Definition of herpes – Definicion.de

Herpes is a rash that is usually chronic and generates stinging and itching. It can appear in isolated spots of the skin and under very different ways. It is possible to distinguish between herpes simplex and herpes zoster. Herpes simplex is an infectious disease characterized by skin lesions formed by small vesicles cluster. These vesicles, which are surrounded by a red halo, are caused by a virus. Although there is no cure for herpes simplex, medicine has developed various forms of treatment that can reduce symptoms and speed healing of injuries. Herpes zoster or shingles, also known as shingles and culebrina, is a disease caused by reactivation of the chickenpox virus. This disorder causes small painful blisters grouped around a dermatome. Shingles can appear on the lips, eyes and genitals. Early symptoms of shingles include fever, sensitivity to light, headache and malaise. After the start tingling, itching and severe pain in the area of ​​the affected nerve until the rash occurs. In some cases, especially in the elderly, pain caused by shingles becomes chronic (post-herpetic neuralgia). The severity of pain may incapacitate the patient.

Shingles, like herpes simplex, can not be cured (ie, the virus can not be removed from the body). There are, however, treatments to relieve symptoms and reduce the severity and extent of the process. emotional consequences of genital herpes While there are physical causes of the emergence of a herpes often the main reason is psychological. Similarly, also the condition of this disease can bring significant emotional conflicts for an individual. Genital herpes can be very common, however, there is still great resistance from people to talk about it. It is that generally feel affected by this problem quite often brings severe emotional consequences. One of the most common to suffer from this disorder advice is to start a psychological treatment to prevent their consequences more severe than those already present physical. It is important that in addition to treating the visible problem with antivirals, or treatment as recommended to us by our specialist, also work on the feelings caused by the inability to lead a normal life. Shame felt by the patient prevents you approach a friend or relative to discuss the subject, why it is so important that there is a therapist who can guide you so you know channel their anxieties in the most appropriate way. Mp do, it is likely that the individual is affected by any emotional illness, the most common is depression. Once the patient is diagnosed, feel serious discomfort, caused by the feeling of seeing wounded his honor. The fact that it is a disease that is contracted through sexual transmission, fills it with greater shame.

Guilt can be a serious impediment for mental health. And if the infection was caused by not taking the recommended precautions, it can achieve greater quantities, they can get even self-loathing or harmful attitudes himself. The consequences of this can be: an aberrant fear that will lead reclusive, avoiding contact even with their friends, even those with whom he felt more united. This voluntary confinement should be discussed with a specialist, who will help the affected solve their emotional problems and make decisions that do not put their mental stability.

INFECTION Cytomegalovirus | Microbes on the Net

INTRODUCTION It is a virus Herpetoviridae family, subfamily B-Herpesviridae. Also called human herpesvirus type 5. Between 40 and 100% of the general population is seropositive for CMV. Male homosexuals have a seropositivity close to 100%. CMV infection can be asymptomatic, it can manifest itself as a mononucleotico syndrome and even present as disseminated infection in immunocompromised individuals. Morphology and Antigenic structure It is a double-stranded DNA virus that replicates in the nucleus of cells to which invades. It presents icosahedral symmetry and a lipoprotein envelope with spicules (see picture). Cytomegalovirus physiopathogeny a) congenital CMV Infection: Congenital infection is acquired:

By primary infection of the mother represents the vast majority of cases. By reactivation of latent maternal infection. b) CMV infection in childhood and adulthood: often associated with a strong T cell response to infection, which can causes a syndrome Mononuclear. Once acquired infection (symptomatic or not) remain indefinitely in the host tissues (latent infection). The virus is transmitted by oropharyngeal secretions, urine, vagina, semen, breast milk and blood. The virus enters therefore, by mouth, genitals, or transfused through the placenta (transplacental) blood. The infection produces “viremia”, especially coupled with polymorphonuclear (PMN). Ductal epithelia infects: salivary gland, kidney, although it can infect other tissues (endothelium). CLINICAL CONGENITAL INFECTION 5% of infected fetuses develop “Cytomegalic disease of the newborn” compromising the reticuloendothelial system and central nervous system. It is characterized by petechiae, hepatosplenomegaly and jaundice (more common triad), microcephaly, cerebral calcifications, intrauterine growth retardation, prematurity, corioretinitis.

