julio 2017 - DERMAGIC EXPRESS / Dermatologia y Bibliografia - Dermatology & bibliography DERMAGIC EXPRESS / Dermatologia y Bibliografia - Dermatology & bibliography: julio 2017

domingo, 30 de julio de 2017

THE MINOCYCLINE IN LYME DISEASE. / LA MINOCICLINA EN LA ENFERMEDAD DE LYME



The Minocycline in the LYME DISEASE, a Terminator Antibiotic ?. 

 

La Minociclina en La ENFERMEDAD DE LYME, un Antibiotico Exterminador ?

 

 

 



 

EDITORIAL ENGLISH
===================
Hello friends of the DERMAGIC EXPRESS network today bring you a very interesting topic THE MINOCYCLE IN LYME DISEASE. First of all I will tell you once again that this is not the first time I speak of this "OLD ANTIBIOTIC" family of tetracyclines which many years ago, I repeat many years ago was discovered the ABILITY or CAPACITY to finish or destroy   many MICROORGANISMS or bacteria which scientists considered practically "INVINCIBLE" or "IMPOSSIBLE" to exterminate.

The first and perhaps most important that I will show you is THE HANSEN'S BACILLI, the MYCOBACTERIUM LEPRAE, a millenary and apocalyptic bacterium, responsible for LEPROSY mentioned in the BIBLE in the LEVITIC'S chapter , described and discovered by the scientist ARMAUER HANSEN in The year of 1.873.

This MYCOBACTERIUM was considered "INVINCIBLE" until SULPHONES appeared, (DDS) diaminodiphenylsulfone, RAFAMPICINE, and CLOFAZIMINE. I am speaking of the years 1940-1945 when these medicines appeared, which together with IMMUNOTHERAPY, decreed the closure of LEPROSERIES throughout the world wide. All this I told you in THE LEPROSY CHAPTERS.

And a few years later came the MINOCYCLINE (MINO), an antibiotic that is changing the history of the evolution of some diseases today. This antibiotic is a family of "old" TETRACYCLINES whose first antibiotic was synthesized in the year 1.940 under the name CHLORTETRACYCLINE (AUREOMYCIN) by the scientist Benjamin Minge Duggar, of LABORATORY LEDERLE.

Subsequent to this discovery, other TETRACYCLINES appeared on the market: OXYTETRACYCLINE, DEMECLOCYCLINE, LYMECYCLINE, MECLOCYCLINE. METHACYCLINE, ROLITETRACYCLINE TIGECYCLINE AND OUR "FAMOUS" MINOCYCLINE.

Specifically MINOCYCLINE (MINO) was born in 1.961 and placed on the market in the year 1.967, under the name MINOCIN, which still exists today. It's been 50 years, half a century since its discovery. Its main use was to combat ACNE bacteria, but other properties were later described.

In March 1.999, 17, I launched the article THE MINOCYCLINE, THE GOOD, THE BAD AND THE UGLY, which was published in the Dermatology's magazine of Chile, and updated on February 10, 2,017 under the name MINOCYCLINE ALZHEIMER AND OTHER NEUROLOGICAL DISORDERS, for its new uses. This means that I have 20 years talking about the benefits of this antibiotic that differentiate it from the rest of its congeneries.

In the 1980s and 1990s, MINOCYCLINE was shown to have a highly potent effect against MYCOBACTERIUM LEPRAE and several therapeutic regimens were designed in conjunction with other antibiotics such as OFLOXACINE, CLARITROMYCIN, AND AMOXYCYLIN to combat LEPROSY, references 3,4,5,6,7,8.

Recently it has been discovered its effect NEUROPROTECTOR, being used today in diseases like ALZHEIMER, PARKINSON, SCHIZOPHRENIA, BIPOLAR DISORDERS, AUTOIMMUNE ENCEPHALOMYELITIS AND MULTIPLE SCLEROSIS.

Then you'll be asking yourself "WHAT HAS" this antibiotic that THAT MAKES IT DIFFERENT FROM ITS CONGENERIES, and I'll tell you: CLEAR and SCIENTIFICALLY

1.) HAS MORE BROAD SPECTRUM THAN OTHER TETRACYCLINES.


2.) HAVE AN AVERAGE LIFETIME IN SERUM: 2 TO 4 TIMES GREATER THAN OTHER TETRACYCLINES.
 

3.) IT HAS GREATER LIPOSOLUBILITY THAN OTHER TETRACYCLINES WHICH ALLOWS IT TO HAVE GREATER PENETRATION IN THE TISSUES AS PROSTATE, BRAIN AND CENTRAL NERVOUS SYSTEM.

Are you understanding me? you are copying me? Are you feeling me ?


That is why today we have found this antibiotic with uses that the human never thought could be useful.

NOW I AM GOING TO EXPLAIN THE RELATIONSHIP OF LYME DISEASE WITH MINOCYCLINE.

If you go to review the most known DATABASES you will find that the antibiotics most used in LYME DISEASE of the group of tetracyclines are OXYTETRACYCLINE, and LATELY TIGECYCLINE, without ruling out the MINOCYCLINE. 


And the most used, family of PENICILLINS, DOXYCYCLINE, Also an old antibiotic that was born in 1.961 and came on the market in 1.967 by the laboratory PFIZER

A few days ago I read an article of a patient with LYME DISEASE who developed BELL'S Paralysis and its treatment with DOXYCYCLINE failure, they prescribed MINOCYCLINE and the patient was healthy. In many articles it appears as a first option against LYME DISEASE DOXYCYLINE, and others, but not the MINOCYCLINE, much less the  G PENICILLIN, of which I did not find almost studies.

But if you get to "DIG" well the databases you find the "SURPRISE" that MINOCYCLINE in the 80s and 90s, was discovered its effectiveness in LYME DISEASE, in fact there are also some (few) Studies where it is shown that PENICILLIN G PROCAINIC is also effective in this disease, and here comes the big question

Why ? these two antibiotics G PENICILLIN AND MINOCYCLINE (MINO) are not used as the FIRST ELECTION against LYME disease? Or in combination with others? I know that some scientists DO USE THE MINOCYCLINE, but very few or almost none of the G PENICILLIN, knowing that the BORRELIA is a SPIROQUETTE like the TREPONEMA PALLIDUM that causes SYPHIILIS and that it "DIES" with PENICILLIN.

This review I am doing to REMEMBER TO SOME SCIENTISTS that MINOCYCLINE was one of the first antibiotics that after THE DAPSONE, RIFAMPICIN and CLOFAZYMINE, has the ability, to eliminate a MICRO-ORGANISM as "HARD DIE" as the MYCOBACTERIUM LEPRAE, this speaks for itself of its "POWER" no matter how "OLD" it is.

What do I want to tell you with this?
That I have knowledge of the "TREMENDOUS" health problem worldwide that is causing the BORRELIA BURGORFERI and you have at your disposal 2 ANTIBIOTICS such as G PENICILLIN and MINOCYCLINE that can help you with all those patients, especially those suffering from NEUROBORRELIOSIS, because of the great capacity it has this antibiotic (MINOCYCICLINE) to penetrate the brain tissues.

You also have OFLOXACIN AND CLARITHROMYCIN, so I suggest researchers use them in LYME DISEASE.


Of course against this LYME DISEASE has been used numerous antibiotics such as: ciprofloxacin, amoxicillin, erythromycin, tetracycline, cephalosporins and others.


Finally, as I said in one of my reviews on LYME DISEASE ...

"...DO NOT STOP CLAIMING YOUR RIGHTS ON HEALTH, TREATMENT AND INSURANCE POLICY, BUT ALSO DO NOT HESITATE TO MAKE A GOOD TREATMENT ... DO NOT GIVE UP ..."
 

And also the old axiom is fulfilled:

"...THE SCIENTIFIC ARTICLES DO NOT PRESCRIBE FOR MORE" OLD "THAT IS THE DATE OF PUBLICATION ..."


And we can also summarize that two old antibiotics like DOXYCYCLINE, a family of penilins and MINOCYCLINE, a family of tetracyclines invented 50 years ago, are the ones who are giving the big battle against LYME DISEASE today. I particularly think MINOCYCLINE is more powerful


Greetings to all

Dr. José Lapenta.
 

 


EDITORIAL SPANISH
===================
Hola amigos de la red DERMAGIC EXPRESS te trae hoy un tema bastante interesante LA MINOCICLINA EN LA ENFERMEDAD DE LYME. Primeramente te voy a decir una vez más, que no es la primera vez que hablo de este "VIEJO ANTIBIOTICO", familia de las tetraciclinas el cual hace muchos años, repito hace muchos años se le descubrió la HABILIDAD o CAPACIDAD de acabar o destruir unos cuantos MICROORGANISMOS o bacterias las cuales los científicos consideraban prácticamente "INVENCIBLES" o "IMPOSIBLES" de exterminar.

El primero y quizá mas importante que te voy a mostrar es EL BACILO DE HANSEN, el MYCOBACTERIUM LEPRAE, bacteria milenaria y apocalíptica, causante de la LEPRA, descrita en la BIBLIA en el capitulo LEVITICO,  descrito y descubierto por el científico Alemán ARMAUER HANSEN en él año de 1.873.

Esta MYCOBACTERIA se le considero " INVENCIBLE" hasta que aparecieron las SULFONAS, (DDS) diaminodifenilsulfona, LA RAFAMPICINA, Y el CLOFAZIMINE. Te estoy hablando de los años 1.940-1.945 cuando aparecieron estas medicinas, que conjuntamente con la INMUNOTERAPIA, decretaron el cierre de las LEPROSERIAS en todo el mundo. Todo esto te lo conté en LOS CAPITULOS SOBRE LA LEPRA.

Y algunos años después llego la MINOCICLINA (MINO), un antibiótico que está cambiando la historia de la evolución de algunas enfermedades hoy día. Este antibiótico es familia de las "viejas" TETRACICLINAS cuyo primer antibiótico fue sintetizado en él año de 1.940 bajo el nombre de CLORTETRACICLINA (AUREOMICINA) por el científico Benjamín Minge Duggar, del LABORATORIO LEDERLE.

Posterior a este descubrimiento fueron apareciendo en el mercado otras TETRACICLINAS: OXITETRACICLINA, DEMECLOCICLINA, LYMECICLINA, MECLOCICLINA. METHACICLINA, ROLITETRACICLINA, TIGECICLINA Y nuestra "FAMOSA" MINOCICLINA.

Especificamente la MINOCICLINA (MINO) nació en él año 1.961 y colocada en el mercado en el año de 1.967, bajo el nombre DE MINOCIN, el cual existe todavía hoy día. Han pasado 50 años, medio siglo desde su descubrimiento. Su uso principal fue destinado a combatir la bacteria del ACNE, pero posteriormente se le describieron otras propiedades.

En el año de 1.999 17, de Marzo, yo lance a la red el articulo LA MINOCICLINA, LO BUENO, LO MALO Y LO FEO, el cual fue publicado en la REVISTA DE DERMATOLOGIA DE EL PAIS CHILE, y lo relance actualizado el 10 de febrero de 2.017 bajo el nombre de MINOCICLINA ALZHEIMER Y OTROS TRASTORNOS NEUROLOGICOS, por sus nuevos usos. Es decir tengo casi 20 años hablándoles de las bondades de este antibiótico que lo diferencian del resto de sus congéneres.

En los años 80 y 90 se demostró que la MINOCICLINA tiene un efecto altamente potente contra el MYCOBACTERIUM LEPRAE y se diseñaron varios esquemas terapéuticos en conjunto con otros antibióticos como la OFLOXACINA, CLARITROMICINA Y AMOXICILINA, para combatir la LEPRA, referencias 3,4,5,6,7,8.

