicpac/recommendations/index.html

FIGURE 1. Adjusted* methicillin-resistant Staphylococcus aureus bloodstream infection rates from population based surveillance - six U.S. Emerging Infections Program sites,† 2005-2016

* Adjusted for year and distribution of age, sex, and race among overall and dialysis population. Community-onset infections comprise health care-associated community-onset and community-associated infections

† California (three counties), Connecticut (statewide), Georgia (eight counties), Minnesota (one county), New York (one county), and Tennessee (one county).

FIGURE 2. Adjusted* hospital-onset and community-onset rates of Staphylococcus aureus bloodstream infections - Premier and Cerner Hospitals, United States, 2012-2017

Abbreviations: MRSA = methicillin-resistant Staphylococcus aureus; MSSA = methicillin-susceptible Staphylococcus aureus.

* Modeled relative to observed rates in 2012. Model adjusts for discharge month and year and hospital region, teaching status, bed size, and distributions of patient age, sex and race, in addition to accounting for repeated measures and clustering by facility.

Suggested citation for this article: Kourtis AP, Hatfield K, Baggs J, et al. Vital Signs: Epidemiology and Recent Trends in Methicillin-Resistant and in Methicillin-Susceptible Staphylococcus aureus Bloodstream Infections - United States. MMWR Morb Mortal Wkly Rep 2019;68:214-219. DOI: .

MMWR and Morbidity and Mortality Weekly Report are service marks of the U.S. Department of Health and Human Services.
Use of trade names and commercial sources is for identification only and does not imply endorsement by the U.S. Department of Health and Human Services.
References to non-CDC sites on the Internet are provided as a service toMMWR readers and do not constitute or imply endorsement of these organizations or their programs by CDC or the U.S. Department of Health and Human Services. CDC is not responsible for the content of pages found at these sites. URL addresses listed inMMWR were current as of the date of publication. All HTML versions of MMWR articles are generated from final proofs through an automated process. This conversion might result in character translation or format errors in the HTML version. Users are referred to the electronic PDF version (https://www.cdc.gov/mmwr) and/or the originalMMWR paper copy for printable versions of official text, figures, and tables. Questions or messages regarding errors in formatting should be addressed to mmwrq@cdc.gov.

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Vital Signs: Epidemiology and Recent Trends ...

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Nearly 120,000 Staphylococcus aureus bloodstream infections and 20,000 associated deaths occurred in the United States in 2017. After years of progress, the rate of decline of MRSA bloodstream infections has slowed in the United States, whereas bloodstream infections caused by methicillin-susceptible S. aureus are increasing slightly in the community (3.9% annually, 2012-2017).

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Untreatable form of Lyme disease COULD HIT 2 MILLION AMERICANS BY 2020 wiki 7 

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Untreatable form of Lyme disease COULD HIT 2 MILLION AMERICANS BY 2020 wiki 7 

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SAMANTHA MITCHELL

As we learned in chapter 23 about Lyme disease. The most common vector-borne illness in the U.S., Lyme disease is caused by the Borrelia burgdorferi bacterium, which is spread by infected ticks. Sufferers can have a fever, headache, chills, fatigue, joint and muscle ache and swollen lymph nodes. In many cases, patients experience an erythema migrans rash that can grow up to 12 inches around the area of the tick bite. Around 329,000 cases are thought to occur each year, although the true number of infections is thought to be higher.

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Scientists predict the number of people to suffer from a little-understood type of Lyme disease could spike to almost 2 million in 2020.

The most common vector-borne illness in the U.S., Lyme disease is a condition caused by the Borrelia burgdorferi bacteria, which is spread by infected ticks. Sufferers are hit by a fever, headache, chills, tiredness, joint and muscle aching, as well as swollen lymph nodes. In many cases, patients experience an erythema migrans rash that can grow up to 12 inches around the area of the tick bite. Around 329,000 cases are thought to occur each year, although the true number of infections is thought to be higher.

In most cases, doctors prescribe antibiotics and the symptoms pass. However, for others the symptoms can linger in what is known as post-treatment Lyme disease (PTLD) or post-treatment Lyme disease syndrome. The condition is characterized by cognitive dysfunction, incapacitating fatigue and chronic pain, according to the authors of the research published in the journal BMC Public Health.

The condition is poorly understood: there is no set diagnosis for it and treatment is controversial, the authors wrote. The cause is unkown-some believe the bug could disrupt the immune system-and it can take months to recover. Past estimates suggest treatments fail in between 10 to 20 percent of cases, which could cost the U.S. economy up to $1 billion per year.

"Although antibiotic therapy cures most LD patients, a significant proportion of patients continue to suffer persisting symptoms that can derail normal life," wrote the team.

It can therefore be tough to find accurate data on the prevalence of PTLD, and diagnosis can involve ruling out other health problems.

For their study, the scientists drew on several pools of data to create a model to estimate the number of PTLD cases which occurred between 2016 and 2020. That included data collected by the United States Center for Disease Control and Prevention as well as past estimates of Lyme disease rates; survival rates; and examples of treatments failing.

A conservative estimate made by the researchers suggested that 69,011 cases of PTLD occurred in 2016, which will gradually rise to 81,509 cases in 2020. In another model, the researchers accounted for cases rising from 1980s combined with treatment failing in 20 percent of cases. That would see a prediction of 1,523,869 cases in 2016 and 1,944,189 forecast for 2020.

The authors acknowledged that it remains unclear which is the most accurate estimation.

"Nevertheless, our findings suggest that there are large numbers of patients living with LD-related chronic illness," they wrote. Further research is now needed to create tests to accurately diagnose and treat the condition, raise public awareness, and arrive at a conclusive figure on the number of sufferers.

While ticks carrying the Lyme disease-causing bacteria can strike at any time of the year, the warmer months of April and September are the riskiest. The CDC advises avoiding grassy, brushy or wooded areas where ticks could lurk, and by treating clothing with 0.5 percent permethrin products, and EPA-approved insect repellents before heading to areas where the bugs might live.

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Untreatable form of Lyme disease could hit two million Americans by 2020, scientists warn

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Scientists predict the number of people to suffer from a little-understood type of Lyme disease could spike to almost 2 million in 2020. The most common vector-borne illness in the U.S., Lyme disease is a condition caused by the Borrelia burgdorferi bacteria, which is spread by infected ticks.

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In class we discussed scabies. In this article there is an outbreak in a hospital. Such little insects can infest and spread rapidly. These scabies cause itching and from the itching can create a second infection. As the article states just reading about bugs makes me itch. They can spread from close contact. Making sense that in a hospital the scabies spread. Not only do they spread from contact but can be in linens as well. The children show symptoms of itching in areas like the wrist and fingers. Adults in the armpits. Reading about and learning about scabies is an itchy subject. No scabies for me.

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Let's be honest. It is the rare few of us who don't start empathetic itching when we even read stories about skin mite infestations or head lice, for example, let alone experience them first hand.

According to the Dayton Daily News, things got all too real for 86 hospital employees at Kettering Hospital when spokesperson, Elizabeth Long, confirmed an outbreak of scabies among the staff. The hospital representative maintains the spread can be traced to a patient and the proper precautions are in place to prevent further issues-maintaining no other patients have been affected.

What better time to clarify some misperceptions about scabies and a few other causes of more acute intense itching than the present?! Especially ones that are readily treatable. To read about causes of chronic itching that could signify more substantial underlying disease, read When Itching is a Bigger Deal.

Scabies is a highly contagious tiny skin mite. It burrows under the skin (and lays eggs) often in a linear array causing intense diffuse itching throughout the body. Children routinely demonstrate these patterns at the wrists, ankles, skin folds, and between the digits, in particular. Whereas adults will commonly include findings in the groin or axilla (aka armpits)-sexual activity and the resultant close body contact is a culprit. The bug can spread throughout a household and family as cramped quarters or shared bedding (of an infested person) are possible sources of transmission. Vigorous scratching can introduce a secondary infection.