His prognosis is bad. perinatal infection The vast majority are asymptomatic. The newborn can become infected during passage through the birth canal or by ingesting breast milk or contact with other drainage from the mother. Approximately 40-60% of children breastfed by HIV-positive mothers for more than a month acquire the virus. The following tables have been linked to perinatal CMV infection: interstitial pneumonitis, hepatitis, anemia, rash and lymphadenopathy. CMV mononucleosis CMV may cause a syndrome of infectious mononucleosis heterophile antibodies without (unlike EBV mononucleosis producing these antibodies). The disease most often affects young sexually active and lasts 2 to 6 weeks. It has prolonged high fever, chills, severe fatigue, malaise, myalgia, headache and splenomegaly. Unlike EBV mononucleosis, exudative pharyngitis and cervical lymphadenopathy they are rare. Rarely it presents: pneumonia or pneumonitis, myocarditis, pleurisy, arthritis, encephalitis and even a Guillain Barre syndrome. CMV infection in immunocompromised hosts

The CMV virus appears to be the most frequently complicated organ transplants (heart, lung, kidney, liver or bone marrow). Especially it affects patients with less than 50-100 CD4 + / mm3. In patients with advanced HIV infection, CMV is an important pathogen that frequently causes: Retinitis: more common presentation. It is a major cause of blindness in immunocompromised patients, especially those with advanced AIDS. The relative risk for developing CMV encephalitis in patients with retinitis, is 9. 5 and increases to 13 when retinitis affects peripapillary region (in these cases, 75% percent have encephalitis). Disseminated infection. It is manifested by: Fever, night sweats, malaise, anorexia and fatigue. Arthralgia and myalgia. There may be respiratory compromise: Tachypnea, hypoxia and nonproductive cough (differential diagnosis with PCP, deep fungal infections and viral or bacterial infections).

It can affect the digestive tract: ulcers in the esophagus, stomach and intestine, which may bleed or punctured. It can also cause encephalitis. DIAGNOSIS The microbiological diagnosis of CMV infection is based on the search for the virus (culture isolation), its antigens or genome (DNA). Samples used: urine, saliva, genital secretions or blood (Remember that the isolation of the virus in urine or saliva may be due to an infection back months or years). Viral isolation in cell cultures: human fibroblast monolayers where its cytopathic effect is observed (if viral titers are high, the cytopathic effect is observed within a few days of culture, otherwise delay weeks or months). Detection of viral antigens (pp65) in peripheral leukocytes Detection of viral DNA in blood, CSF or tissue (PCR). Detection of seroconversion: one determination of antibodies is not useful for the diagnosis, it is necessary to determine a seroconversion. TREATMENT Antivirals action against CMV: Gancliclovir: Selective inihibidor of CMV DNA polymerase.

Valganciclovir: derived from the use enteral ganciclovir. Foscarnet: is used in cases of resistance to ganciclovir. Cidofovir: prolonged half-life allowing intermittent intravenous administration (weekly). Epidemiology and Prophylaxis It has a cosmopolitan distribution. In the United States, 1% of newborns infected with CMV. In less developed countries (such as countries in South America) the percentage is even higher. It is known that viral shedding favors the fact of living in closed communities, poor hygiene, prolonged and intimate contact between two people. In adolescents and young adults, the virus is sexually transmitted (is transmitted by semen and cervical secretions of people usually asymptomatic). Once infected, an individual immunocompetent has latent virus probably for life. If you experience any event that compromises their immunity may suffer a disease ocacionada by viral reactivation. The vaccine is experimental. BIBLIOGRAPHY

MEDICAL VIROLOGY: CARBALLAL, OUBIÑA. SHOWCARD professor of MICROBIOLOGIA MEDICA 1999 – UNT. “CYTOMEGALOVIRUS AND HUMAN HERPES TYPE 6,7 and 8”. CAP 166. EDITION OF THE 16 ° HARRISON’S PRINCIPLES OF INTERNAL MEDICINE.