Últimamente se le descubrió su efecto NEUROPROTECTOR, siendo utilizado hoy día en enfermedades como el ALZHEIMER, PARKINSON, ESQUIZOFRENIA, TRASTORNOS BIPOLARES ENCEFALOMIELITIS AUTOINMUNE Y ESCLEROSIS MULTIPLE.

Entonces te estarás preguntando que "TIENE" este antibiótico que lo diferencia de sus congéneres, y te lo voy a decir: CLARO y CIENTIFICAMENTE

1.) TIENE UN MAYOR AMPLIO ESPECTRO QUE OTRAS TETRACICLINAS.


2.) TIENE UN TIEMPO DE VIDA MEDIA EN EL SUERO: 2 A 4 VECES MAYOR QUE OTRAS TETRACICLINAS.

3.) TIENE MAYOR LIPOSOLUBILIDAD QUE LAS DEMAS TETRACICLINAS LO CUAL LE PERMITE TENER UNA MAYOR PENETRACION EN LOS TEJIDOS COMO PROSTATA, CEREBRO Y SISTEMA NERVIOSO CENTRAL.

Me estas entendiendo? me estas copiando? Me estas sintiendo ?

Es por ello que hoy día se le ha encontrado a este antibiótico con MEDIO SIGLO EN EL MERCADO usos que el humano jamás pensó que podría ser útil.

AHORA VOY A EXPLICARTE LA RELACION DE LA ENFERMEDAD DE LYME CON LA MINOCICLINA.


Si te pones a revisar las más conocidas BASES DE DATOS te encontraras que los antibióticos más utilizados en la ENFERMEDAD DE LYME del grupo de las tetraciclinas son la OXITETRACICLINA, y ULTIMAMENTE la TIGECICLINA, sin descartar por supuesto la MINOCICLINA.


Y el más utilizado, de la familia de las PENICILINAS, LA DOXICICLINA, También un antibiótico antiguo que nació en 1.961 y salió al mercado en 1.967 por el laboratorio PFIZER

Hace unos días leí un artículo de un paciente con ENFERMEDAD DE LYME que desarrollo parálisis de BELL y su tratamiento con DOXICICLINA fracaso, le recetaron MINOCICLINA y el paciente se sano. En muchos artículos aparece como primera opción contra la ENFERMEDAD DE LYME la DOXICILINA, y otros, pero no la MINOCILINA y mucho menos la PENICLINA G, de la cual no encontré casi estudios.

Pero si te pones a "ESCARBAR" bien las bases de datos te encuentras con la "SORPRESA" de que la MINOCICLINA en los años 80s y 90s, se le descubrió su efectividad en la ENFERMEDAD DE LYME, de hecho también hay algunos (pocos) estudios donde se demuestra que la PENICILINA G PROCAINICA también es efectiva en esta enfermedad, y aquí viene la gran pregunta ?

Porque estos dos antibióticos PENICILINA G Y MINOCICLINA (MINO) no son utilizados como PRIMERA ELECCION CONTRA enfermedad de LYME? O en combinación con otros? Yo se que algunos científicos SI UTILIZAN LA MINOCICLINA, pero muy pocos o casi ninguno la PENICILINA sabiendo que la BORRELIA ES UNA ESPIROQUETA como el TREPONEMA PALLIDUM que causa la SIFILIS y que "MUERE" con PENICILINA.

Esta revisión la estoy haciendo para RECORDARLES A ALGUNOS CIENTIFICOS que la MINOCICLINA fue uno de los primeros antibióticos que luego de LA DAPSONA, RIFAMPICINA Y CLOFAZIMINA, tiene la habilidad, capacidad de ELIMINAR UN MICRO-ORGANISMO tan "DURO DE MATAR" como el MYCOBACTERIUM LEPRAE, esto habla por sí solo de su "POTENCIA" no importa lo "VIEJO" que sea.

Que quiero decirte con esto ? que tengo conocimiento del TREMENDO problema de salud a nivel mundial que está ocasionando la BORRELIA BURGORFERI y tienes a tu disposición 2 ANTIBIOTICOS como PENICILINA G Y MINOCICLINA que pueden ayudarte con todos esos pacientes, sobre todo los que padecen de NEUROBORRELIOSIS, por la gran capacidad que tiene este antibiótico (MINOCICLINA) de penetrar los tejidos cerebrales.

También tienes OFLOXACINA Y CLARITROMICINA, entonces les sugiero a los investigadores UTILIZARLOS en la ENFERMEDAD DE LYME.


Por supuesto contra esta ENFERMEDAD DE LYME se ha utilizado numerosos antibióticos como: ciprofloxacino, amoxicilina, eritromicina, tetraciclina, cefalosporinas y otros

Para finalizar, como te dije en una de mis revisiones sobre la ENFERMEDAD DE LYME...

 "NO DEJES DE RECLAMAR TUS DERECHOS SOBRE SALUD, TRATAMIENTOS Y POLIZAS DE SEGURO, PERO TAMBIEN NO DEJES DE HACER UN BUEN TRATAMIENTO... NO SE RINDAN..."

Y también se cumple el viejo axioma:


"...LOS ARTICULOS CIENTIFICOS NO PRESCRIBEN POR MAS "VIEJA" QUE SEA LA DATA DE PUBLICACION..."


Y tambien podemos resumir que dos viejos antibioticos como la DOXICICLINA, familia de las penilinas y la MINOCICLINA, familia de las tetraciclinas inventadas hace 5o años, son quienes estan dando la gran batalla contra LA ENFERMEDAD DE LYME hoy dia. Yo particularmente creo que la MINOCICLINA es mas potente


Saludos a todos

Dr. José Lapenta.
 


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REFERENCIAS BIBLIOGRAFICAS/ BIBLIOGRAPHICAL REFERENCES
 =======================================================================

1.) Progression of Lyme disease to Bell's Palsy despite treatment with doxycycline.
2.) Minocycline as A Substitute for Doxycycline in Targeted Scenarios: A Systematic Review.
3.) Minocycline in lepromatous leprosy.
4.) Efficacy of minocycline in single dose and at 100 mg twice daily for lepromatous leprosy.
5.) Field trial on efficacy of supervised monthly dose of 600 mg rifampin, 400 mg ofloxacin and 100 mg minocycline for the treatment of leprosy; first results.
plus minocycline, with or without rifampin, against Mycobacterium leprae in mice and in lepromatous patients.
single-lesion paucibacillary leprosy. Single-lesion Multicentre Trial Group.
minocycline, with or without ofloxacin, against Mycobacterium leprae in patients.
9.) Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
10.) In-vitro and in-vivo antibiotic susceptibilities of Lyme disease Borrelia isolated in China.
11.) Erythema migrans: three weeks treatment for prevention of late Lyme borreliosis.
12.) No detection of Borrelia burgdorferi-specific DNA in erythema migrans lesions after minocycline treatment.
13.) Susceptibility of the Lyme disease spirochete to seven antimicrobial agents.
14.) Antibiotic therapy in early erythema migrans disease and related disorders.
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1.) Progression of Lyme disease to Bell's Palsy despite treatment with doxycycline.
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Int J Infect Dis. 2017 Jul 10. pii: S1201-9712(17)30182-0. doi: 10.1016/j.ijid.2017.07.004. [Epub ahead of print]

Marcos LA1, Yan Z2.
Author information

1
Department of Medicine, Division of Infectious Diseases, Stony Brook University, Stony Brook, USA. Electronic address: Luis.marcos@stonybrookmedicine.edu.
2
Department of Radiology, Stony Brook University, Stony Brook, USA. Electronic address: zengmin.yan@stonybrookmedicine.edu.

Abstract

A 54 year-old healthy woman presented to the emergency department with a right sided facial paralysis. About 3 weeks ago, she woke up and noticed an attached engorged tick in her right lower extremity. A week later, she noticed a mild to moderate right jaw pain which progressed to a severe right facial pain so she visited her doctor. On physical, II to XII cranial nerve examination was unremarkable. Doppler ultrasound did not show any vascular abnormalities in temporal artery. Her inflammatory markers were within normal limits (C-reactive protein:0.3mg/dL; sedimentation rate:6mm/h). Further brain imaging by MRI reveled no abnormalities. Lyme serology (antibodies against purified VlsE-1 and PepC10 antigens) was negative (index value 0.6;≤0.90 negative). Complete blood count and metabolic panel were within normal limits. Only objective physical finding was a right erythematous ear canal so the patient was prescribed a 7-day course of amoxicillin/clavulonic acid. Two days later, the rash in right leg increase in size. It was described as 4cm rash circular with erythematous edges, clearing and central erythema consistent with erythema migrans (EM) (bull's eye). She was prescribed doxycycline 100mg orally twice a day. Five days later went to see a neurologist due to worsening right facial shooting pain. Patient had minimal gastrointestinal side effects from the antibiotic and continued taking it every 12hours without interruption. Physical exam revealed face symmetric, numbness in right chin in nerve distribution. She was diagnosed with possible Lyme cranial neuritis. Doxycycline was continued and pregabalin was started. On day #10 of doxycycline, she woke up and noticed that her right face was paralyzed and unable to close the right eye so she went to the local emergency department. The EM was improved from 4 to 2cm residual rash. Because of her headaches, a lumbar puncture and brain MRI were recommended. Cerebrospinal spinal fluid analysis revealed only 3 WBCs, protein 30.2g/dL, glucose 62mg/L, Lyme serology pair CSF fluid O.D.=0.114 (borderline), serum Lyme serology pair O.D.=0.409 (reactive), serum IgM western blot was positive (bands present: 23 and 41kDa), serum IgG western blot was indeterminate (bands: 41,58 and 93kDa), CRP remained less than 0.1mg/dL. MRI of brain showed new increased enhancement involving right facial nerve (Fig. 1). She was discharged on minocycline 100mg orally twice a day for 21 days. Two days later, her right side headaches improved significantly. The facial paralysis completely resolved after 1 week. At 3 months follow-up, she recovered completely without any complications.
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2.) Minocycline as A Substitute for Doxycycline in Targeted Scenarios: A Systematic Review.
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Open Forum Infect Dis. 2015 Nov 25;2(4):ofv178. doi: 10.1093/ofid/ofv178. eCollection 2015 Dec.

Carris NW1, Pardo J2, Montero J3, Shaeer KM4.
Author information

1
Department of Pharmacotherapeutics and Clinical Research , University of South Florida College of Pharmacy ; Departments of Family Medicine.
2
Department of Pharmacy , North Florida/South Georgia Veterans Health System , Gainesville.
3
Internal Medicine , University of South Florida, Morsani College of Medicine , Tampa.
4
Department of Pharmacotherapeutics and Clinical Research , University of South Florida College of Pharmacy ; Internal Medicine , University of South Florida, Morsani College of Medicine , Tampa.