Traditionally, the mite is spread via protracted exposure to direct, skin-to-skin contact of an infected person. Nursing homes and other crowded conditions of close proximity like prisons or child care facilities- as per the CDC - can serve to accelerate spread. Anyone can contract scabies as it may even be spread before symptoms arise.

The form described in this recent hospital outbreak was stated to be of the crusted variety which tends to afflict those who are profoundly immune suppressed, elderly or bed-ridden due to disabling diseases. This type tends to be spread more easily on more limited exposure being able to contaminate inanimate objects like linens and towels. Aggressive treatment is vital to avoiding outbreaks. (Review scabies in detail here)

Head Lice impacts an estimated 6-12 million children ages 3-11 years old in the United States annually, according to the CDC. Spread is due to head-to-head contact as the lice feed off the blood of the scalp. Live lice or the nits are typically found in the scalp, the nape of the neck and behind the ears being the highest real estate. Like scabies, they can be an even bigger menace at night. Eyelashes and eyebrows are less common locales.

Pin Worms, an intestinal parasite,are another joy of parenting as they tend to impact children-though parents rarely acquire them, household contacts and caregivers are fair game. They are very small, white threadlike worms that prefer to come out of the anus at night and lay their eggs. It is possible for them to linger in bedding, clothing etc.. Common and not particularly virulent-though undesirable-they shouldn't be feared as treatment is swift and typically easy. Reinfection not unlikely. Intense perianal itching is a suspicious sign. The route of spread is fecal-oral, so proper hand washing is key for avoiding these and many infections. For instance, someone can ingest pinworm eggs by unwittingly putting them in their mouth or through contaminated items.

Bites from mosquitoescan be another source of itching. Your body tends to release histamine at the site of the offending agent, hence, why we itch. This is more pronounced in some people than others. Scratching, like in all similar itching conditions, can introduce further infection. Ticks prefer to ascend and are attracted to hairy, moist locations-like the genitals or groin, axilla, and scalp. They can also spread disease, so discussing any and all bite forms with your doctor is always advisable for prevention purposes and the avoidance of further complication.
In conclusion...
The take home message: If you are restless-especially at night, itching or discover any bites, a discussion with and potential evaluation by your doctor is always the safest bet.

Sweet dreams! Don't let the bed bugs bite. Will get into those another time, I think you have endured enough.

By Jamie Wells, M.D.

Dr. Jamie Wells, MD, FAAP, is an award-winning Board-Certified physician with over a decade of experience caring for patients and the Director of Medicine at the American Council on Science and Health. She served as a Clinical Instructor/Attending at NYU Langone, Mt. Sinai-Beth Israel and St. Vincent's Medical Centers in Manhattan. Dr. Wells graduated from Yale University with honors, was inducted as a junior and elected President of Jefferson Medical College's Alpha Omega Alpha National Medical Honor Society and has been named a New York Super Doctor, repeatedly, in the NY Times magazine supplement listing the top 5% of physicians in over 30 medical specialties as chosen by their peers. A National Merit Scholar, Dr. Wells was identified for her academic excellence early on when she was selected by the Center for Excellence in Education (CEE) for its prestigious Research Science Institute (RSI) and was featured as one of the top twenty high school students in the nation in USA TODAY as a recipient of their scholarship. At Yale, she was President of the Yale Science and Engineering Association, majored in American Studies and concentrated in media and film, spending her final year researching her senior essay entitled, "Ebola: The Making of an Epidemic"-- exploring the power of the governmental, political, public health and media machines and their desire to work in harmony when there is a common economic concern. In medical school, she maintained various leadership and elected positions (such as Editorials Editor of the school paper and editing guides to passing Board Exams) while creating mentoring and tutoring programs and spearheading countless volunteer activities that served the school and local Philadelphia communities. During this time, she did research for the Department of Neurosurgery at the University of Pennsylvania School of Medicine in deep brain stimulation of the subthalamic nucleus of patients with Essential Tremor and Parkinson's Disease. She was a grant reviewer for Komen's 2018-2019 Community Grants Program and has judged the local, district and world championships for Dean Kamen's F.I.R.S.T. (For Inspiration & Recognition of Science & Technology) robotics competition as well as the Miss America's Outstanding Teen scholarship competition for which she was recently nominated and, subsequently, elected to be a member of its Board of Directors. Dr. Wells is on the Leadership Council of The Wistar Institute (the nation's first independent biomedical research facility and certified cancer center). She has been awarded America's Top Pediatricians, America's Top Physicians Honors of Distinction and Excellence, Compassionate Doctors Award, Patients Choice Award (honors given by patients to less than 3% of the nation's 720,000 active physicians) and been recognized for her exemplary care of those with Cystic Fibrosis. Dr. Wells was named a Doctor of Excellence which profiles the world's leading doctors who have demonstrated success and leadership in their profession. For the better part of a decade, she answered all of the medical inquiries on line for the Boomer Esiason Cystic Fibrosis Foundation's website in a section entitled, ASK DR. WELLS. Whether she is published, for example, in the acclaimed journal Neoreviews for a case involving a near drowning of an infant via water birth, USA Today regarding the mysterious illness of US diplomats in Cuba or the Huffington Post in response to the Dolce & Gabbana controversy or 10 ways to Save Your Life or the Life of a Loved One, it is a longstanding passion of hers to make science and health understanding accessible to all. She champions empowering others to be their own advocate in healthcare and has given talks to various audiences from struggling expectant mothers and parenting groups to undergraduates, spoken on panels as well as emphasized education to patients under her care. Believing she wanted to be a brain surgeon, she began her first residency in neurosurgery, ultimately switching fields to pediatrics. As a result, her knowledge is vast in the medical realm and sought after by innumerable media outlets. Dr. Wells' greatest asset is making complicated material palatable for people in a nonthreatening, often humorous way. Her opinion as a medical expert has been showcased on live and taped local, national and international television programs that run the gamut from CNN, Fox National News Channel, ABC News, BBC, Reuters, Al Jazeera TV, NY 1, CBS, TLC, Fox Business Network, Fox 5, Parent TV, CUNY-TV, My 9, Arise TV and so on having been featured in an hour length show on Discovery Health and, repeatedly, on Sirius Radio for Martha Stewart Living. She is a huge proponent of the health benefits of animals and was certified with her adorable and gifted English Bulldog, Mollie Joe, as a therapy team. We asked New York City to guess her profession and no one got it right:

If you want to reach her by email: jamie@acsh.org

A small sample of her media appearances:

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Scabies Outbreak and Things That Go Itch in the Night

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Let's be honest. It is the rare few of us who don't start empathetic itching when we even read stories about skin mite infestations or head lice, for example, let alone experience them first hand. According to the Dayton Daily News, things got all too real for 86 hospital employees at Kettering Hospital when spokesperson, Elizabeth Long, confirmed an outbreak of scabies among the staff.

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Polio and the last surviving iron lung users. 

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Polio and the last surviving iron lung users. 

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In class, we went over polio which is a viral disease that reached pandemic levels levels in the 1950's. Once infected with the virus it can enter your blood stream. From your blood stream it can enter your central nervous system (CNS) where it has a high affinity for motor nerve cells. As the virus replicates in nerve cells the nerve cells die and it causes paralysis. often with paralytic polio respiratory failure was common due to paralyzed chest wall muscles. A Dallas attorney is one of the last people in the untied states who uses an out dated mechanical ventilator called the iron lung. Because his lungs our too weak for modern ventilators he is still confined to the iron lung which uses positive and negative pressure to allows him to breath.