Fat embolism | NeuroWikia

EMBOLISM GREASE This entity should be encompassed in the differential diagnosis of changes in level of consciousness. The main clinical symptoms include psychomotor agitation, decreased level of consciousness, increased breathing and heart rate, fever, petechiae and subconjunctival chest. – The most common cause is long bone fracture (femur, tibia, fibula), being more frequent in comminuted and closed. It can also occur as a complication of other diseases (pancreatitis, burns), cosmetic procedures where the remodeling of adipose tissue-extraction (liposuction) and in patients used to support cardiopulmonary bypass during surgery occurs. – Clinical symptoms usually appear 24-72 hours after the underlying event that triggers, with a higher incidence in males. In addition due to the greater amount of fat young bone it is more common in the first decades of life. – The strongest pathophysiological substrate is spread (mainly traumatic) fatty marrow elements circulatory level that produces consistently platelet aggregation and formation of microembolisms systemically with involvement of multiple target organs. Another theory states that the involvement of the level of consciousness is secondary to hypoxia-hypoperfusion secondary to pulmonary and cardiac involvement. – The clinical-therapeutic management of this disease is based on the maintenance of tissue perfusion, with albumin for their palatability to peripheral fatty elements, which are fixed, preventing them from reaching plungers fatty pulmonary and cerebral level, and measures invasive ventilatory support-if the clinical situation warrants. This entity is critical early fracture stabilization, avoiding the discharge of fat molecules into the bloodstream, and evaluate the hemodynamic status of the patient and good control of perfusion / diuresis allowing “wash” fatty blood level elements. Bibliography Bettermann, K.

(2006) Transient global amnesia: Continuing the quest for a source. Arch Neurol; 63: 1336. Caminero A. (2005) posterior reversible encephalopathy syndrome. Neurology, 20: 327-331. Commission on Classification and Terminology of the International League Against Epilepsy (1989) Epilepsy. ; 30: 389. Fulde GW, Harrison P. (1991) Fat embolism – a review. Arch Emerg Med; 8: 233. Hinchey J, Chaves C, Apiggnani B, J Breen, Pao L, Wang A. reversible posterior leukoencephalopathy syndrome A (1996) N Engl J Med. ; 334: 494-500.

Jacobson D, Terrence C, O. Reinmuth (1986) The neurologic manifestations of fat embolism. Neurology; 36: 847. Manzano S, Kurtis M, Caicoya A, Mark A. (2005) posterior reversible encephalopathy syndrome. Neurology; 20: 380-381. Maurice M, Allan M. (2004) Cerebrovascular Diseases. In: Victor M, M Rebollo, Ricart C. Hypertensive encephalopathy. In Martí-Vilalta JL. cerebral vascular diseases. 2nd edition.

(Pp 357-362) . Barcelona. Editorial Prous. Raschilas F, Wolff M, Delatour F. (2002) Outcome of and prognostic factors for herpes simplex encephalitis in adult Patients: results of a multicenter study. Clin Infect Dis; 35: 254. Roach, ES (2006). Transient global amnesia: look at Mechanisms not causes. Arch Neurol; 63: 1338. Ropper AH, Brown RH (2007) Delirium and other acute confusional states Definition. Ropper AH, Brown RH Principles of Neurology. 8th edition. (Pp 355-366).

Mexico. Editorial Mc Graw-Hill. Sander K Sander D. (2005) New insights into the global amnesia: recent imaging and clinical findings. Lancet Neurology; 4: 437-44 CJ Vaughan, In Front N. (2000) Hypertensive emergencies. Lancet; 356: 411 Whitley, RJ. Viral encephalitis (1990). N Engl J Med; 323: 242. 2364 readings

Genital HSV 1. What am I Dealing with? – Herpes

Thank you so much for your reply and information. Could you just read If what is below and offer any insight lesson That May possibly my stress and worries about this, by god you are a saint. I Have Been Having real battle trying to figure out what to do about this, as well as viruses and putting esta situation into perspective. I am not afraid of virus esta Because in the grand scheme of things it is a Relatively insignificant infection. so i am more afraid of contracting the virus and then a esta things not working out Between the two of us. I am afraid That it will hinder my abilities to find another woman due to the overall social perspective of the virus. I am guilty of being very ignorant on the subject, like MOST of us Because we are Taught to fear STDs in high school / sexed cources etc. I am even guilty of advising a friend to stay away from someone Who Had Told him openly HSV She Had . . . And now for This I feel so awful and wish i could take back everything i said to him. If i were to contract esta virus from her and we lived happily ever after, then a by god i could give two shizz About the virus. Its my fear of contracting it and it not working out That worries me most .

. . I personally never seen a cold Have sore ever in my life, or rather i have never seen anything of significance on someones sheer lip to make me think it was a cold sore. I think my best friend dated a Girl Who May or May not of had a cold sore every now again, but I does not show any signs of cold sores . . . If the girl im dating Told me she HAD had a cold sore on her lip at one point in her life say 4 years ago? how would i feel about it? idk what i would think . . . i would probably be like “cold sore? eleven?