Abstract

Doxycycline, a commonly prescribed tetracycline, remains on intermittent shortage. We systematically reviewed the literature to assess minocycline as an alternative to doxycycline in select conditions, given doxycycline's continued shortage. We identified 19 studies, 10 of which were published before 2000. Thirteen of the studies were prospective, but only 1 of these studies was randomized. Based on the available data, we found minocycline to be a reasonable substitute for doxycycline in the following scenarios: skin and soft-tissue infections and outpatient treatment of community-acquired pneumonia in young, otherwise healthy patients or in patients with macrolide-resistant Mycoplasma pneumoniae, as well as Lyme disease prophylaxis and select rickettsial disease should doxycycline be unavailable.
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3.) Minocycline in lepromatous leprosy.
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Author
Fajardo TT Jr; Villahermosa LG; dela Cruz EC; Abalos RM; Franzblau SG;
Walsh GP
Address
Clinical Research Branch, Leonard Wood Memorial Center, Cebu City, The
Philippines.
Source
Int J Lepr Other Mycobact Dis, 63(1):8-17 1995 Mar
Abstract
Twelve patients were treated with three dose levels of minocycline for 30 days, primarily to detect the dose-related effects on Mycobacterium leprae viability, followed by another 5 months of daily minocycline for overall efficacy and persistence of clinical and antibacterial effects. Subsequently, the patients were given standard WHO/MDT chemotherapy for multibacillary leprosy. Clinical improvement was recognizable during the first month, occurring much earlier among those on minocycline 200 mg daily than those who received minocycline 100 mg daily. A similar change also was observed in one patient 11 days after three daily doses of 100 mg of minocycline. At the end of 6 months, all patients were clinically improved with a slight reduction in the average bacterial index (BI) and logarithmic index of bacilli in biopsy (LIB). The effects of minocycline on viability by mouse foot pad inoculation and palmitic acid oxidation assays were noted beginning at 10 to 14 days of daily dosing and becoming more definite after 30 days of treatment. Both tests correlated fairly well. Doses of 200 mg daily did not appear to be more efficient than minocycline 100 daily. Phenolic glycolipid-I (PGL-I) antigen determinations done on some patients during the first month remained positive and did not correlate with changes in viability results. At the end of 6 months, after 5 months of 100 mg of
minocycline monotherapy, no viable organisms could be demonstrated by mouse foot pad inoculation and palmitic acid oxidation assays; assays for PGL-I antigen were all negative.(ABSTRACT TRUNCATED AT 250 WORDS)

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4.) Efficacy of minocycline in single dose and at 100 mg twice daily for lepromatous leprosy.
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Int J Lepr Other Mycobact Dis (United States), Dec 1994, 62(4) p568-73
AUTHOR(S): Gelber RH; Murray LP; Siu P; Tsang M; Rea TH
AUTHOR'S ADDRESS: San Francisco Regional Hansen's Disease Program, CA 94115.

PUBLICATION TYPE: CLINICAL TRIAL; JOURNAL ARTICLE

ABSTRACT:
A clinical trial of minocycline in a total of 10 patients with previously untreated lepromatous leprosy was conducted in order to evaluate the efficacy of a single, initial, 200-mg dose and 100 mg twice daily of minocycline for a total duration of up to 3 months. Patients improved remarkably quickly. Although single-dose therapy did not result in a significant killing of Mycobacterium leprae, viable M. leprae were cleared from the dermis regularly by 3 months of twice-daily therapy, a rate similar to that achieved by minocycline 100 mg once daily. Because more side effects were noted herein than previously with 100 mg daily, we recommend that minocycline, when applied, be administered at 100 mg daily to leprosy patients.

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5.) Field trial on efficacy of supervised monthly dose of 600 mg rifampin, 400 mg ofloxacin and 100 mg minocycline for the treatment of leprosy; first results.
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Author
Mane I; Cartel JL; Grosset JH
Address
Institut de Leprologie Appliquee, Dakar CD Annexe, Senegal.
Source
Int J Lepr Other Mycobact Dis, 65(2):224-9 1997 Jun
Abstract
In 1995, a field trial was implemented in Senegal in order to evaluate the efficacy of a regimen based on the monthly supervised intake of rifampin 600 mg, ofloxacin 400 mg and minocycline 100 mg to treat leprosy. During the first year of the trial, 220 patients with active leprosy (newly
detected or relapsing after dapsone monotherapy) were recruited: 102 paucibacillary (PB) (60 males and 42 females) and 118 multibacillary (MB) (71 males and 47 females). All of them accepted the new treatment (none requested to be preferably put under standard WHO/MDT), no clinical sign which could be considered as a toxic effect of the drug was noted, and none of the patients refused to continue treatment because of any clinical trouble. The compliance was excellent: the 113 patients (PB and MB) detected during the first 6 months of the trial have taken six monthly doses in 6 months, as planned. The rate of clearance and the progressive decrease of cutaneous lesions was satisfactory. Although it is too soon to give comprehensive results, it should be noted that no treatment failure was observed in the 56 PB patients who have completed treatment and have been followed up for 6 months. The long-term efficacy of the new regimen is to be evaluated on the rate of relapse during the years following the
cessation of treatment. If that relapse rate is acceptable (similar to that observed in patients after treatment with current standard WHO/ MDT), the new regimen could be a solution to treat, for instance, patients very irregular and/or living in remote or inaccessible areas since no selection of rifampin-resistant Mycobacterium leprae should be possible (a monthly dose of ofloxacin and minocycline being as effective as a dose of dapsone and clofazimine taken daily for 1 month). Nevertheless, until longer term results of this and other trials become available, there is no justification for any change in the treatment strategy, and all leprosy patients should be put under standard WHO/MDT.
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6.) Bactericidal activity of a single-dose combination of ofloxacin plus minocycline, with or without rifampin, against Mycobacterium leprae in mice and in lepromatous patients.
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Author
Ji B; Sow S; Perani E; Lienhardt C; Diderot V; Grosset J
Address
Facult´e de M´edecine Piti´e-Salp^etri`ere, Paris, France.
bacterio@biomath.jussieu.fr
Source
Antimicrob Agents Chemother, 42(5):1115-20 1998 May

Abstract

To develop a fully supervisable, monthly administered regimen for treatment of leprosy, the bactericidal effect of a single-dose combination of ofloxacin (OFLO) and minocycline (MINO), with or without rifampin (RMP), against Mycobacterium leprae was studied in the mouse footpad system and in previously untreated lepromatous leprosy patients. Bactericidal activity was measured by the proportional bactericidal method. In mouse experiments, the activity of a single dose of the combination OFLO-MINO was dosage related; the higher dosage of the combination displayed bactericidal activity which was significantly inferior to that of a single dose of RMP, whereas the lower dosage did not exhibit a bactericidal effect. In the clinical trial, 20 patients with previously untreated lepromatous leprosy were treated with a single dose consisting of either 600 mg of RMP plus 400 mg of OFLO and 100 mg of MINO or 400 mg of OFLO plus 100 mg of MINO. The OFLO-MINO combination exhibited definite bactericidal activity in 7 of 10 patients but was less bactericidal than the RMP-OFLO-MINO combination. Both combinations were well tolerated. Because of these promising results, a test of the efficacy of multiple doses of ROM in a larger clinical trial appears justified.
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7.)Efficacy of single dose multidrug therapy for the treatment of single-lesion paucibacillary leprosy. Single-lesion Multicentre Trial Group.
====================================================
Source
Indian J Lepr, 69(2):121-9 1997 Apr-Jun
Abstract
A multicentre double-blind controlled clinical trial was carried out to compare the efficacy of a combination of rifampicin 600 mg plus ofloxacin 400 mg plus minocycline 100 mg (ROM) administered as single dose with that of the standard six-month WHO/MDT/PB regimen. The subjects included 1483 cases with one skin lesion who were previously untreated, were smear-negative, and had no evidence of peripheral nerve trunk involvement, and they were randomly divided into study and control groups. The total duration of the study from the day of intake was 18 months, and 1381 patients completed study. Only 12 patients were categorized as treatment
failure and no difference was observed between the two regimens. Occurrence of mild side-effects and leprosy reactions were minimal (less than 1%) in both groups. This study showed that ROM is almost as effective as the standard WHO/MDT/PB in the treatment of single lesion PB leprosy.
====================================================
8.) Bactericidal activity of single dose of clarithromycin plus minocycline, with or without ofloxacin, against Mycobacterium leprae in patients.
====================================================
Author
Ji B; Jamet P; Perani EG; Sow S; Lienhardt C; Petinon C; Grosset JH
Address
Facult´e de M´edecine Piti´e-Salp^etri`ere, Paris, France.
Source
Antimicrob Agents Chemother, 40(9):2137-41 1996 Sep
Abstract
Fifty patients with newly diagnosed lepromatous leprosy were allocated randomly to one of five groups and treated with either a month-long standard regimen of multidrug therapy (MDT) for multibacillary leprosy, a single dose of 600 mg of rifampin, a month-long regimen with the dapsone (DDS) and clofazimine (CLO) components of the standard MDT, or a single dose of 2,000 mg of clarithromycin (CLARI) plus 200 mg of minocycline (MINO), with or without the addition of 800 mg of ofloxacin (OFLO). At the end of 1 month, clinical improvement accompanied by significant decreases of morphological indexes in skin smears was observed in about half of the patients of each group. A significant bactericidal effect was demonstrated
in the great majority of patients in all five groups by inoculating the footpads of mice with organisms recovered from biopsy samples obtained before and after treatment. Rifampin proved to be a bactericidal drug against Mycobacterium leprae more potent than any combination of the other drugs. A single dose of CLARI-MINO, with or without OFLO, displayed a
degree of bactericidal activity similar to that of a regimen daily of doses of DDS-CLO for 1 month, suggesting that it may be possible to replace the DDS and CLO components of the MDT with a monthly dose of CLARI-MINO, with or without OFLO. However, gastrointestinal adverse events were quite frequent among patients treated with CLARI-MINO, with or without OFLO, and
may be attributed to the higher dosage of CLARI or MINO or to the combination of CLARI-MINO plus OFLO. In future trials, therefore, we propose to reduce the dosages of the drugs to 1,000 mg of CLARI, 100 mg of MINO, and 400 mg of OFLO.
=====================================================================
9.) Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
=====================================================================
Med Hypotheses. 2005;64(3):438-48.

Fritzsche M1.
Author information

1
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. markus.fritzsche@gmx.ch

Abstract

Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.
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10.) In-vitro and in-vivo antibiotic susceptibilities of Lyme disease Borrelia isolated in China.
====================================================================
J Infect Chemother. 2000 Mar;6(1):65-7.

Li M1, Masuzawa T, Wang J, Kawabata M, Yanagihara Y.
Author information

1
International Center for Medical Research, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650, Japan. muqingl@kobe-u.ac.jp

Abstract

The antibiotic susceptibilities of seven Borrelia burgdorferi sensu lato isolates from Ixodes persulcatus in China were examined by in-vitro microdilution minimum inhibition concentration (MIC) and macrodilution minimum bactericidal concentration (MBC) methods. All isolates tested were susceptible to amoxicillin, erythromycin, and minocycline. The MICs of these drugs for the Chinese isolates were 0.025-0.1 microg/ml, <0.012-0.05 microg/ml, and <0.012-0.05 microg/ml, respectively. The MBCs were 0.1-0.39 microg/ml, <0.012-0.2 microg/ml, and 0.025-0.39 microg/ml, respectively. The in-vivo antimicrobial susceptibilities of the Chinese Borrelia isolates to two test drugs, amoxicillin and minocycline, were evaluated using ddY mice. Mice were infected by subcutaneous inoculation into the right hind footpad. When infection was confirmed, the mice were treated by subcutaneous injection of the test drugs into the back. Amoxicillin and minocycline, which possessed high in-vitro activities against Lyme disease Borrelia, provided good protection against borreliosis in this animal model. Higher doses of these drugs resulted in elimination of the Lyme disease spirochete from all animals receiving this course of treatment. The 50% curative doses (CD50) of amoxicillin and minocycline were 8.7 mg/kg and 3.1 mg/kg, respectively. This suggested that amoxicillin and minocycline could be useful for the treatment of Chinese Borrelia infection.
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11.) Erythema migrans: three weeks treatment for prevention of late Lyme borreliosis.
====================================================================
Infection. 1996 Jan-Feb;24(1):69-72.