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Attorney Paul Alexander looks out from inside his iron lung at his home in Dallas on Friday, April 27.

By MARC RAMIREZ, The Dallas Morning News

DALLAS (AP) - The machine is what people see first. The submarine-like metal cylinder dominates the room, rhythmically humming and pulsating as it helps keep Paul Alexander alive.

The Dallas Morning News reports it is simple but effective: A big tube, a motor, a moving arm. As the paralyzed Dallas lawyer lies inside, his head protrudes from a velvety, airtight closure at one end, propped on a pillow on a height-adjusted table.

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Alexander has spent much of his life in a can, a childhood victim of a once-epidemic disease that menaced the nation and now leaves him at the mercy of a mechanical respirator. Though unable to move from the neck down, he refused to be limited by his metal prison, finding success in both the classroom and the courtroom.

At the University of Texas at Austin, where he earned his bachelor's and law degrees, students crowded his open dorm door and gawked. Later, clients visiting his home waited awhile before they ultimately asked: What is that thing you're in? Is it a sauna?

No, he would say. It's an iron lung. I had polio as a kid.

Then, some would ask: What's polio?

No one makes iron lungs anymore. Barely a handful of people still use the hulking respirators, which apply negative pressure to enable breathing for those unable to do so on their own.

Alexander, 72, is among the few. The semi-retired bankruptcy lawyer has been using one since he was 6, his lungs and muscles ravaged by paralytic polio. He's a living reminder of a time when fears of the crippling, infectious disease gripped the country and parents kept kids away from playmates, pools and birthday parties for so much as a sniffle.

"Polio was the horror of the day," Alexander says, his speech punctuated with clicks, wheezes and silent breaks as he pauses to gulp in air. "It was like the Black Plague."

The disease destroys nerve cells in the spinal cord. It spread silently, explained Steve Cochi, senior adviser at the global immunization division of the Centers for Disease Control and Prevention. For every one person who contracted paralytic polio, another 200 might display few or no symptoms.

"It was a disease that terrorized a community," Cochi said. Its most famous victim was President Franklin D. Roosevelt.

Until 1955, when Jonas Salk became a hero by developing the vaccine that would largely eradicate the disease globally, polio reached pandemic levels. The worst year was 1952, according to PolioToday.org, with nearly 58,000 reported cases causing 3,100 deaths and leaving more than 21,000 in varying stages of paralysis.

That summer, on a hot and rainy day, 6-year-old Paul Alexander was playing outside his Pleasant Grove home, when he suddenly felt like going back inside.

As he walked in, dripping and muddy, he said, he let the screen door slam - an act that would normally draw scolding from his mom, who was mopping the kitchen.

Instead, she saw him and her face froze. "Oh, my God," he remembers her saying.

She told Paul to run out and get his shoes. When he came back in, she cleaned him up and told him to go to bed.

"She knew instantly," he says. He still wonders how.

He was pampered. His parents brought him crayons and coloring books featuring his beloved cowboys. It was pretty great, though he had the sense something wasn't right. And so he colored, page after page, like there would be no tomorrow.

Inside his canary-yellow machine in his Love Field-area home, Alexander's rigid body lies under a white sheet, fingernails long as talons and resting on his chest. He depends on a caregiver to help him eat, wash his face in the morning, brush his teeth and shave. He can be bathed, or his sheets adjusted, through portholes on the machine's sides.

On the table, his head is ringed by technology linking him to the outside world - a computer, a pushbutton telephone, an Amazon Echo. What's the Echo for? He grins. "Rock 'n' roll," he says.

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Closer to Alexander's face, a straw pokes from a tall water cup; on his chin rests one end of a long, plastic T-square-like implement that he operates with his mouth, pecking out emails or answering and hanging up the phone.

It's been about 30 years since his longtime caretaker, Kathryn Gaines, answered Alexander's newspaper ad: "Disabled professional seeking part-time help."

When other caretakers flaked, she stepped up. Eventually, she moved in.

For 15 years they lived together, then Gaines moved next door, and now she lives down the block. "We just kind of get along," she says. "I haven't killed him yet."

One typical morning, she showed up at 7, Alexander's human alarm clock, and gathered the implements of his morning routine, starting with a toothbrush, a metal bowl and a glass of water.

Gaines brushed his front teeth, then let Alexander take over as he worked the brush around his back teeth with practiced movements. She put the straw to his mouth; he took a swig from the glass and swirled before ejecting the wash back through the straw into the metal bowl.

Similar routines followed as she rubbed his face with a wet towel and lathered him up for a shave, the two reading each other's body language.

Like an old married couple, they've had their moments, but Gaines has proved reliable where others haven't.

"People need people," she says.

As young Paul's polio set in, his back and neck stiffened and pain shot through his limbs; by the next day, he said, he was hallucinating, with a high fever. By week's end, he was too weak to sit on the toilet.

"My hands were gone," he says. "I couldn't color."

The family had kept Paul home after their doctor suggested he'd be better off recovering there than at a hospital teeming with sick kids. But when the practically immobile boy had trouble breathing, it seemed he wouldn't be among the lucky ones whose symptoms eventually passed.

He was rushed to the hospital, where he underwent a tracheotomy and woke up in a plastic, steam-filled tent. By then, he was already in an iron lung, with no idea what was happening. "I figured I'd gone to hell," he says.

Doctors tried to get him to breathe on his own, but their sink-or-swim methods were terrifying to him and unsuccessful. It would be 18 months before he went home, paralyzed from the neck down.

With the help of a physical therapist, Paul gradually overcame fears of breathing on his own and learned to gulp for air - "kind of like a fish," he says. "I was using my throat muscles and my tongue to gulp in breath and swallow it into my lungs."

Motivated by the prospect of a puppy, he learned to breathe for three minutes at a time, and eventually for much of his waking day. "It's exhausting," he says. "People think I'm chewing gum. I've developed it into an art."

But for a boy who wanted nothing more than to go to school, it was a turning point.

"I knew that was the road to a future," he says. "To become something."

Iron lungs haven't been mass-produced for half a century, and insurance stopped covering Alexander's repairs long ago. His chest muscles too damaged to use the portable ventilators that have become common for others with breathing issues, he's dependent on a nearly obsolete machine.

When his iron lung began to leak air several years ago and he found it hard to breathe, he didn't know whom to call.

Around the same time, Brady Richard, whose boyhood how-does-this-work curiosity led him to launch Environmental Testing Laboratory in northwest Dallas, was trying to cobble together a working iron lung from the shells of others abandoned in a nearby workshop.

"I like old stuff, so I read up on it," he says, not knowing who might need it.

About a month later, a woman came into Richard's business, which tests machinery and technology under simulated weather and seismic conditions, and asked if he had any iron lungs. A guy she knew named Paul Alexander really needed one.

Alexander's existing machine was "flat worn out," Richard says.

Using existing parts and a few he crafted himself, Richard eventually replaced it with another. The key was figuring out how the machine worked, its bellows moving back and forth to create a vacuum that makes the user's chest expand.

He's tried it himself. "It's a weird feeling," he says.

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He's fascinated by the machine's beautiful simplicity.

"It's basic and bulletproof," he says. "There's no chips, no electronics. It's built to run forever."

But for Alexander, its purpose is singularly crucial. Without it, he'd eventually run out of breath.

In 2008, a Tennessee woman who'd used an iron lung for 60 years died after a power failure deactivated her machine. Earlier this year, Alexander's own electricity went out temporarily.

"That's how close I walk the line between life and death," he says.

One of the Dallas Independent School District's first homeschooled students, Alexander learned to memorize instead of taking notes. He graduated second in his class from W.W. Samuell High in 1967 - "The only reason I didn't get first," he said, "is because I couldn't do the biology lab."