NBD? ” and probably would Have Carried on a relationship With Her With no second thoughts . . . So should i really look at this any differently from That scenario? Facts are just . . . she has the exact same virus causes cold sores That, only it’s in a different region of her body, and it so happens to be her sex organs . . . She Had 1 outbreak . .

. her first and only 4 years ago. Is it really any different than Having a coldsore on her lip? She contracted it from a guy down on her WHO Went with a cold sore . . . That tells me but she kissed him before must of all this right? so why doesnt she orally as well HSV1 Have? (She has never had a cold sore orally) But at the same time then a, i keep telling myself that i could very well Already Have This virus . . . I Talked to my dad about this.

He Said I hasnt Known of anyone in our family to have a cold sores. but i’ve kissed a “fair” share of girls in my day . . . never one with a cold sore i believe. Any who . . . I have not had sex With Her yet. I am not that sexually active . . . never Have Been Because i have always Looked for someone to spend the rest of my life with.


I have never had sex With anyone i didnt think at one point i would want to spend the rest of my life with. 2 people my whole life and I am 2 years out of college. I really just want to do the right thing here, and i do not want to make any decision i regret . . . The most frustrating part about prep all this is not exactly what i am Knowing dealing with. Its the lack of sufficient information That is bothering the hell out of me. Ive read so much about this and yet nothing is ever in September it stone . . . So say i do not carry it . . .

That Means i can contract it still . . . She has HSV1 vaginally . . . She has HAD ONE initial outbreak 4 years ago, nothing else . . . The virus supposedly sheds 5% of roughly 18 days days a year. She Takes oral meds Which supposedly you reduce shedding / obs 50%, 18 days to 9 days now . . .

If i use a condom That you reduce transmission by 30% even supposedly lessening the likelihood of transmission. 4 years Have gone by since her initial and only ob . . . meaning her body has probably continued to build antibodies Which supposedly even more so lessons the likelihood of shedding . . . And we say Conducted to moderately healthy sexual relationship, sex 1-3 times a week, the odds are pretty damn good That never contract the virus ill would not already say? I pretty dag on good immune system Should help too would not you say? Say i carry the virus orally and Have Never Had an OB . . . the odds of me contracting it genitally decrease even more so .

. . Also she could very well be one of these “non shedders” and the virus Could possibly be dormant for the rest of her life? Possibility This has never been ruled out . . . has there Been Any indication of the virus doing Such a thing above the waste? meaning maybe you had a cold sore you were a child When and Then it lay dormant for the rest of life? Been there ever have cases of people contracting the virus and then a not Outbreaks or even Having shed? esta has to be to Possibility. Also I read something somewhere That is the amount of shedding Directly correlated to the amount of OBs a person has . . .

The frustration With This virus . . . i tell ya . . . I have never been tested for the virus . . . have never felt the need Until now . . . Have we fooled around a couple of times, no oral sex or intercourse .

. . our privates May Have briefly brushed together but that’s about it. I apologize for my writing . . . its more like a series of thoughts than a proper blog post haha. Thanks again “catinbarefeet” and anyone else WHO Responds . . . I feel for all those WHO carry virus esta . . .

live your lives and be happy with who you are. There is someone out there for all of you. I still dont know what i am going to do about my situation. I could very well continue to see her, who knows maybe i will marry her . . . But in the end, everything is gonna be alright.

HSV1 G Transmission – Westover Heights Clinic

1) there is no firm Understanding data, Practically speaking, how worried should we be about prep genital-genital or genital-oral transmission When symptoms / prodromes are not present? I have read from you and others genital-genital HSV1 That is almost unheard-transmission of, but what do you do whos Suggest partners HSV1 When one has G and the other has not HSV at all? (Vacyclovir, condoms, nothing? ) I don,Äôt think you need to be terribly genital to genital Worried About transmission, though it can happen. I think you know That We Do not have any data transmission of genital HSV About 1 to a sex partner. What About You should do a little bit transmission is up to you and your partner. Some people are much more worried about this than others. If your partner is very concerned acerca de esta just from getting to th you I would suppressive therapy and daily Suggest condom use. I am a little bit concerned about prep since you got your testing rather than testing IgG IgM testing and IgM testing is notoriously poor. I,Äôm wondering what kind of testing to determine got your partner is not infected That She With HSV 1. Remember That the ELISA screening test is traditionally That used, the IgG tes, t Misses About one- or two out of 10 cases of HSV 1 infection. The most reliable test for HSV 1 antibody Western blot is the herpes available through the University of Washington.