Breier F1, Kunz G, Klade H, Stanek G, Aberer E.
Author information

1
Universitätsklinik für Dermatologie, Wien, Austria.

Abstract

An open, randomized, prospective study was carried out to compare the clinical efficacy and safety of phenoxymethylpenicillin with that of minocycline in the treatment of erythema migrans. Sixty patients (minocycline 30, penicillin 30) were enrolled in the study. The two groups of patients were statistically homogeneous regarding age and sex distribution. IgG and IgM antibodies against Borrelia burgdorferi were determined by ELISA before and after treatment and 1 year thereafter. Thirty-nine patients completed the study. All these patients (penicillin 21, minocycline 18) who received a 21-day course of treatment were free of clinical symptoms of late Lyme borreliosis after 1 year. Serum antibodies against B. burgdorferi could be detected before treatment in 6/21 patients treated with penicillin and 3/18 patients treated with minocycline. After 1 year 8/39 patients were seropositive without any evidence of ongoing disease. In the remaining 21 patients treatment could not be completed with the initial antibiotic due to side effects (penicillin 9/30, minocycline 12/30). One patient, who stopped penicillin treatment at day 14 and one patient who stopped minocycline at day 4, developed fatigue and memory impairment within the observation period. A 3-week course of treatment with penicillin or minocycline is equally effective in treating patients with erythema migrans and preventing late symptoms of Lyme borreliosis.
=====================================================================
12.) No detection of Borrelia burgdorferi-specific DNA in erythema migrans lesions after minocycline treatment.
=====================================================================
Arch Dermatol. 1995 Jun;131(6):678-82.

Muellegger RR1, Zoechling N, Soyer HP, Hoedl S, Wienecke R, Volkenandt M, Kerl H.
Author information

1
Department of Dermatology, Karl-Franzens University, Graz, Austria.

Abstract
BACKGROUND AND DESIGN:

Early treatment of erythema migrans is important to prevent late complications. Minocycline possesses several attributes, making it potentially useful in the treatment of borrelial infections. In our study, minocycline was administered to 14 patients with erythema migrans. Punch biopsy specimens were obtained from the (affected) skin of all patients before and after therapy. The formalin-fixed, paraffin-embedded specimens were analyzed by polymerase chain reaction for the presence of Borrelia burgdorferi-specific DNA.
RESULTS:

Polymerase chain reaction assay succeeded in amplifying B burgdorferi-specific DNA from the first biopsy specimen, obtained from the border of erythema migrans before initiating treatment, in eight (57%) of 14 patients. At the end of minocycline therapy, however, polymerase chain reaction analysis disclosed no B burgdorferi-specific DNA in any of the 14 patients. The good clinical response of our patients with erythema migrans substantiates our molecular findings.

CONCLUSIONS:

The presented polymerase chain reaction data, together with the clinical outcome, indicate that minocycline may be useful for treatment of early Lyme borreliosis.
=====================================================================
13.) Susceptibility of the Lyme disease spirochete to seven antimicrobial agents.
=====================================================================
Yale J Biol Med. 1984 Jul-Aug;57(4):549-53.

Johnson SE, Klein GC, Schmid GP, Feeley JC.
Abstract

The antimicrobial susceptibility of five Lyme disease spirochete strains (two human and three tick isolates) was determined. A macrodilution broth technique was used to determine on three separate test occasions the minimal inhibitory concentrations (MICs) of seven antibiotics. The Lyme disease spirochete was most susceptible to erythromycin with a MIC of less than or equal to 0.06 micrograms/ml. The spirochete was also found to be susceptible to minocycline, ampicillin, doxycycline, and tetracycline-HCL with respective mean MICs of less than or equal to 0.13, less than or equal to 0.25, less than or equal to 0.63, and less than or equal to 0.79 micrograms/ml. The spirochete was moderately susceptible to penicillin G with a mean MIC of 0.93 micrograms/ml. All strains were resistant to rifampin at the highest concentration tested (16.0 micrograms/ml).
=====================================================================
14.) Antibiotic therapy in early erythema migrans disease and related disorders.
=====================================================================
Zentralbl Bakteriol Mikrobiol Hyg A. 1987 Feb;263(3):377-88.

Weber K, Neubert U, Thurmayr R.
Abstract

Between December 1978 and July 1985, we used various antibiotics for the treatment of 97 adult patients with early erythema migrans disease (EMD). Six patients with borrelial lymphocytoma (BL) and 20 with acrodermatitis chronica atrophicans (ACA) were treated similarly. Follow-up was for a median of 20, 14, and 12 months, respectively. The erythema migrans and all associated symptoms resolved within a median of 3 weeks (0.5-18.4), BL within 7 weeks (4-16), and ACA partly or completely within several months. A Jarisch-Herxheimer (-like) reaction was observed in 8 patients with EMD. Fourteen patients with EMD and one with ACA developed an exacerbation of symptoms or new manifestations between the 2nd and 20th day, and 28 patients with EMD and one with ACA continued to have or acquired various symptoms greater than or equal to 3 weeks after initiation of therapy. Arthralgia, neurologic and constitutional symptoms, and in one instance a slight pulmonary interstitial edema developed in EMD. More severe initial illness was a risk factor for the development of later symptoms in EMD. Retreatment was more often necessary in ACA than in EMD. A patient with ACA had a recurrence after 5 1/2 years. IgG antibody titers rose at least fourfold in 5 patients with ACA and in 1 with EMD despite therapy. We tentatively recommend minocycline or high doses of parenteral penicillin for the treatment of these disorders. 

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  Produced by Dr. Jose Lapenta R. Dermatologist

                 Maracay Estado Aragua Venezuela 2.017  

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THE POWASSAN VIRUS, A REVIEW. / EL VIRUS DE POWASSAN, REVISION

 

 

The Powassan Virus a Review, A killer Tick, !! 


El Virus de Powassan, Revision, Una garrapata que mata. !!








EDITORIAL ENGLISH
=================
Hello friends of the DERMAGIC EXPRESS network brings you today another interesting topic related to TICKS and the transmission of VIRUS. In this case it is the POWASSAN VIRUS (POWV), THE REVIEW. Virus widely distributed in nature that was isolated and discovered in the village of POWASSAN, in 1.958 locality of ONTARIO (CANADA), in a young man who died of the infection. Subsequently described in CANADA IN 1.998 and in other countries.
 
The virus has been found in many areas of our planet: it is practically spread throughout the Continent of North America, Russia, and Central Asia, being isolated in regions such as:
 
1.) UNITED STATES: NEW YORK, CALIFORNIA, COLORADO, DAKOTA, WISCONSIN, NEW ENGLAND: Maine, New Hampshire, Vermont, Massachusetts, Rhode Island and Connecticut. ROCKY MOUNTAINS.
 
2.) MEXICO: Sonora.
 
3.) RUSSIA.
 
4.) CENTRAL ASIA,
 
The virus POWASSAN (POWv) is also found in warm weather through EUROPE and ASIA, where it is part of the tick-borne ENCEPHALITIS virus complex. In other words, it is widely distributed in nature.
 
It is an RNA virus of the family FLAVIVIRIDAE, genus FLAVIVIRUS, species: POWASSAN VIRUS. After being discovered began to report cases of this disease whose predominant symptom is ENCEPHALITIS, with a 10% mortality and 50% of those affected with neurological squeal. So that it is not a "SIMPLE" virus, it is a "LETAL" virus that can cause you to DIE.

                                   LINEAGE I


The vector: TICKS, among which stand out: IXODES COOKEI, and IXODES SCAPULARIS, also IXODES MARXI, IXODES SPINIPALPUS and other ticks as: DERMACENTOR ANDERSONI AND DERMACENTOR VARIABILIS.
 

NOW I WILL TELL YOU THE ANIMALS that are part of this disease which is an ENZOOTIC, which means that it is distributed in several or many species of animals in some region and transmitted to the human by a vector, in this case THE TICKS.
The POWASSAN VIRUS (POWv) is considered as explained by a VIRUS RNA, which is divided into 2 COMPLEXES or LINEAGES, each with a different enzootic cycle:
                                                                                               LINEAGE I
 

1.) LINEAGE I: CONSIDERED AS THE "PROTOTYPE" which is linked to the TICK IXODES COOKEI and is presented mainly in the WOODCHUCKS (Marmot Momax), STRIPED SHUNKS (Mephitis mephitis) and also the WHITE-FOOD LEGS MOUSE (Peromyscus Leucopus). (see photos).
 
                                      LINEAGE II


2.) LINEAGE II: Which has the greatest genetic variation and is linked to TICK IXODES SCAPULARIS and is presented mainly in DEER being denominated VIRUS DEER TICK (VDT). (View the first photo)
 
Also POWASSAN virus (POWv) has been isolated from other animals such as: THE RACCOON (Procyon lotor), COYOTES (Canis Latrans), and FOXES.
 

Both LINEAGES have had confirmed cases of POWASSAN VIRUS (POWv) disease in both North America and Russia. The viruses of both LINEAGES belong to the same viral species, there is only difference in the composition of the RNA and it is believed that the "DIVERGED" of both viruses occurred more than 200 years ago. In conslusion two lineages are “serologically indistinguishable".
 

Before continuing I will tell you that it has been ISOLATED from the TICK IXODES SCAPULARIS POWASSAN VIRUS (POWv / DTV) and the "FEARED" BORRELIA BURGDORFERI, causing the LYME DISEASE, in fact the geographic distribution for both is the same.
 
In other words we are fighting against a LEGION OF TICKS that transmit THE POWASSN VIRUS (POWv) that causes a SEVERE ENCEPHALITIS, AND THE BORRELIA BURGODORFERI, SPIROCHAET, that causes the already known LYME DISEASE, Which is a tremendous health problem in the Northern Hemisphere today.

                                         
LINEAGE II
 
SYMPTOMS OF POWASSAN VIRUS INFECTION:
 
INITIAL STAGE:
=============
 
THE SYMPTOMS CAN BE PRESENTED BETWEEN 1 WEEK AND 1 MONTH AFTER THE BIT OF THE INFECTED TICK:
 
1.) FEVER.
2.) HEADACHE.
3.) NAUSEAS.
4.) WEAKNESS.
5.) CONFUSION.
6.) VOMITING.
7.) LOSS OF MEMORY.
8.) SEIZURES
 
SEVERE STAGE:
==============
 
POWASSAN VIRUS (POWv) CAN ATTACK THE NERVOUS SYSTEM PRODUCING BRAIN INFLAMMATION:
 
1.) LOSS OF CONSCIOUSNESS.
2.) MENINGITIS.
3.) ENCEPHALITIS: MORTALITY 10%, 50% OF THE SURVIVORS HAVE PERMANET NEUROLOGICAL SEQUELS: RECURRENT HEADACHE, MUSCLE WEAKNESS, MEMORY PROBLEMS.
 
Unlike LYME DISEASE, the POWASSAN virus has NO SPECIFIC TREATMENT, OR NO VACCINE. Treatment is symptomatic. Another detail is that virus transmission is faster than in LYME DISEASE where the TICK must be adhered to the skin between 36 and 48 hours. In the case of POWASSAN only in a few hours the VIRUS is transmitted by the bite.
 