Next came Southern Methodist University, where he got around with the help of volunteers from Alpha Phi Omega fraternity before transferring to UT, along with his iron lung. There, he earned his bachelor's degree in 1978, then his law degree in 1984.

He spent his career practicing family law and helping people filing for bankruptcy fight off creditors.

He was more flexible then. His 125-pound body has since stiffened, and he's unable to use a wheelchair as he once did, a situation he hopes to correct with surgery so he can return to lawyering.

He admits to one great love, an SMU classmate whom he says he couldn't allow himself to commit to because it didn't feel fair. "You like to dance," he says he told her. "But I can't dance with you, and that makes me feel bad for you."

To this day, the words he recalls her saying make him emotional: "When I'm dancing with others," she said, "in my head I'm dancing with you."

That's among the tales he wants to share in a book he hopes to self-publish - an autobiography, but also a plea to Americans to make sure polio never returns.

In the two years before Salk's vaccine was widely available, the average number of U.S. polio cases topped 45,000. By 1962, it had fallen to 910. Today, the CDC's Cochi says, polio is nearly gone: Only eight cases, all thought to be connected, have been reported in 2018, in Afghanistan and neighboring Pakistan.

But until it's fully wiped out, he says, "this disease can come back with a vengeance. As long as there's polio virus circulating in the world, everyone is at risk."

That's a prospect that horrifies Alexander as growing numbers of U.S. parents refrain from vaccinating their kids. What if just one affected person were to make it into the country?

When he was younger, some tried to discourage Alexander from imagining he could accomplish what he's done, and occasionally, he's faced those demons himself.

"Why did God let this happen to me?" he's wondered. "I would get so angry with him. I won't accept for a single moment that Paul Alexander is not good enough to stand before God and ask, 'Why? What'd you do this for?'"

Faith powers him onward, and he credits his motivation to succeed to a spirit of defiance and, most of all, to his late parents, whom he describes as "extraordinary souls. Magical."

"They just loved me," he says. "They said, 'You can do anything.' And I believed it."

Information from: The Dallas Morning News, http://www.dallasnews.com

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Dallas Attorney, 72, Who Survived Polio Lives in Iron Lung

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Attorney Paul Alexander looks out from inside his iron lung at his home in Dallas on Friday, April 27. By MARC RAMIREZ, The Dallas Morning News DALLAS (AP) - The machine is what people see first. The submarine-like metal cylinder dominates the room, rhythmically humming and pulsating as it helps keep Paul Alexander alive.

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A 20-year-old woman in Dallas, Tex., rushed to the hospital after waking one morning with a bumpy rash on her hands, arms, legs, scalp and torso. She was later informed the unusual skin lesions were caused by a sexually transmitted disease (STD).

The woman, whose case was documented last week in The New England Journal of Medicine, arrived at the University of Texas Southwestern Medical Center in Dallas with muscle aches, fever and pain in both of her ankles in addition to the rash.
NUMBER OF AMERICAN ADULTS NOT HAVING SEX REACHES ALL-TIME HIGH, REPORT SAYS
After a series of tests, the woman, who has not been identified publically, was diagnosed with gonorrhea - an STD that most commonly affects those aged 15 to 24, per the Centers for Disease Control and Prevention (CDC). The woman reportedly told doctors she had unprotected sex with a new partner a couple of weeks before experiencing symptoms.

"There was mild swelling and pain with passive motion in the right ankle and tenosynovitis involving the tendons of both ankles," doctors wrote in the case review, noting there was "high suspicion for disseminated gonococcal infection" before tests officially confirmed that was the case.

Gonorrhea - colloquially referred to as "the clap" - is an STD that can affect both men and women, typically causing "infections in the genitals, rectum and throat," the CDC says. Most people become infected with gonorrhea after having intercourse with someone who has the disease.

Men who have the STD can experience a burning sensation when urinating, discharge from the penis (it's usually green, yellow or white in color) and swollen testicles. For women, however, symptoms are less obvious - if they're apparent at all.

"Even when a woman has symptoms, they are often mild and can be mistaken for a bladder or vaginal infection," the federal health agency says, noting women with gonorrhea "are at risk of developing serious complications from the infection, even if they don't have any symptoms."
JIM CARREY PENS ARIANA GRANDE SWEET MESSAGE AFTER SINGER SHARES DEPRESSION QUOTE
If a woman does experience symptoms, however, they typically include a burning sensation when peeing, increased vaginal discharge and bleeding between periods, among other signs.

The disease can cause serious complications if left untreated. The gonorrhea bacterium is capable of spreading through an untreated person's bloodstream and eventually infecting other parts of their body, causing joint pain and a skin rash, much like the woman experienced, according to the Mayo Clinic. If the disease is left untreated altogether, it can also lead to infertility in both men and women.

As for the Texas woman, she was prescribed antibiotics to rid her of the infection. Three months later, she was "feeling well, with no recurrence of skin lesions or joint pain," the doctors said.

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Texas woman receives gonorrhea diagnosis after rash erupts on hands, body

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A 20-year-old woman in Dallas, Tex., rushed to the hospital after waking one morning with a bumpy rash on her arms, legs, scalp and torso - and was soon after informed her unusual skin lesions were caused by a sexually transmitted disease (STD) that can cause serious complications if left untreated.

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Angelina Salvo
A warning has hit the local media in Colorado about the dangers of the kissing bug. The Reduviid bug, better known as the kissing bug is directly linked to the spread of Changas'  Disease, or American Trypanosomiasis. Changas' was predominantly found in tropical countries but has found its way into the U.S.  It has a tendency to bite humans after feeding on various mammals such as rodents. The feces carried on the bugs feet is then left In the new portal of entry and itching or scratching causing the infection to spread.  If left untreated or undiagnosed heart damage may occur in young children.  Esophageal damage leading to difficulty swallowing is also another effect of prolong exposure to trypanosoma. This relates to the microbial Diseases of the cardiovascular and lymphatic systems covered in chapter 23, but hits a little to close to home.

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FORT COLLINS, Colo. - A blood-sucking bug that can spread disease and is nicknamed for biting people around their mouths has been sighted in Colorado.

The Coloradoan reports the Centers for Disease Control and Prevention says the "kissing bug," or Triatoma sanguisuga, has been making its way into the U.S. from South and Central America.

The bugs' bite is often painless, but the insect can pass parasites though their feces that cause Chagas' disease.

The CDC says the disease can be deadly, but it usually causes symptoms that include severe redness, itching, swelling, welts and hives.

The insect usually has a band around the edge of the body that is striped with orange or red markings. It looks similar to the box elder bug that's commonly found in Colorado.

Trademark and Copyright 2019 The Associated Press. All rights reserved.

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CDC warns blood-sucking 'kissing bug' sighted in Colorado

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FORT COLLINS, Colo. - A blood-sucking bug that can spread disease and is nicknamed for biting people around their mouths has been sighted in Colorado. The Coloradoan reports the Centers for Disease Control and Prevention says the "kissing bug," or Triatoma sanguisuga, has been making its way into the U.S.