I ask Both short- and long-term. I understand I am fairly likely to get another outbreak, and then a increasingly unlikely after that. Also I Understand That an absence of Outbreaks Is not Necessarily an absence of viral shedding, but I do presumed That as the risk or frequency of Outbreaks diminishes, the same happens With shedding. It is true That Generally the rate of herpes virus in the genital tract shedding decreases over time. Because of the infrequency However HSV 1 sheddingin of the genital tract, we don ‘t have specific data acerca whether or not shedding over time Increases or decreases over time with HSV 1 infection. 2) If you do Consider there to be significant risk of me transmitting the HSV1 virus from my genital area, does the fact That my outbreak was on the head of my penis make it unlikely That I Could shed the virus from elsewhere in the groin? (I. e. are a pretty sure bet condoms for protection? ) Viral shedding can Occur anywhere from the genital tract not just the penis. Virus is not really shed from the groin but it can be shed from the top of the penis, the top of the scrotum and the anus from. Certainly Condoms do reduce transmission but again not perfect They are.

3) My research Indicates I got this from most likely to receiving oral sex unprotected from someone with a history of cold sores. Whenever I got the virus, there would Have Been Present heavy kissing. Did I most likely to contract the virus as well orally, Should I refrain from kissing for a period of time? The last partner I Had Besides my primary was 2 months ago. Yes The most common source of genital HSV 1 is receiving oral sex from someone Who has to oral HSV-1 infection. It is impossible to say you acquired Whether or not esta orally. Again it needs to be a decision you and your partner Between how careful you want to be acerca the whole issue HSV 1 transmission. In my personal opinion refraining from kissing When you,Äôve never had a cold sore Seems a little bit of overkill. 4) I understand That it is possible to carry the HSV2 virus for a long time, and pass it to others, all without symptoms. Is this true for genital HSV1 Present? In These cases, does the person still Develop antibodies? Or Could I (or my partner) Have had esta virus for a long time, dormant, DESPITE negative blood tests over the years? Again Because of the in accuracy of the ELISA test is it possible that you ‘ADH are your partner could,Äôve this for a long time and it has not shown up in blood antibody test.

5) Finally, do you have any advice on my previous Contacting partners. Should I contact I Have Been With everyone since my last test (8 months)? I ask for the sake of informing People Who May be infected or at risk, not out of a desire to find the source of my own infection. I honestly don,Äôt think it is Necessary to contact all of your partners in the past eight months to tell them about prep your HSV 1 infection. More than half of the population in the US Between the ages of 14 and 49 Have HSV 1 and so it is likely some of Those People That Already have one HSV on Their Own. Because the test That We Have to look for it isn,Äôt great I think the whole exercise Might Be one of futility. I know you are trying to be very thorough and you can inform people if you Certainly wish. Terri

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Hyaluronic acid injections for facial paralysis

Beyond achieving more voluminous lips, injections of hyaluronic acid could improve the quality of life of people with facial paralysis. For the first time, scientists from Johns Hopkins and Stanford University have found a group of 25 patients with this problem. As highlighted in an article published in the journal JAMA Facial Plastic Surgery, the results demonstrate its effectiveness in improving the labial force. When the facial nerve (there is one on each side of the face) suffers an injury or inflammation, the person loses voluntary muscle movement of the affected area of ​​the face, according to the damaged branch. It usually occurs on one side of the face. “The most common is Bell’s palsy and is related to viral infections,” explains Caesar Casado, chief of Plastic Hospital Universitario La Paz in Madrid Surgery. Such as the herpes virus, Epstein-Barr virus (which causes mononucleosis) or flu. It has also been associated with Lyme disease. Another of the most common causes of this problem are “injuries or accidents and oncological” for example as a result of parotid cancer. Depending on the degree of deterioration, affected individuals may feel some weakness, as if one side of the face is off-hook, or feel a significant rigidity that prevents them from moving at all one side of the face. As a result, the patient will have difficulties to completely close the eye, thus suffer dry eye, will experience problems to taste food through the affected side of the tongue and even the loudest sounds heard by the injured ear. Consequences and stigma This condition “causes both physical and psychological problems,” says Kofi Boahene, one of the study authors, facial plastic surgeon Department of Otolaryngology at the Faculty of Medicine at Johns Hopkins University (Baltimore, USA).