LYME DISEASE if not treated in time can also produce inflammation of the brain and give symptoms known today as NEUROBORRELIOSIS. The number of cases of POWASSAN VIRUS (POWv) is much smaller than LYME DISEASE. But both diseases can cause DEATH and leave NEUROLOGICAL SEQUELS.
 
The diagnosis of POWASSAN VIRUS is done by the test: Reverse Transcriptase Polymerase Chain Reaction (RT-PCR).
 
Given these facts, we can conclude that our population is not being invaded by "ALIENS", here the only "ALIENS" are these TICKS that step by step want to diminish the existence of HUMANITY.
 
As an anecdotal fact I can also conclude that the human "INVADED" the territory of these animals (Deer, woodchucks, coyote, raccoon, skunk, fox, etc.) even made ZOO where people go to see them. Many of them are in captivity and are carriers of TICKS transmitting LYME DISEASE and POWASSAN VIRUS.
 
Here is the great PROBLEM with these two diseases, both transmitted by TICKS, because if the patient does NOT have ENCEPHALITIS, it can easily be confused with LYME DISEASE, (the symptomatology is similar), whose serologic diagnosis we know is difficult, because of the capacity of The SPIROCHETA to "EVADE" the laboratory tests. In both cases, a good medical history must be made and definitely the laboratory tests will say whether it is POWASSAN VIRUS OR LYME DISEASE. So that... 

"... NOT ALL BITTEN BY TICKS IN ZONES WHERE LYME'S DISEASE IS ENDEMIC INDICATE THAT IS BORRELIA... COULD  BE THE POWASSAN VIRUS ..."
 
Therefore the best way to combat this pest must be directed to "ELIMINATE" where possible the TICKS to avoid being bitten by them.
 
In the references, the facts, in the attach some of the animals and vectors.
 
I want to thank all the people who fight every day against LYME DISEASE and especially the people of Madison Area Lyme Support Group.
 
Greetings to all.
 
Dr. José Lapenta.



EDITORIAL ESPAÑOL
=================
Hola amigos de la red DERMAGIC EXPRESS te trae hoy otro interesante tema relacionado con LAS GARRAPATAS y la transmisión de VIRUS. En este caso se trata del VIRUS DE POWASSAN (POWv), LA REVISION. Virus ampliamente distribuido en la naturaleza que fue aislado y descubierto en el pueblo de POWASSAN, en 1.958 localidad de ONTARIO,(CANADA) en un joven quien murió de por la infección. Posteriormente descrito en CANADA EN 1.998 y en otros países.

El virus se ha encontrado en en numerosas aéreas de nuestro planeta: prácticamente se encuentra diseminado en todo el continente de América del Norte, Rusia, y Asia Central, siendo aislados en regiones como:

1.) ESTADOS UNIDOS: NUEVA YORK, CALIFORNIA, COLORADO, DAKOTA, WISCONSIN, NUEVA INGLATERRA: Maine, Nuevo Hampshire, Vermont, Massachusetts, Rhode Island y Connecticut. MONTAÑAS ROCOSAS.

2.) MEXICO: Sonora.

3.) RUSIA.

4.) ASIA CENTRAL,

El virus POWASSAN(POWv) también se encuentra en el clima cálido a través de EUROPA Y ASIA, donde es parte del complejo de virus de la ENCEFALITIS transmitida por garrapatas. En otras palabras, está ampliamente distribuido en la naturaleza.

Se trata de un virus tipo ARN de la familia FLAVIVIRIDAE, genus FLAVIVIRUS, especie: POWASSAN VIRUS. Luego de ser descubierto comenzaron a reportarse casos de esta enfermedad cuyo sintoma predominante es la ENCEFALITIS, con un 10% de mortalidad y el 50% de los afectados queda con secuelas neurologicas. De modo de que no se trata de un "SIMPLE" virus, se trata de un virus "LETAL" el cual puede causarte la muerte.

El vector: GARRAPATAS, entre las que se destacan IXODES COOKEI, y IXODES SCAPULARIS, también IXODES MARXI, IXODES SPINIPALPUS y otras garrapatas como: DERMACENTOR ANDERSONI Y DERMACENTOR VARIABILIS.

AHORA TE HABLARE DE LOS ANIMALES QUE forman parte de esta enfermedad la cual es una ENZOOTIA, lo cual significa que está distribuida en varias o muchas especies de animales en una determinada región y transmitida al humano por un vector, en este caso LA GARRAPATA.

Se considera al VIRUS DE POWASSAN (POWv) como ya te lo explique un RNA VIRUS, el cual está dividido en 2 COMPLEJOS O LINAJES, cada uno con un ciclo enzootico diferente:

1.) LINAJE I: CONSIDERADO COMO EL "PROTOTIPO" el cual está vinculado a la GARRAPATA IXODES COOKEI y se presenta principalmente en las MARMOTAS (Marmota Momax)), LA MOFETA RAYADA (Mephitis mephitis) y también en el RATON DE PATAS BLANCAS. (Ver fotos)

2.) LINAJE II: El cual tiene la mayor variación genética y está vinculado a la GARRAPATA IXODES SCAPULARIS y se presenta principalmente en CIERVOS O VENADOS siendo denominado VIRUS DE LA GARRAPATA DEL CIERVO (DTV= Deer Tick Virus).

También el virus de POWASSAN(POWv) ha sido aislado de otros animales como: EL MAPACHE (Procyon lotor), COYOTES (Canis Latrans), y ZORROS.

Ambos LINAJES
han tenido casos confirmados de enfermedad por el VIRUS DE POWASSAN(POWv) tanto en América del Norte como en Rusia. Los virus de ambos LINAJES pertenecen a la misma especie viral, solo hay diferencia en la composición del ARN y se cree que la "DIVISION" de ambos virus ocurrió hace mas de 200 años. En conclusión los dos LINAJES son "serológicamente indistinguibles".

Antes de continuar te contare que ha sido AISLADA de la GARRAPATA IXODES SCAPULARIS EL VIRUS DE POWASSAN(POWv/DTV) y la "TEMIDA" BORRELIA BURGDORFERI, causante de la ENFERMEDAD DE LYME, de hecho la distribución geográfica para ambas es la misma. 

En otras palabras estamos luchando contra una LEGION DE GARRAPATAS que transmiten EL VIRUS DE POWASSN(POWv) que causa una ENCEFALITIS GRAVE, Y LA ESPIROQUETA BORRELIA BURGODORFERI, que ocasiona la ya CONOCIDA ENFERMEDAD DE LYME, la cual es un tremendo problema de salud en el Hemisferio Norte hoy dia.

SINTOMAS DE LA INFECCION POR EL VIRUS DE POWASSAN:

ETAPA INICIAL:

=============
LOS SINTOMAS PUEDEN PRESENTARSE ENTRE 1 SEMANA Y 1 MES LUEGO DE LA PICADURA DE LA GARRAPATA INFECTADA:

1.) FIEBRE.
2.) DOLOR DE CABEZA.
3.) NAUSEAS.
4.) DEBILIDAD.
5.) CONFUSION.
6.) VOMITOS.
7.) PERDIDA DE LA MEMORIA.
8.) CONVULSIONES.

ETAPA SEVERA:
============

EL VIRUS DE POWASSAN(POWv) ATACA EL SISTEMA NERVIOSO PRODUCIENDO INFLAMACION CEREBRAL:

1.) PERDIDA DE LA CONCIENCIA.
2.) MENINGITIS.
3.) ENCEFALITIS: MORTALIDAD 10%, EL 50% QUEDA CON SECUELAS NEUROLOGICAS: DOLOR DE CABEZA RECURRENTE, DEBILIDAD MUSCULAR, PROBLEMAS DE LA MEMORIA.


A diferencia de la ENFERMEDAD DE LYME el virus de POWASSAN NO TIENE TRATAMIENTO ESPECIFICO NI EXISTE VACUNA CONTRA EL MISMO. El tratamiento es sintomático. Otro detalle es que la transmisión del virus es mas rápido que en la ENFERMEDAD DE LYME donde la GARRAPATA debe estar adherida a la piel entre 36 y 48 horas. En el caso de POWASSAN solo en pocas horas el VIRUS es transmitido por la picadura. 

LA ENFERMEDAD DE LYME si no es tratada a tiempo también puede producir inflamación del cerebro y dar síntomas conocidos hoy día como NEUROBORRELIOSIS. El número de casos del VIRIS DE POWASSAN(POWv), es mucho menor que la ENFERMEDAD DE LYME. Pero ambas enfermedades pueden causar la MUERTE y dejar SECUELAS NEUROLOGICAS.

El diagnostico del VIRUS DE POWASSAN
se hace mediante la prueba: Reacción en Cadena de Polimerasa de Transcriptasa Reversa (RT-PCR).

Ante estos hechos descritos previamente, podemos concluir que nuestra población no está siendo invadida por "EXTRATERRESTRES", aquí los únicos "ALIENS" son estas GARRAPATAS que paso a paso quieren disminuir la existencia de la HUMANIDAD.

Como hecho anecdótico también puedo concluir que el ser humano "INVADIO" el territorio de estos animales (Ciervo, venado, marmota, coyote, mapache, mofeta, etc.) incluso hizo ZOOLOGICOS donde la gente va a verlos. Muchos de ellos están en cautiverio y son portadores de GARRAPATAS que transmiten ENFERMEDAD DE LYME Y VIRUS DE POWASSAN.


He aquí el gran PROBLEMA con estas dos enfermedades, ambas transmitidas por GARRAPATAS, porque si el paciente NO presenta ENCEFALITIS, puede fácilmente confundirse con ENFERMEDAD DE LYME, (la sintomatología es parecida), cuyo diagnostico serológico sabemos que es difícil, por la capacidad de la ESPIROQUETA de "ESCONDERSE" ante las pruebas de laboratorio. En ambos casos hay que hacer una buena historia clínica y definitivamente las pruebas de laboratorio dirán si se trata del VIRUS DE POWASSAN O ENFERMEDAD DE LYME. De modo que...

 "... NO TODO PICADO POR GARRAPATA EN ZONAS DONDE LA ENFERMEDAD DE LYME ES ENDEMICA INDICAN QUE SEA UNA BORRELIA... PODRIA TRATARSE DEL VIRUS DE POWASSAN..."
 

Por ello la mejor manera de combatir esta plaga debe estar dirigida a "ELIMINAR" en lo posible las GARRAPATAS para evitar ser mordido por ellas.

En las referencias, los hechos, en el adjunto fotos de algunos animales y vectores.

Quiero dar las gracias a toda la gente que pelea día a día contra la ENFERMEDAD de LYME y muy especialmente a la gente de Madison Area Lyme Support Group.


Saludos a todos.