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Gas Gangrene The bacteria disease Gas Gangrene caused by Clostridium perfringens is a spore-forming Gram-positive anaerobe bacterium.  The bacterium is found in soil and in the gut some animal. The bacteria ability to cause gas gangrene is to the production a protein toxin. Gas gangrene is a disease that occur in compromised individual such as, muscle injuries, severely damaged tissues, wounds that are very deep, and wounds that are contaminated with stool or dirt, especially those that might occur on a farm. Gas gangrene is a disease which affects the muscle and is often referred to as clostridial myonecrosis. Severe traumatic that damage the circulatory system has poor blood flow and low oxygen to the affected area. Smoking also plays a factor in poorly oxygenated tissues. Gas Gangrene can spread into surrounding tissues if the blood supply into these tissues is reduced and if the ability of the host to raise an inflammatory response involving phagocytes is suppressed. The infection can spread rapidly from healthy tissues, and an entire limb may become gangrenous within the space of a few hours.  Amputation of the infected limb or removal of all the infected tissues is the only effective treatment. Therefore, without some type of treatment, the toxins produced by the bacteria will eventually kill the patient.  Flora Colson

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Gas Gangrene The bacteria disease Gas Gangrene caused by Clostridium perfringens is a spore-forming Gram-positive anaerobe bacterium.  The bacterium is found in soil and in the gut some animal. The bacteria ability to cause gas gangrene is to the production a protein toxin. Gas gangrene is a disease that occur in compromised individual such as, muscle injuries, severely damaged tissues, wounds that are very deep, and wounds that are contaminated with stool or dirt, especially those that might occur on a farm. Gas gangrene is a disease which affects the muscle and is often referred to as clostridial myonecrosis. Severe traumatic that damage the circulatory system has poor blood flow and low oxygen to the affected area. Smoking also plays a factor in poorly oxygenated tissues. Gas Gangrene can spread into surrounding tissues if the blood supply into these tissues is reduced and if the ability of the host to raise an inflammatory response involving phagocytes is suppressed. The infection can spread rapidly from healthy tissues, and an entire limb may become gangrenous within the space of a few hours.  Amputation of the infected limb or removal of all the infected tissues is the only effective treatment. Therefore, without some type of treatment, the toxins produced by the bacteria will eventually kill the patient.  Flora Colson

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Walckenaer E, Poirel L, Leflon-Guibout V, et al.

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Normandi Guarienti THE RESURGENCE OF CHICKENPOX

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Normandi Guarienti THE RESURGENCE OF CHICKENPOX

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Many years ago chickenpox seemed to be a common outbreak in which effected populations. In the 2900's vaccines were created in order to stop the outbreaks of killing off populations and protect the people. For this wiki I chose to google recent outbreaks of chickenpox's. One of the main causes for recent outbreaks is the cause of people who do not vaccinate their children. Of course even in recent outbreaks the symptoms are the same initially with fever, malaise, fatigue, and a headache, followed by an itchy, full-body rash. Earlier this week, there was a chickenpox outbreak in Asheville, North Carolina. North Carolina is the largest state that has seen since the creation of a vaccine. The case count currently stands at 36, up from 28 at the beginning of November. This outbreak is centered around the Asheville Walford School, a private school with the highest religious vaccination exemption rate in the county.

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Despite growing international , outbreaks of vaccine-preventable diseases are becoming increasingly common worldwide. In particular, an overall rise in measles incidence in multiple countries in addition to a number of high-profile outbreaks have generated considerable media coverage. Outbreak Observatory has discussed measles on several occasions, covering topics like its reemergence in the Americas and the cost of outbreak response , and since our last post, New York has faced a large measles outbreak . However, while press reports often focus on measles, it is important to remember that outbreaks of other vaccine-preventable diseases continue to occur in places where vaccine is widely available. To that end, this week's Outbreak Thursday will discuss a recent outbreak in the United States (US) of another vaccine-preventable disease: chickenpox. Specifically, we look at the public health consequences of this outbreak and what public health officials can do to combat increased risks posed when populations choose not to vaccinate.

A Dangerous History

Chickenpox is caused by the varicella zoster virus, a kind of herpesvirus. It initially with fever, malaise, fatigue, and a headache, followed by an itchy, full-body rash. The rash then turns into fluid-filled blisters, which then scab and fall off. The disease is spread through contact with the fluid inside the blisters as well as through coughing and sneezing. The varicella zoster vaccine has been publicly available in the United States since 1996. Since , the US Advisory Committee on Immunization Practices (ACIP) has recommended that children and any other healthy individuals with no evidence of immunity to chickenpox receive 2 doses of vaccine. Routine childhood vaccination includes the first dose at age 12-15 months and the second dose at 4-6 years. Overall, vaccine coverage for varicella vaccine is high in the United States: the CDC reports that in 2017 , the percentage of teens with no history of varicella disease who had received 2 or more doses of vaccine was 88.6%. But there are variations in coverage between states and within states, and pockets of low vaccination coverage increases the risk of outbreaks.

Prior to the release of a varicella vaccine, chickenpox was a common childhood disease. Each year, it sickened a new cohort of children, such that by the time that individuals reached adulthood, most had been infected at some point or another and acquired immunity. While once a common childhood affliction, chickenpox was not necessarily the harmless rite of passage that many perceive it to be. Infected individuals were at risk for developing severe complications , such as infections of the blisters, pneumonia, and encephalitis. Prior to the availability of a vaccine, an estimated 11,000 Americans were hospitalized each year due to chickenpox. The US CDC reports that an average of 103 deaths due to chickenpox were reported each year between 1990 and 1996. Interestingly, most deaths occur in immunocompetent children and adults. Since the development of the vaccine, however, hospitalizations and deaths associated with chickenpox have fallen by more than 70% and 88%, respectively.

Beyond the typical complications, chickenpox can produce other serious outcomes. For example, , a disease caused by the reactivation of dormant varicella zoster virus. Shingles is a painful condition that can affect anyone who has had chickenpox, but immunosuppressed and elderly individuals are at the highest risk. In 2017, the US FDA approved a second vaccine for shingles, which is now the preferred vaccine for for use in individuals over 50 years of age .

Chickenpox Outbreaks in the US

Earlier this week, a chickenpox outbreak in Asheville, North Carolina became the largest the state has seen since the creation of a vaccine. The case count currently stands at 36, up from 28 at the beginning of November. Notably, this outbreak is centered around the Asheville Walford School, a private school with the highest religious vaccination exemption rate in the county. Although North Carolina requires 2 doses of varicella vaccine for children entering kindergarten, it for medical and religious exemptions. Medical exemptions require the completion of a form by a physician licensed in North Carolina; however, religious exemptions only require the submission of a parental written statement, which does not need to be "notarized, signed by a religious leader, or prepared by an attorney". This outbreak has once again rekindled the debate over mandatory vaccinations. So far, the Buncombe County Medical Director has taken a firm stance against those who decline to vaccinate, stating, "We want to be clear: vaccination is the best protection from chickenpox."

This is not the first time North Carolina has experienced a chickenpox outbreak. In 2006, an occurred in Yadkin County, just 2 hours from Buncombe County. The outbreak affected at least 50 children across 3 elementary schools and caused one death.

North Carolina is not alone. From August 2015 to January 2014, 89 outbreaks of chicke npox were re ported to the , with the majority of cases occurring among unvaccinated individuals. In 2017, the state of reported 390 cases of chickenpox-the highest number of cases since 2013-most of which occurred in private or charter schools with lower vaccination rates. More recently, a primary school in Washington state saw 5 confirmed cases of chickenpox. In response, the local health department required any students without proof of immunization to stay home for 3 weeks.

Proposed Strategies for Encouraging Vaccination

Though childhood vaccine coverage in the US remains high , significant outbreaks of vaccine-preventable diseases continue to occur, in part due to parents' hesitancy or refusal to vaccinate their children . In understanding how to develop strategies to increase vaccine coverage, it is important to recognize that there is no one type of "anti-vaxxer." Rather, the reasons why people do not vaccinate may vary considerably. Parents' concerns about vaccine safety is often discussed as a contributing factor, but perceptions of low vaccine efficacy may be another reason why parents choose not to vaccinate their children. As one study points out , people may differ in how they perceive risks-eg, some may favor "natural risks" (disease) over perceived unnatural risks (vaccines). Access to vaccines and costs associated with vaccination have also been identified as important factors in vaccine coverage.