Dr. José Lapenta
 
=======================================================================
REFERENCIAS BIBLIOGRAFICAS/ BIBLIOGRAPHICAL REFERENCES
=======================================================================
1.) Serologic Evidence of Powassan Virus Infection in Patients with Suspected Lyme Disease1.
2.) Potential role of deer tick virus in Powassan encephalitis cases in Lyme disease-endemic areas of New York, U.S.A.
3.) Emerging Cases of Powassan Virus Encephalitis in New England: Clinical Presentation, Imaging, and Review of the Literature.
4.) Powassan Virus: An Emerging Arbovirus of Public Health Concern in North America.
5.) Tick Saliva Enhances Powassan Virus Transmission to the Host, Influencing Its Dissemination and the Course of Disease.
6.) Isolation of deer tick virus (Powassan virus, lineage II) from Ixodes scapularis and detection of antibody in vertebrate hosts sampled in the Hudson Valley, New York State.
7.) Powassan/Deer Tick Virus and Borrelia Burgdorferi Infection in Wisconsin Tick Populations.
8.) Powassan meningoencephalitis, New York, New York, USA.
9.) Powassan Virus
10.) Tickborne Powassan virus infections among Wisconsin residents.
11.) Prevalence and genetic characterization of Powassan virus strains infecting Ixodes scapularis in Connecticut.
12.) Increased recognition of Powassan encephalitis in the United States, 1999-2005.
13.) Another Dies From Powassan / New York Man Dies From Tick Carrying Brain Swelling Virus
14.) Powassan virus encephalitis, Minnesota, USA.
15.) Powassan virus in mammals, Alaska and New Mexico, U.S.A., and Russia, 2004-2007.
16.) Tick-borne encephalitis among U.S. travelers to Europe and Asia - 2000-2009.
Centers for Disease Control and Prevention (CDC).
17.) Tick-Borne Encephalitis Virus in Ticks and Roe Deer, the Netherlands.
18.) Stable prevalence of Powassan virus in Ixodes scapularis in a northern Wisconsin focus.
19.) Seroprevalence of Powassan virus in New England deer, 1979-2010.
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 1.) Serologic Evidence of Powassan Virus Infection in Patients with Suspected Lyme Disease1.
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 Emerg Infect Dis. 2017 Aug;23(8):1384-1388. doi: 10.3201/eid2308.161971.
 
 Frost HM, Schotthoefer AM, Thomm AM, Dupuis AP 2nd, Kehl SC, Kramer LD, Fritsche TR, Harrington YA, Knox KK.
 Abstract
 
 Powassan virus (POWV) lineage II is an emerging tickborne flavivirus with an unknown seroprevalence in humans. In a Lyme disease-endemic area, we examined the seroreactivity to POWV in 2 patient cohorts and described the clinical features of the POWV-seroreactive patients. POWV disease might be less neuroinvasive than previously thought.
 KEYWORDS:
 
 Lyme disease; Powassan virus; United States; deer tick virus; encephalitis viruses; meningitis/encephalitis; serology; tick-borne encephalitis; tickborne; vector-borne infections; viruses; zoonoses
 
 ================================================================
 2.) Potential role of deer tick virus in Powassan encephalitis cases in Lyme disease-endemic areas of New York, U.S.A.
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 Emerg Infect Dis. 2013 Dec;19(12):1926-33. doi: 10.3201/eid1912.130903.
 
 El Khoury MY, Camargo JF, White JL, Backenson BP, Dupuis AP 2nd, Escuyer KL, Kramer L, St George K, Chatterjee D, Prusinski M, Wormser GP, Wong SJ.
 Abstract
 
 Powassan virus, a member of the tick-borne encephalitis group of flaviviruses, encompasses 2 lineages with separate enzootic cycles. The prototype lineage of Powassan virus (POWV) is principally maintained between Ixodes cookei ticks and the groundhog (Marmota momax) or striped skunk (Mephitis mephitis), whereas the deer tick virus (DTV) lineage is believed to be maintained between Ixodes scapularis ticks and the white-footed mouse (Peromyscus leucopus). We report 14 cases of Powassan encephalitis from New York during 2004-2012. Ten (72%) of the patients were residents of the Lower Hudson Valley, a Lyme disease-endemic area in which I. scapularis ticks account for most human tick bites. This finding suggests that many of these cases were caused by DTV rather than POWV. In 2 patients, DTV infection was confirmed by genetic sequencing. As molecular testing becomes increasingly available, more cases of Powassan encephalitis may be determined to be attributable to the DTV lineage.
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 3.) Emerging Cases of Powassan Virus Encephalitis in New England: Clinical Presentation, Imaging, and Review of the Literature.
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 Piantadosi A1, Rubin DB2, McQuillen DP3, Hsu L4, Lederer PA1, Ashbaugh CD5, Duffalo C6, Duncan R3, Thon J2, Bhattacharyya S2, Basgoz N1, Feske SK2, Lyons JL2.
 Author information
 
 1
 Division of Infectious Disease, Massachusetts General Hospital.
 2
 Department of Neurology, Brigham and Women's Hospital, Boston.
 3
 Department of Infectious Diseases, Lahey Hospital & Medical Center, Tufts University School of Medicine, Burlington.
 4
 Department of Radiology.
 5
 Division of Infectious Disease, Brigham and Women's Hospital, Boston, Massachusetts.
 6
 Christiana Care Health System, Division of Infectious Diseases, Newark, Delaware.
 
 Abstract
 BACKGROUND:
 
 Powassan virus (POWV) is a rarely diagnosed cause of encephalitis in the United States. In the Northeast, it is transmitted by Ixodes scapularis, the same vector that transmits Lyme disease. The prevalence of POWV among animal hosts and vectors has been increasing. We present 8 cases of POWV encephalitis from Massachusetts and New Hampshire in 2013-2015.
 METHODS:
 
 We abstracted clinical and epidemiological information for patients with POWV encephalitis diagnosed at 2 hospitals in Massachusetts from 2013 to 2015. We compared their brain imaging with those in published findings from Powassan and other viral encephalitides.
 RESULTS:
 
 The patients ranged in age from 21 to 82 years, were, for the most part, previously healthy, and presented with syndromes of fever, headache, and altered consciousness. Infections occurred from May to September and were often associated with known tick exposures. In all patients, cerebrospinal fluid analyses showed pleocytosis with elevated protein. In 7 of 8 patients, brain magnetic resonance imaging demonstrated deep foci of increased T2/fluid-attenuation inversion recovery signal intensity.
 CONCLUSIONS:
 
 We describe 8 cases of POWV encephalitis in Massachusetts and New Hampshire in 2013-2015. Prior to this, there had been only 2 cases of POWV encephalitis identified in Massachusetts. These cases may represent emergence of this virus in a region where its vector, I. scapularis, is known to be prevalent or may represent the emerging diagnosis of an underappreciated pathogen. We recommend testing for POWV in patients who present with encephalitis in the spring to fall in New England.
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 4.) Powassan Virus: An Emerging Arbovirus of Public Health Concern in North America.
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 Hermance ME1, Thangamani S1,2,3.
 Author information
 
 1
 1 Department of Pathology, University of Texas Medical Branch , Galveston, Texas.
 2
 2 Institute for Human Infections and Immunity, University of Texas Medical Branch , Galveston, Texas.
 3
 3 Center for Tropical Diseases, University of Texas Medical Branch , Galveston, Texas.
 
 Abstract
 
 Powassan virus (POWV, Flaviviridae) is the only North American member of the tick-borne encephalitis serogroup of flaviviruses. It is transmitted to small- and medium-sized mammals by Ixodes scapularis, Ixodes cookei, and several other Ixodes tick species. Humans become infected with POWV during spillover transmission from the natural transmission cycles. In humans, POWV is the causative agent of a severe neuroinvasive illness with 50% of survivors displaying long-term neurological sequelae. POWV was recognized as a human pathogen in 1958 when a young boy died of severe encephalitis in Powassan, Ontario, and POWV was isolated from the brain autopsy of this case. Two distinct genetic lineages of POWV are now recognized: POWV (lineage I) and deer tick virus (lineage II). Since the index case in 1958, over 100 human cases of POWV have been reported, with an apparent rise in disease incidence in the past 16 years. This recent increase in cases may represent a true emergence of POWV in regions where the tick vector species are prevalent, or it could represent an increase in POWV surveillance and diagnosis. In the past 5 years, both basic and applied research for POWV disease has intensified, including phylogenetic studies, field surveillance, case studies, and animal model development. This review provides an overview of POWV, including the epidemiology, transmission, clinical disease, and diagnosis of POWV infection. Recent research developments and future priorities with regard to the disease are emphasized.
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 5.) Tick Saliva Enhances Powassan Virus Transmission to the Host, Influencing Its Dissemination and the Course of Disease.
 =================================================================
 J Virol. 2015 Aug;89(15):7852-60. doi: 10.1128/JVI.01056-15. Epub 2015 May 20.
 
 Hermance ME1, Thangamani S2.
 Author information
 
 1
 Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
 2
 Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA Galveston National Laboratory, University of Texas Medical Branch, Galveston, Texas, USA sathanga@utmb.edu.
 
 Abstract
 
 Powassan virus (POWV) is an encephalitic tick-borne flavivirus which can result in serious neuroinvasive disease with up to a 10% case fatality rate. The study objective was to determine whether the salivary gland extract (SGE) from Ixodes scapularis ticks facilitates the transmission and dissemination of POWV in a process known as saliva-activated transmission. Groups of BALB/c mice were footpad inoculated with either a high dose of POWV with and without SGE or a low dose of POWV with and without SGE. Mice from each group were sacrificed daily. Organ viral loads and gene expression profiles were evaluated by quantitative real-time PCR. Both groups of mice infected with high-dose POWV showed severe neurological signs of disease preceding death. The presence of SGE did not affect POWV transmission or disease outcome for mice infected with the high dose of POWV. Neuroinvasion, paralysis, and death occurred for all mice infected with the low dose of POWV plus SGE; however, for mice infected with the low dose of POWV in the absence of SGE, there were no clinical signs of infection and no mice succumbed to disease. Although this group displayed low-level viremias, all mice were completely healthy, and it was the only group in which POWV was cleared from the lymph nodes. We conclude that saliva-activated transmission occurs in mice infected with a low dose of POWV. Our study is the first to demonstrate virus dose-dependent saliva-activated transmission, warranting further investigation of the specific salivary factors responsible for enhancing POWV transmission.
 IMPORTANCE:
 
 Powassan virus (POWV) is a tick-borne flavivirus that continues to emerge in the United States, as is evident by the surge in number and expanding geographic range of confirmed cases in the past decade. This neuroinvasive virus is transmitted to humans by infected tick bites. Successful tick feeding is facilitated by a collection of pharmacologically active factors in tick saliva. In a process known as saliva-activated transmission, tick bioactive salivary molecules are thought to modulate the host environment, making it more favorable for the transmission and establishment of a pathogen. This phenomenon has been demonstrated for several tick-borne pathogens; however, a systematic investigation of the role of tick saliva on dissemination and pathogenesis of a tick-borne viral disease has never been attempted before. This study will fill that gap by systematically examining whether the presence of tick saliva contributes to the transmission and dissemination of POWV in mice.
 
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 6.) Isolation of deer tick virus (Powassan virus, lineage II) from Ixodes scapularis and detection of antibody in vertebrate hosts sampled in the Hudson Valley, New York State.
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 Parasit Vectors. 2013 Jul 15;6:185. doi: 10.1186/1756-3305-6-185.
 
 Dupuis AP 2nd1, Peters RJ, Prusinski MA, Falco RC, Ostfeld RS, Kramer LD.
 Author information
 
 1
 The Arbovirus Laboratories, Wadsworth Center, New York State Department of Health, 5668 State Farm Rd, Slingerlands, NY, 12159, USA. kramer@wadsworth.org.
 
 Abstract
 BACKGROUND:
 
 Deer tick virus, DTV, is a genetically and ecologically distinct lineage of Powassan virus (POWV) also known as lineage II POWV. Human incidence of POW encephalitis has increased in the last 15 years potentially due to the emergence of DTV, particularly in the Hudson Valley of New York State. We initiated an extensive sampling campaign to determine whether POWV was extant throughout the Hudson Valley in tick vectors and/or vertebrate hosts.
 METHODS:
 
 More than 13,000 ticks were collected from hosts or vegetation and tested for the presence of DTV using molecular and virus isolation techniques. Vertebrate hosts of Ixodes scapularis (black-legged tick) were trapped (mammals) or netted (birds) and blood samples analyzed for the presence of neutralizing antibodies to POWV. Maximum likelihood estimates (MLE) were calculated to determine infection rates in ticks at each study site.
 RESULTS:
 
 Evidence of DTV was identified each year from 2007 to 2012, in nymphal and adult I. scapularis collected from the Hudson Valley. 58 tick pools were positive for virus and/or RNA. Infection rates were higher in adult ticks collected from areas east of the Hudson River. MLE limits ranged from 0.2-6.0 infected adults per 100 at sites where DTV was detected. Virginia opossums, striped skunks and raccoons were the source of infected nymphal ticks collected as replete larvae. Serologic evidence of POWV infection was detected in woodchucks (4/6), an opossum (1/6), and birds (4/727). Lineage I, prototype POWV, was not detected.
 CONCLUSIONS:
 
 These data demonstrate widespread enzootic transmission of DTV throughout the Hudson Valley, in particular areas east of the river. High infection rates were detected in counties where recent POW encephalitis cases have been identified, supporting the hypothesis that lineage II POWV, DTV, is responsible for these human infections.
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 7.) Powassan/Deer Tick Virus and Borrelia Burgdorferi Infection in Wisconsin Tick Populations.
 =================================================================
 Vector Borne Zoonotic Dis. 2017 Jul;17(7):463-466. doi: 10.1089/vbz.2016.2082. Epub 2017 May 10.
 
 Knox KK1, Thomm AM1, Harrington YA1, Ketter E2, Patitucci JM3, Carrigan DR4.
 Author information
 
 1
 1 Coppe Healthcare Solutions , Waukesha, Wisconsin.
 2
 2 Stowers Institute for Medical Research , Kansas City, Missouri.
 3
 3 Marshfield Clinic Research Foundation , Marshfield, Wisconsin.
 4
 4 Wisconsin Viral Research Group , Waukesha, Wisconsin.
 
 Abstract
 
 Powassan/Deer Tick Virus (POWV/DTV) is an emerging cause of arboviral neuroinvasive disease in the upper Midwest. These studies describe the prevalence and geographic distribution of Wisconsin ticks carrying POWV/DTV as well as the high frequency of Ixodes scapularis ticks coinfected with both POWV/DTV and Borrelia burgdorferi, the causative agent of Lyme disease. These findings suggest that concurrent transmission of POWV/DTV and B. Burgdorferi from coinfected ticks is likely to occur in humans.
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 8.) Powassan meningoencephalitis, New York, New York, USA.
 =================================================================
 Emerg Infect Dis. 2013;19(9). doi: 10.3201/eid1909.121846.
 
 Sung S1, Wurcel AG, Whittier S, Kulas K, Kramer LD, Flam R, Roberts JK, Tsiouris S.
 Author information
 
 1
 Department of Pathology, Columbia University, 830 West 168th St, New York City , NY 10032, USA. ss3768@columbia.edu
 
 Abstract
 
 Disease caused by Powassan virus (POWV), a tick-borne flavivirus, ranges from asymptomatic to severe neurologic compromise and death. Two cases of POWV meningoencephalitis in New York, USA, highlight diagnostic techniques, neurologic outcomes, and the effect of POWV on communities to which it is endemic.
 =================================================================
 9.) Powassan Virus
 =================================================================
 Source: CDC (Center for Control and Disease Prevention)
 
 Powassan (POW) virus is transmitted to humans by infected ticks. Approximately 75 cases of POW virus disease were reported in the United States over the past 10 years. Most cases have occurred in the Northeast and Great Lakes region. Signs and symptoms of infection can include fever, headache, vomiting, weakness, confusion, seizures, and memory loss. Long-term neurologic problems may occur. There is no specific treatment, but people with severe POW virus illnesses often need to be hospitalized to receive respiratory support, intravenous fluids, or medications to reduce swelling in the brain.
 
 You can reduce your risk of being infected with POW virus by using tick repellents, wearing long sleeves and pants, avoiding bushy and wooded areas, and doing thorough tick checks after spending time outdoors. If you think you or a family member may have POW virus disease, it is important to consult your healthcare provider.
 
 Symptoms
 ========
 Many people who become infected with Powassan (POW) virus do not develop any symptoms.
 The incubation period (time from tick bite to onset of illness) ranges from about 1 week to 1 month.
 POW virus can infect the central nervous system and cause encephalitis (inflammation of the brain) and meningitis (inflammation of the membranes that surround the brain and spinal cord).
 Symptoms can include fever, headache, vomiting, weakness, confusion, loss of coordination, speech difficulties, and seizures.
 Approximately half of survivors have permanent neurological symptoms, such as recurrent headaches, muscle wasting and memory problems.
 Approximately 10% of POW virus encephalitis cases are fatal.
 
 Treatment
 =========
 There are no vaccines or medications to treat or prevent POW virus infection.
 If you think you or a family member may have POW virus disease, see your health care provider for evaluation and diagnosis.
 Persons with severe POW illnesses often need to be hospitalized. Treatment may include respiratory support, intravenous fluids, and medications to reduce swelling in the brain.
 
 prevention
 =========
 
 Reducing exposure to ticks is the best defense against Powassan virus disease, Lyme disease, Rocky Mountain spotted fever, and other tickborne infections. There is no vaccine for Powassan virus . There are several steps you and your family can take to prevent and control Powassan virus disease as demonstrated on the Lyme disease website.
 
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 10.) Tickborne Powassan virus infections among Wisconsin residents.
 ================================================================
 WMJ. 2010 Apr;109(2):91-7.
 
 Johnson DK1, Staples JE, Sotir MJ, Warshauer DM, Davis JP.
 Author information
 
 1
 Bureau of Communicable Diseases and Emergency Response, Wisconsin Division of Public Health, Madison, WI 53701-2659, USA. diep.hoangjohnson@wi.gov
 
 Abstract
 INTRODUCTION:
 
 Powassan virus (POWV) is a tickborne Flavivirus that causes a rare but potentially life-threatening illness. The first reported case of POWV infection in a Wisconsin resident occurred in 2003. Enhanced surveillance and testing detected 2 additional cases.
 METHODS:
 
 Patient specimens with a positive or equivocal immunoglobulin M (IgM) antibody to an arbovirus were sent from commercial laboratories to the Wisconsin State Laboratory of Hygiene and forwarded to the Centers for Disease Control and Prevention (CDC) for confirmatory testing. Patients with laboratory confirmed POWV infections were interviewed to obtain demographic, clinical, and epidemiologic information.
 RESULTS:
 
 POWV infections were confirmed in 3 adult Wisconsin residents in 2003, 2006, and 2007; illness onsets occurred during May and June. Two patients were hospitalized and all survived. One patient had a dual infection with POWV and Anaplasma phaghocytophilum. Specimens from all 3 patients were initially reported as positive for IgM antibody to either St Louis encephalitis or California serogroup viruses; POWV-specific antibody was detected during confirmatory testing at the CDC. Each patient had exposures to known or likely tick habitats in different counties within 30 days before illness onset.
 CONCLUSIONS:
 
 These are the first diagnosed human POWV infections in Wisconsin. Because all 3 patients were initially identified as having other arboviral infections using commercial screening kits, routine confirmatory testing is essential for proper diagnosis of most arboviral infections. Wisconsin residents should be educated regarding risks of acquiring and ways to prevent POWV infection and other tickborne diseases when spending time outdoors.
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 11.) Prevalence and genetic characterization of Powassan virus strains infecting Ixodes scapularis in Connecticut.
 ==================================================================
 Am J Trop Med Hyg. 2012 Oct;87(4):754-9. doi: 10.4269/ajtmh.2012.12-0294. Epub 2012 Aug 13.
 
 Anderson JF1, Armstrong PM.
 Author information
 
 1
 Department of Entomology and Center for Vector Biology and Zoonotic Diseases, The Connecticut Agricultural Experiment Station, New Haven, CT 06504-1106, USA. John.F.Anderson@CT.Gov
 
 Abstract
 
 A total of 30 Powassan virus (POWV) isolates from Ixodes scapularis collected from Bridgeport and North Branford, CT in 2008, 2010, 2011, and 2012 and one earlier isolate from Ixodes cookei collected in Old Lyme, CT in 1978 were characterized by phylogenetic analysis of their envelope gene sequences. Powassan virus sequences segregated into two major groups termed the deer tick virus (DTV) and Powassan (POW) lineages. The lineage from I. cookei was POW. The remaining viruses from I. scapularis grouped with the DTV lineage. Powassan viruses from Bridgeport were nearly identical and clustered with a virus strain from a human in New York. Viruses from North Branford were homogeneous and grouped with viruses from Massachusetts, northwestern Connecticut, and Ontario. These findings suggest that POWV was independently introduced into these geographical locations in Connecticut and maintained focally in their respective environments. An improved method of isolation of POWV in vitro is described.
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 12.) Increased recognition of Powassan encephalitis in the United States, 1999-2005.
 ================================================================
 Vector Borne Zoonotic Dis. 2008 Dec;8(6):733-40. doi: 10.1089/vbz.2008.0022.
 
 Hinten SR1, Beckett GA, Gensheimer KF, Pritchard E, Courtney TM, Sears SD, Woytowicz JM, Preston DG, Smith RP Jr, Rand PW, Lacombe EH, Holman MS, Lubelczyk CB, Kelso PT, Beelen AP, Stobierski MG, Sotir MJ, Wong S, Ebel G, Kosoy O, Piesman J, Campbell GL, Marfin AA.
 
 Author information
 
 1
 Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, U.S. Public Health Service, Department of Health and Human Services, Fort Collins, Colorado 80522, USA.
 
 Abstract
 
 Powassan virus (POWV) disease is a rare human disease caused by a tick-borne encephalitis group flavivirus maintained in a transmission cycle between Ixodes cookei and other ixodid ticks and small and medium-sized mammals. During 1958-1998, only 27 POWV disease cases (mostly Powassan encephalitis) were reported from eastern Canada and the northeastern United States (average, 0.7 cases per year). During 1999-2005, nine cases (described herein) of serologically confirmed POWV disease were reported in the United States (average, 1.3 cases per year): four from Maine, two from New York, and one each from Michigan, Vermont, and Wisconsin. The Michigan and Wisconsin cases are the first ever reported from the north-central United States. Of these nine patients, 5 (56%) were men, the median age was 69 years (range: 25-91 years), and 6 (67%) had onset during May-July. All but one patient developed encephalitis with acute onset of profound muscle weakness, confusion, and other severe neurologic signs. In one case, no neurologic symptoms were present but the presence of pleocytosis, an elevated cerebrospinal fluid (CSF) protein concentration, and POWV-specific immunoglobulin M in CSF suggested neuroinvasion. All patients recovered from their acute disease, but most had long-term neurologic sequelae. Periresidential ecologic investigations were performed in three cases, including tests of local mammals and ticks for evidence of POWV infection. Woodchucks (Marmota monax), striped skunks (Mephitis mephitis), and a raccoon (Procyon lotor) collected at two of the Maine case-patients' residences had neutralizing antibody titers to POWV. I. cookei were found on woodchucks and skunks and questing in grassy areas of one of these residences; all were negative for POWV. Although POWV disease is rare, it is probably under-recognized, and it causes significant morbidity, and thus is an additional tick-borne emerging infectious disease entity. Because no vaccine or specific therapy is available, the basis of prevention is personal protection from ticks (or "tick hygiene") and reduced exposure to peridomestic wild mammals.
 =================================================================
 13.) Another Dies From Powassan / New York Man Dies From Tick Carrying Brain Swelling Virus
 =================================================================
 by lymecoordinator56
 
 source: hudsonvalleypost.com/new-york-man-dies-from-rare-tick-carrying-brain-swelling-virus/
 
 New York Man Dies From Tick Carrying Brain Swelling Virus
 By Bobby Welber July 13, 2017 10:27 AM
 
 
 The daughter of a man who lived just outside the Hudson Valley is warning the public after her father died from a tick that carries a rare brain swelling virus.
 