Clinicians can also play an important role in parents' decisions regarding vaccination. In , parents who changed their minds about either delaying or refusing a vaccination for their child listed "information or assurances from health care provider" as the main reason. In light of this, some researchers have begun to investigate strategies that best enable clinicians to encourage parents to vaccinate their children. Various approaches have been proposed, but studies have had mixed results with respect to the success of these approaches. Additional research is needed on this front to better equip clinicians to address the complex challenges surrounding vaccine hesitancy and reluctance among parents.

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Despite growing international , outbreaks of vaccine-preventable diseases are becoming increasingly common worldwide. In particular, an overall rise in measles incidence in multiple countries in addition to a number of high-profile outbreaks have generated considerable media coverage.

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Risks vs benefits of the rabies vaccine 

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Risks vs benefits of the rabies vaccine 

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The rabies vaccine is routinely given to animals and those who are considered high risk for contact like veterinary workers, however normally not given otherwise unless exposure occurs. The unusually long incubation period of the disease makes the vaccine effective when given after exposure, but carries a higher risk of side effects than some other vaccines. The following article discusses why the rabies vaccine is more beneficial when used on this case by case basis rather than routinely given. https://www.quora.com/Why-dont-humans-get-anti-rabies-vaccinations-since-rabies-is-nearly-100-fatal

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There is currently a vaccine for conjunctiva (pink eye) in cattle. This was developed because of how quickly it spreads through a heard of cattle. It's a dose of 2ml IM into the neck before any onset of pinkeye. In the future this could help us develop a vaccination for humans. Especially for young children where this infection is most common.

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In class we talked about Rubella also known as the German Measles. Rubella is a virus which causes a fever, respiratory problems, and a rash of pinkish red-ish spots. It can cause mild symptoms but it also causes arthritis, encephalitis, and neuritis. I thought that this article was interesting because the website gave a little bit of history about the vaccine to help prevent rubella. The article explains that the first Rubella vaccine was created in 1969 and was used in combination with the measles and mumps vaccine. Ten years later in 1979, Plotkin developed the RA27/3 vaccine which has now offered protection against the disease and has replaced the original Rubella vaccine. It is still used today and is recommended by doctors in the United States.

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In chapter one we briefly discussed what the rabies virus is. I recently did some more research on the virus and feel the need to talk about some interesting facts. Most cases of rabies come from wild animals such as bats, foxes, skunks, and raccoons. This virus begins with your basic symptoms such as fever and headache then progresses to anxiety, confusing and some paralysis. When bitten the amount of saliva also increases this is why we see foaming at the mouth. The rabies virus when in the system will act very carefully making sure the immune system doesn't notice any changes. On the many downsides to rabies one the saddest things is possibly having to euthanize your animal if infected by the virus.

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Rabies is a fatal but preventable viral disease. It can spread to people and pets if they are bitten or scratched by a rabid animal. In the United States, rabies is mostly found in wild animals like bats, raccoons, skunks, and foxes. However, in many other countries dogs still carry rabies, and most rabies deaths in people around the world are caused by dog bites.

The rabies virus infects the central nervous system. If a person does not receive the appropriate medical care after a potential rabies exposure, the virus can cause disease in the brain, ultimately resulting in death. Rabies can be prevented by vaccinating pets, staying away from wildlife, and seeking medical care after potential exposures before symptoms start.

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history of rabies; signs of rabies; symptoms of rabies; effects of rabies; human rabies vaccine; rabies vaccine; rabies symptoms; treatments for rabies; rabies virus; rabies information; rabies facts; bats; dogs; cats

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Rabies is a preventable viral disease of mammals usually transmitted through the bite of an infected animal. The rabies virus infects the central nervous system; ultimately causing disease in the brain and death. Information is included on rabies basics; prevention; and more.

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In class we have talked alot about measles. I find it interesting because with the measle outbreak we can clearly see how much a vaccine can do. According to the CDC this year is highest outbreak since it was reportedly eradicated in 2000, there was also a outbreak in 2014 on smaller scale of about 300 cases. Now that their are those against vaccines, we are seeing more and more eradicated diseases coming back. There are now 22 states that have reported measles cases all adding to a number of over 600 cases total.
https://www.cdc.gov/measles/cases-outbreaks.html

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As we discussed skin disease in chapter 21, one that stuck out to me was impetigo. I had heard about it and knew the gist of it, but found it very intriguing. (and gross, but that's beside the point). In the year of 2000 there was an increase in impetigo cases. (caused by staphylococcus aureus resistance). However, an article posted by the American Society for Clinical Investigation studied the interrelation between the bacteria common with impetigo (streptococci and staphylococcus aureus).
Streptococci was recovered from 361 lesions at 21 percent, while staphylococcus at 8 percent. Streptococci were often in the beginning phase of the lesions, occurring in phases. However, the site of sequence for staphylococcus aureus spread from normal skin to skin lesions, migrating to various parts of the body. So while strep and staph are both predominant bacterial genera recovered from impetigo lesions, staphylococci are considered second invaders.

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Abstract

Intensive observations on 37 children in a population with endemic skin infections provided an opportunity to study the interrelationships between and the significance of the bacterial genera commonly associated with impetigo. Cultures of the respiratory tract, three normal skin sites, and lesions, when present, were taken three times weekly from July to October 1969. Impetigo developed in all 37 children. Group A streptococci alone were recovered from 21% of 361 lesions, Staphylococcus aureus alone from 8%, Staphylococcus epidermidis alone from 5% and mixtures of streptococci and staphylococci from 61%.

Vesicular or pustular lesions were more often pure streptococcal than pure staphylococcal. Streptococci alone were more often recovered from early stage lesions rather than from later ones. The pure staphylococcal lesions characteristically occurred early in the season whereas streptococcal or mixed lesions had later peaks.

Serial observations on 74 lesions revealed longer persistence of streptococci than staphylococci in mixed lesions. In 85% of the instances the same streptococcal serotype was recovered repeatedly from an individual lesion, whereas staphylococcal types changed in 57% of instances.

Phage type 75 accounted for the majority of staphylococcal isolates from all sites, whereas phage type 54 was recovered only from skin lesions.

In contrast to streptococci, the site sequence of staphylococcal spread was from the nose to normal skin to skin lesions.

These studies reveal important differences in the migration of staphylococci (as compared with streptococci) to various body sites and suggest a subsidiary role for staphylococci in nonbullous impetiginous lesions yielding both organisms.

Selected References

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Natural history of impetigo: II. Etiologic agents and bacterial interactions

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Intensive observations on 37 children in a population with endemic skin infections provided an opportunity to study the interrelationships between and the significance of the bacterial genera commonly associated with impetigo. Cultures of the respiratory tract, three normal skin sites, and lesions, when present, were taken three times weekly from July to October 1969.

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Mammoth Bio-sciences is making headlines again, no not for resurrecting a mammoth as has previously caused stirs in the scientific communities, but for advances in diagnostic testing that may soon bring disease testing directly to the patients home. Similar to the concept that is used for donation databases, parental, and ancestry DNA testing, using urine or saliva samples, Crispr proteins are gathered with at home testing kit that will speed up the process of identifying diseases such as HPV and Malaria by detecting viruses genetic codes.
With diagnostics being a medical field not getting much attention this is a great step in the right direction that may eventually save time and money.

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You'd be hard-pressed to read one of the many published lists of "world-changing" technologies and not spot an entry about Crispr. Scientists think the nascent gene-editing technique could eventually be used for anything from engineering disease-resistant crops to eradicating illnesses.

Another long-shot possibility: bringing back extinct animals like the woolly mammoth. That's where the year-old startup Mammoth Biosciences got its name.