 In early May or late April, 74-year-old Charles Smith of Saratoga County discovered a tick bite near his elbow. Ten days later, Smith became very sick and was rushed to a hospital.
 
 After a number of tests, he was diagnosed with the Powassan virus and died in early
 June, reports WYNT.
 
 The Powassan virus is spread by the same deer tick that carries Lyme disease. Powassan, which in some cases has been fatal, attacks the nervous system and can cause a dangerous brain swelling.
 
 Other symptoms can include vomiting, weakness, confusion, seizures and memory loss.
 
 There is currently no treatment for the virus, which according to the CDC kills around 10% of people who become sick. Half are left with permanent neurological problems.
 
 At the families urging, on Wednesday, the New York State Department of Health confirmed that Smith was diagnosed with the Powassan virus.
 
 “Why has it taken us to to contact you to make people aware?” Stephanie wondered to WYNT.
 
 To decrease your risk of being infected with the Powassan virus the CDC recommends using tick repellents, wearing long sleeves and pants, avoiding bushy and wooded areas and doing thorough tick checks after spending time outdoor.
 
 Correction: This article originally stated that the death of 17-year-old Poughkeepsie High School Joseph Elone in 2013 was from Powassan virus.
 While Powassan virus was initially suspected, Elone in fact died of Lyme carditis, according to the Lyme Action Network.
 
 **Comment**
 
 If you've read the articles I've posted this summer about Powassan you will realize it can no longer be called "rare." Too many have died in such a short period of time.
 
 Also, the daughter of the deceased makes a valid point: she had to contact authorities. This is a huge reason why they are stating it is "rare." How many people are going to think of contacting authorities when they are grieving a loved one? This should be a reportable disease in every state, requiring health professionals to report it. This should also hold true for every other tick borne infection. Those of us with boots on the ground know full well these infections are NOT rare - just rarely diagnosed and reported.
 
 Despite what authorities say, there are things you can do for viruses besides hydrate people: Source: madisonarealymesupportgroup.com/2016/03/28/combating-viruses/
 
 Source:newsmax.com/Health/Health-News/ozone-therapy-treatment-cancer/2015/03/20/id/631395/ Ozone was first used in medicine at the end of the 19th century to treat tuberculosis. During World War I, medics used it to disinfect wounds. Since the 1950s, ozone therapy has gained popularity throughout the world. More than 45,000 physicians in 50 countries now administer ozone. Ozone is typically administered with one of two different IV methods:
 
 Major Auto-Hemotherapy (MAH), in which blood is drawn from the patient, exposed to ozone and re-injected into the patient.
 
 Direct Intravenous Ozone Therapy (DIV), in which oxygen and ozone are directly infused into the patient’s bloodstream.
 
 Source: medicalozone.info/ozone-therapy-infected-blood/ Here ozone has an inhibitory effect upon parasites. The parasites are subjected to an increased oxidative stress, and their reproductive cycle is disrupted. Ozonation was carried out at a concentration of 80 µg/ml in a RBC suspension. Optimal growth inhibition was obtained by applying ozone twice, i.e. immediately before and after infection.
 
 Source: oxygenhealingtherapies.com/Why_Ozone_Therapy.html More About Viruses
 "In each reproducing cell in our bodies there are two substances: RNA and DNA – the ‘helix' form discovered by Crick and Watson. They contain the genetic blueprint for the cell, and the whole body. Viruses are not cells, they are either RNA or DNA genetic material - but not both - surrounded by a coat of protein. Since they have only half of the genetic material, they cannot reproduce on their own. They multiply by attaching themselves to the inner RNA or DNA of normal cells, taking it over and forcing the cell to make more of the virus. Picture slave labor. They wait there and emerge when our defenses are down! Outside of their host cell they are basically inert so it is clear that they are ‘hiding out' in the cells, and must be uncovered within the cell to be destroyed before they manifest their destructive potential. This is where the amazing property of ozone to invade diseased cells, uncovering and destroying the disease or virus, is so effective."
 
 Although MAH improves many diseases and conditions, it rarely eliminates them. So many doctors prefer DIV, which is safer to perform, yet more powerful in its effects. “DIV is the only way you can get rid of something,” says Robins. According to proponents, ozone therapy is broadly effective because it attacks and removes disease-causing agents, including viruses, bacteria, fungi, molds, yeast, and toxic metals.
 
 Although ozone therapy is often denigrated by mainstream physicians in the U.S., in other countries such as Germany, it is considered safe and a standard of care. “When people ask why ozone therapy isn’t more available in the United States, I say it’s because it’s not a patentable medicine and the drug companies can’t make any money off it,” says Robins. “That’s probably the main reason why it’s been suppressed.”
 
 For a list of ozone therapists, go to oxygentherapyexperts.com.
 
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 14.) Powassan virus encephalitis, Minnesota, USA.
 =================================================================
 Emerg Infect Dis. 2012 Oct;18(10):1669-71. doi: 10.3201/eid1810.120621.
 
 Birge J1, Sonnesyn S.
 Author information
 
 1
 Abbott Northwestern Hospital, Minneapolis, Minnesota, USA. birgejustin@gmail.com
 
 Abstract
 
 Powassan virus (POWV) is a rare tick-borne agent of encephalitis in North America. Historically, confirmed cases occurred mainly in the northeastern United States. Since 2008, confirmed cases in Minnesota and Wisconsin have increased. We report a fatal case of POWV encephalitis in Minnesota. POWV infection should be suspected in tick-exposed patients with viral encephalitis.
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 15.) Powassan virus in mammals, Alaska and New Mexico, U.S.A., and Russia, 2004-2007.
 =================================================================
 Emerg Infect Dis. 2013 Dec;19(12):2012-6. doi: 10.3201/eid1912.130319.
 
 Deardorff ER, Nofchissey RA, Cook JA, Hope AG, Tsvetkova A, Talbot SL, Ebel GD.
 Abstract
 
 Powassan virus is endemic to the United States, Canada, and the Russian Far East. We report serologic evidence of circulation of this virus in Alaska, New Mexico, and Siberia. These data support further studies of viral ecology in rapidly changing Arctic environments.
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 16.) Tick-borne encephalitis among U.S. travelers to Europe and Asia - 2000-2009.
 Centers for Disease Control and Prevention (CDC).
 =================================================================
 MMWR Morb Mortal Wkly Rep. 2010 Mar 26;59(11):335-8.
 
 Abstract
 
 Tick-borne encephalitis virus (TBEV) is the most common arbovirus transmitted by ticks in Europe. Approximately 10,000 cases of tick-borne encephalitis (TBE) are reported annually in Europe and Russia. Although TBE is endemic in parts of China, information regarding its incidence is limited. TBEV is closely related to Powassan virus (POWV), another tick-borne flavivirus that is a rare cause of encephalitis in North America and Russia; TBEV and POWV can cross-react in serologic tests. Before 2000, two cases of TBE in North American travelers to Europe were reported. State health officials or clinicians send specimens from patients with unexplained encephalitis to CDC as part of routine surveillance and diagnostic testing. CDC recently reviewed all 2000-2009 laboratory records to identify cases of TBE among U.S. travelers; the five cases identified are summarized in this report. All five cases had TBEV or POWV immunoglobulin M (IgM) antibodies in serum and were confirmed as acute TBE cases by plaque-reduction neutralization tests against both viruses. All four patients who had traveled to Europe or Russia had biphasic illnesses (a common feature of TBE) and made nearly complete recoveries. The fifth patient, the first reported case of TBE in a U.S. traveler to China, had a monophasic illness with severe encephalitis and neurologic sequelae. Health-care providers should be aware of TBE, should counsel travelers about measures to reduce exposure to tick bites, and should consider the diagnosis of TBE in travelers returning from TBE-endemic countries with meningitis or encephalitis.
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 17.) Tick-Borne Encephalitis Virus in Ticks and Roe Deer, the Netherlands.
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 Jahfari S, de Vries A, Rijks JM, Van Gucht S, Vennema H, Sprong H, Rockx B.
 Abstract
 
 We report the presence of tick-borne encephalitis virus (TBEV) in the Netherlands. Serologic screening of roe deer found TBEV-neutralizing antibodies with a seroprevalence of 2%, and TBEV RNA was detected in 2 ticks from the same location. Enhanced surveillance and awareness among medical professionals has led to the identification of autochthonous cases.
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 18.) Stable prevalence of Powassan virus in Ixodes scapularis in a northern Wisconsin focus.
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 Am J Trop Med Hyg. 2008 Dec;79(6):971-3.
 
 Brackney DE1, Nofchissey RA, Fitzpatrick KA, Brown IK, Ebel GD.
 Author information
 
 1
 University of New Mexico School of Medicine, Department of Pathology, Albuquerque, New Mexico 87131, USA.
 
 Abstract
 
 Deer tick virus (DTV), a variant of Powassan virus (POWV), appears to be maintained in nature in an enzootic cycle between Ixodes scapularis ticks and small mammals. Although POWV infection of human beings is rare, a recent report suggests increasing incidence and the possibility that POWV may be an emerging tick-borne zoonosis. Therefore, we assessed the long-term stability of the POWV transmission cycle in northwestern Wisconsin. Adult I. scapularis and Dermacentor variabilis were collected from Hayward and Spooner, Wisconsin, screened for infection by reverse transcriptase polymerase chain reaction (RT-PCR), and virus was isolated. Seventeen of 1,335 (1.3%) of I. scapularis and 0 of 222 (0%) of D. variabilis ticks were infected. All isolated virus belonged to the DTV genotype of POWV. These findings suggest stable transmission of POWV in this focus over ten years and highlight the potential for this agent to emerge as a public health concern.
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 19.) Seroprevalence of Powassan virus in New England deer, 1979-2010.
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 Am J Trop Med Hyg. 2013 Jun;88(6):1159-62. doi: 10.4269/ajtmh.12-0586. Epub 2013 Apr 8.
 
 Nofchissey RA1, Deardorff ER, Blevins TM, Anishchenko M, Bosco-Lauth A, Berl E, Lubelczyk C, Mutebi JP, Brault AC, Ebel GD, Magnarelli LA.
 Author information
 
 1
 University of New Mexico School of Medicine, Albuquerque, NM, USA. rnofchissey@salud.unm.edu
 
 Abstract
 
 Powassan virus and its subtype, deer tick virus, are closely related tick-borne flaviviruses that circulate in North America. The incidence of human infection by these agents appears to have increased in recent years. To define exposure patterns among white-tailed deer, potentially useful sentinels that are frequently parasitized by ticks, we screened serum samples collected during 1979-2010 in Connecticut, Maine, and Vermont for neutralizing antibody by using a novel recombinant deer tick virus-West Nile virus chimeric virus. Evidence of exposure was detected in all three states. Overall our results demonstrate that seroprevalence is variable in time and space, suggesting that risk of exposure to Powassan virus is similarly variable.
 
 
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