Twenty-nine-year-old co-founder and CEO Trevor Martin admits that it's mostly a joke. In reality, his company's goal is much more grounded: Mammoth wants to use Crispr to simplify the process of diagnosing illnesses, which can often require several tests and days of waiting for lab results--and still isn't always accurate.

The startup is developing technology that could someday allow customers to check themselves for serious diseases. In the meantime, it's working on getting its diagnostic tests into the hands of doctors and lab technicians.

'Falling in love'

While earning his doctorate at Stanford, Martin took a course that focused on how to combine biology with other fields--math, statistics, physics, etc.--to open up new scientific possibilities. "I ended up falling in love with this idea that you could leverage different fields to create something more than the sum of its parts," he says.

Martin thought about how that concept could be applied to health care. As he saw it, the area of therapeutics was getting most of the attention in that field; far fewer companies focused on diagnostics. "It was seen as less cool," he says. "So immediately I fell in love with it."

Martin and several classmates agreed to form a company with the goal of making diagnostics faster, simpler, and more precise. They still needed a way to accomplish it. That's when they came across newly published research from Berkeley professor and Crispr co-inventor Jennifer Doudna that detailed how to use the technique for exactly that purpose.

He cold-emailed Doudna. After a few months of dialogue, Martin and his classmates officially joined forces with Doudna and several of her teammates to form Mammoth Biosciences. The startup secured a spot in an accelerator program run by early stage investor NFX Venture Capital, which also provided $3 million in seed money.

Instant gratification

Mammoth says it's developing technology that uses saliva or urine samples to nearly instantly diagnose diseases, such as malaria and HPV. Using Crispr proteins, the company creates tests that detect a virus's genetic code in a person's cells. If a disease is present in the sample, the liquid will change color, indicating a positive test.

To start, the company is focusing on integrating its product into existing lab and hospital tests to make them faster and more accurate. The long-term goal is to create consumer kits that let anyone test themselves at home. Martin isn't naive--he knows getting there will take years. The company is still pre-revenue. Mammoth will need to continue developing and refining its technology to make it scalable and simple enough to use at home, and earn approval from the FDA. It might also face stiff competition if public Crispr companies like Intellia and Editas Medicine decide to expand their focus from therapeutics to diagnostics.

For now, the 20-person company is building out a staff that can get there. "We've assembled literally the best Crispr team that you can possibly put together," says Martin. "But that's not enough. To create a diagnostic product, we need to assemble the best commercialization team as well, people who are critical to actually delivering a useful product to consumers."

Commercialization likely will mean extending beyond its own products, as Mammoth will look to license its technology to other companies. That possibility attracted Ursheet Parikh, VC at Mayfield Fund, which led Mammoth's $23 million Series A round last year. "The traditional approach that most diagnostics and therapeutics companies have taken is to try to build this walled garden where they can use the technology just for their own products," Parikh says. "With Mammoth, we see an opportunity to create a broad platform that enables hundreds of new applications."

Even though the company is starting with diagnostics, Martin won't dismiss the possibility that the company pursues some of Crispr's other potential uses, like therapies or gene editing, in the future. "We want to create products that improve people's quality of life," he says. "We're really interested in pushing the boundaries of CRISPR, seeing what is possible at the absolute limit."

Even if that doesn't mean resurrecting prehistoric beasts.

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The Future of Disease Testing Could Be a Kit That Lets You Do It Yourself in the Comfort of Your Home

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Getting tested for a disease often means waiting days--or weeks--for the results to come back, and even then they aren't always accurate. Mammoth Biosciences is using the gene-editing technique Crispr to speed up the process and make it more reliable.

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Sea Change:A normally land-based microbiologist sets sail to find the building blocks of novel antibiotics in marine bacteria.

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Sea Change:A normally land-based microbiologist sets sail to find the building blocks of novel antibiotics in marine bacteria.

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Around 25,000 people a year in Europe alone, die due to complications from antibiotic-resistant bacteria.

Microbiologists do all they can to find new synthetic chemicals and compounds that will destroy these resistant bacteria, and now they have gone a step further....They are heading out to SEA!!

William Fenical states, “Seawater has a million microbes per milliliter, with even more potential for diversity in sediment and on-shore surfaces,”...This article looks at one Microbiologist from Denmark, who is putting on her sea hat for an expedition in microbe hunting!!

Resistant bacteria are surely becoming more intense, but thankfully we have many motivated scientists in the world, that aggressively meet pathogen challenges head on!!

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THOMAS BREDOL/WWW.BREDOL.DK/PHOTO In 2006 and 2007, systems biologist Lone Gram sailed the seven seas-returning with a boatload of bacteria. Gram, a professor at the Technical University of Denmark (DTU), was a member of Galathea 3, a round-the-world research expedition that used a rebuilt Danish naval vessel as its mother ship. Her team took microbial samples from "anything that was brought on board-seaweed, sediment, deepwater sponges, Arctic ice fish . . ."

Gram and colleagues were on the hunt for new drugs-mainly antibiotic and antivirulence compounds. Most of our current antibacterial medicines are derivatives of compounds from microbes such as the mold Penicillium and Actinobacteria. However, our current arsenal of antibiotics is losing its usefulness, thanks to an upsurge in the number of resistant strains. Every year in Europe alone, antibiotic-resistant bacteria kill an estimated 25,000 people.

Drug development is experiencing a sea change, looking to the ocean for potential medicines.

To find new antibiotics, researchers have explored libraries of synthetic chemicals and compounds from land-based microorganisms. But drug development is experiencing a sea change, looking to the ocean for potential medicines. "Seawater has a million microbes per milliliter, with even more potential for diversity in sediment and on-shore surfaces," says William Fenical, director of the Center for Marine Biotechnology and Biomedicine, Scripps Institution of Oceanography. Because many marine microbes are symbiotic, they naturally produce bioactive compounds to influence the physiology of other organisms.

Gram and her research team are now exploring a collection of 1,500 marine bacterial isolates, many of which have been classified using ribosomal RNA gene sequencing. All were harvested during the Galathea 3 expedition, which was sponsored by the Danish government and named after previous marine collecting trips in 1845 and 1950. On Galathea 3, a 370-foot ship, the Vaedderen, housed more than 50 projects, studying topics from geology to history to climate change. Gram participated in several legs of the 9-month voyage, including cruises to Greenland, Australia, Antarctica, and South America. She says, "The other scientists quickly realized that our samples couldn't be contaminated-we didn't want to isolate Staphylococcus from the captain-so they gave us first access to everything."

CHRIS TACHIBANA Before the saltwater dried on their rubber boots, Gram's team put their marine samples to the test. Microbes were cultured on seawater-simulating agar plates in the shipboard container that served as the microbiology laboratory. Colonies were transferred onto plates with the bacterial fish pathogen Vibrio anguillarum. At least 3 percent of all collected bacteria inhibited pathogen growth in this test. Any that passed a second screen for antibiotic activity were immediately frozen. "It was like what Alexander Fleming did with Penicillium, but more high-throughput," says Gram.

Gram was introduced to marine microbiology through a collaboration with aquaculturists who wanted to protect fish larvae from bacterial infections without using antibiotics. She and her colleagues found that Phaeobacter gallaeciensis bacteria are probiotic: that is, they are not harmful to fish larvae themselves, but larvae fed algae laced with P. gallaeciensis are protected against pathogenic bacteria. The probiotic bacteria are in the Roseobacter clade, which is common in the ocean. Just as Gram was wondering how to get more Roseobacter to study, the Danish government put out a call for scientific projects to be conducted as part of Galathea 3.

Gram wrote a modest application to collect marine bacteria on just two of the expedition's eighteen legs. She received a two-sentence letter granting her space on the entire journey. "I was euphoric for 12 hours," she recalls, "then realized I'd never worked at sea; never done marine experiments; and never equipped such a project." Nine months of frantic planning ensued. Fortunately, postdoctoral fellow Jesper Bruhn, faculty members Jørn Smedsgaard and Kristian Fog Nielsen, and laboratory manager Ellen Kirstine Lyhne, all from DTU, signed up to work expedition legs when Gram needed to be in Denmark for teaching and other faculty duties.

Back on land, the researchers figured out how to grow the microbes, then started characterizing the bioactive compounds they produced. So far, in addition to several already identified antibiotics, the scientists have identified new antivirulence compounds. These don't kill pathogenic bacteria but reduce their disease-causing potential, for example by preventing them from producing toxins. Gram's bacterial collection has yielded two novel compounds that interfere with the pathogenicity of Staphylococcus aureus and a third that blunts the bite of Pseudomonas aeruginosa, which is particularly dangerous for people who are immunocompromised.

I was euphoric for 12 hours, then realized I'd never worked at sea; never done marine experiments; and never equipped such a project.-Lone Gram
Technical University of Denmark

DTU postdoctoral researchers Nikolaj Vynne and Maria Månsson are trying to spur bacteria that produce antibiotics and antivirulence compounds to diversify their output. Genetic analysis hints that some of the bacteria might harbor the ability to make additional compounds, because they have more genes for making bioactive products, such as nonribosomal peptides and organic molecule polyketides, than are required to make the molecules they currently produce. Such additional genes could just be waiting for the researchers to find conditions that unleash novel pathways.

As for Gram, her seafaring days might not be over. She is now part of an explorer-scientist network that tapped her team's expertise for three additional expeditions, one to northeastern Greenland and two to the North Pole. "We didn't sample humpback whales," she muses. "Maybe we'll get to do that on Galathea 4."

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THOMAS BREDOL/WWW.BREDOL.DK/PHOTO In 2006 and 2007, systems biologist Lone Gram sailed the seven seas-returning with a boatload of bacteria. Gram, a professor at the Technical University of Denmark (DTU), was a member of Galathea 3, a round-the-world research expedition that used a rebuilt Danish naval vessel as its mother ship.

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There is a crazy pull between religious beliefs and sciences understanding and stance on vaccination. There has been an extreme outbreak of measles in New York, more specifically within a Jewish community. The jewish community is under attack because their religious stance is not to vaccinate. Other city residents believe these zip codes should face consequences/ the law should come down more strictly if unvaccinated because of the exponential spread/growth rate of measles case. So this article was interesting to me, because the battle of religion/law/health is sticky.

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An order to require immunizations in the ultra-Orthodox Jewish community seemed to mobilize vaccine skeptics. Others worried that the effort did not address the root of the problem: misinformation.

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In Williamsburg, one of the areas of Brooklyn where unvaccinated individuals are required to receive the measles vaccine under a public health emergency declared this week. Credit Credit John Taggart for The New York Times

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Vaccine skeptics were planning a lawsuit against New York City. A Hasidic woman was heckled when she boarded a public bus. Family members were avoiding weddings for fear of encountering unvaccinated relatives.

When Mayor Bill de Blasio announced on Tuesday an emergency health order requiring measles vaccinations, he said the step was necessary to curtail the large measles outbreak in the ultra-Orthodox Jewish community. But as health officials plunged into Brooklyn's Williamsburg neighborhood to enforce the mandate, tensions only escalated.

Mr. de Blasio's effort seemed to mobilize an already well-organized network of vaccine skeptics. Their latest tactic: circulating court affidavits for community members to sign so they can express opposition to mandatory vaccinations ahead of a planned lawsuit.

"I am a religious Jew, whose religious convictions are being blatantly violated by the vaccine Diktats, which are a clear violation of the Nuremberg Code, which forbids forcing medical procedures on anyone without their fully-informed consent," the form says.

It continues: "Childhood diseases, like measles and chickenpox, unlike smallpox and ebola, are not a legitimate public health menace, and do not justify an emergency declaration."

On Tuesday, Mr. de Blasio said unvaccinated residents in certain ZIP codes in Brooklyn must receive a measles vaccination or face a $1,000 fine. The next day, 20 city health inspectors began auditing vaccination records at yeshivas, and 15 disease detectives started interviewing those who had potentially been exposed to the highly contagious virus, the Health Department said.

But many who support vaccines say they worry that the city is missing the mark by not addressing the crucial issue: the misinformation flooding Hasidic communities that tells them to be wary of vaccines. Literature and hotlines spread debunked theories about immunizations, falsely warning that they cause autism and lead to other health problems.

Blima Marcus, an ultra-Orthodox nurse practitioner at Memorial Sloan Kettering Cancer Center, said she understood the city's actions, but she raised concerns about whether they would be effective. In the last week alone, 60 new cases of measles were confirmed in New York City, according to the Centers for Disease Control and Prevention, and suburban Westchester County reported its first eight cases.

"It's a public health problem," Ms. Marcus said. "But ultimately, I don't think it will help in the long term because this doesn't get to the root of the problem, which is widespread misinformation and no corresponding education."

Ms. Marcus said she and other Hasidic health professionals were putting the finishing touches on a pro-vaccination magazine and creating a hotline to dispel myths promulgated by the anti-vaccine movement. The magazine, which will be called Parents Informed and Educated, or Pie, is a direct response to Peach, a 40-page publication that is a main vehicle of misinformation.

"We're seeing a lot more interest in people wanting to get involved," Ms. Marcus said. "They're really angry at the anti-vax movement. They're ashamed."

City officials say countering the anti-vaccine movement is a priority, and they are holding meetings with rabbis, doctors and community members. Health care providers have distributed 8,000 more vaccines between October and April than they did in the same period in the previous year, officials said.

But Dr. Peter Hotez, the director of the Texas Children's Hospital Center for Vaccine Development, echoed Ms. Marcus's concerns, saying the city's efforts could fall short.

"Unless you begin dismantling this anti-vaccine media empire, you're not going to have a big impact on any specific public health measure," he said.

In the wake of the emergency order, Jewish leaders say they fear a continued rise in anti-Semitism. In recent months, Hasidic neighborhoods have been the targets of a slew of anti-Semitic hate crimes, and Jewish leaders reported another one on Thursday.

Rabbi David Niederman, the president of the United Jewish Organizations of Williamsburg, said a city bus driver tried to refuse service to a Hasidic woman in Brooklyn. The driver eventually let the woman board, Mr. Niederman said, but then shouted "measles" at her and directed her to move to the back of the bus.

Maxwell Young, a spokesman for the Metropolitan Transportation Authority, which oversees the city's buses, said the agency was investigating the episode and had "absolutely zero tolerance for discrimination."

Mr. de Blasio's administration has also faced criticism for not reacting quickly enough to the measles outbreak, which began last fall after unvaccinated children returned from Israel.

"I don't think they moved fast enough, but now that they're moving, I'm with them," said Arthur Caplan, a bioethicist at the New York University School of Medicine.

Mr. Caplansaid that the emergency order was appropriate given the scale of the outbreak, and that he believed it would survive any legal challenges.

"There's more saber rattling here than there is restriction of liberty," he said.
Follow Tyler Pager on Twitter: @tylerpager.

A version of this article appears in print on , on Page A24 of the New York edition with the headline: Fear and Misinformation After Vaccination Order. Order Reprints | Today's Paper | Subscribe

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Tensions Rise as New York City Steps Up Response to Measles

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An order to require immunizations in the ultra-Orthodox Jewish community seemed to mobilize vaccine skeptics. Others worried that the effort did not address the root of the problem: misinformation. [What you need to know to start the day: Get New York Today in your inbox .]