Without control of the lips, “patients have to fight drooling, eludes them saliva. They can not eat or drink without spilling and have difficulty pronouncing words that require the complete closure of the lips, such as containing the letters ‘b’ and ‘p’. ” “Those affected are highly stigmatized. One side of the face does not move anything,” the Spanish Married to comment on this work. To alleviate this facial asymmetry, experts consulted by THE WORLD point out that there are two types of techniques: dynamic and static. Among the dynamics are nerve reconstruction through grafts (from the other side of the face) and replacement of paralyzed muscles. Between static, trying to get improvement without surgery in the mouth, you are using botulinum toxin. What is done is to “inject this substance on the healthy side of the lips to reduce muscle tone and achieve greater symmetry about the paralyzed side,” argues Jesus Benito, vice president of the Spanish Society of Plastic and Reconstructive Surgery (Secpre). “It is an aesthetic and cosmetic effect,” nonfunctional, explains the expert. Following a patient who was not diagnosed with muscular dystrophy, but “had a weak face and speech problems,” Boahene found, after an injection of hyaluronic acid, the muscle tone of your lips improved, the muscles of his face “it seemed stronger” and lip joint “improved dramatically”. In order to study this serendipity, Boahene and his team have applied the procedure based on hyaluronic acid in 22 patients (14 women and eight men) with facial paralysis on one side of the face and three people with muscular dystrophy who had lost control of both sides of his mouth. optimistic results Before treatment, study participants underwent a test that measured the pressure of his lips, from the left, center and right of his mouth.

The researchers identified the weakest points causing those affected to blow air through pursed lips. In places where the air is escaping, scientists injected hyaluronic acid. The results, says Boahene, “were surprising,” especially in the three patients with muscular dystrophy, whose lips strength increased from six to seven times. In participants with only a paralyzed hand, the lip force increased an average of 1. 4 times in the paralyzed side. On the other hand, a speech examined before and after each of the participants. He is evaluating both speech and action of eating and drinking without spilling the liquid or food. In this sense, “the 25 showed a marked improvement and no side effects,” notes the author. The mechanism of action of hyaluronic acid is that increases muscle volume atrophied area, which is greater competition labial and the patient is easier to close the mouth. That is, this substance “does not cause the muscle to recover, but improves continence and stiffness of the lip, there is more resistance,” says Benito. “Few patients”, agree that the two Spanish experts. It is a very preliminary work. Is a need for larger studies.

Themselves responsible for this article are preparing an analysis with about 100 patients. When their benefits are confirmed, they conclude both surgeons, it could be an alternative for patients who are unwilling to reconstructive surgical treatments, which are effective. It should be noted, however, that the effect of these injections for aesthetic purposes lasts between six months and a year or so, so it would have to repeat the process periodically.

How is the perfect kiss?

Kissing is a sign of love, affection and recognition. Give a kiss involves using many muscles of the face and generally makes us feel good. It is a wonderful gesture which, unfortunately, can become very unpleasant if we think in bad breath, on the lip cracking in the cold and bacteria that are transmitted with the kiss (from the common cold to those of the kissing disease). Therefore, we present some brief advice on oral hygiene and lip care. Be aware of both factors is an essential step to perfect kisses. The next step has to give you. “Many people have the herpes virus Once infected with the virus, can not get rid of him. I remain dormant until lowering our defenses facilitating its manifestation. ” perfect kisses It’s easy to invite the lips that kiss dedicating a little care. We tell you how: chapped lips

Dry, chapped lips are unsightly and can be very painful. The good news is that you really have a solution with minimal effort and expense: Use every day lip balm (men too). Petrolatum is also effective. Put sunscreen on your lips when you go outdoors on sunny days. Avoid excessive sun exposure. Avoid licking your lips to keep them moist. If the damage is done Do not overdo the tongue over his lips, as it will only provide temporary relief and secarás further. Try chapped lips with a lip balm that contains beeswax or phenol. You can also use Vaseline. “Boqueras” The rágades or rhagades, popularly known as “cold sores” are caused by a common contagious viral infection (herpes simplex or HSV-1).

This virus is from the same family as the virus that causes genital herpes. The rágades occur around the mouth. They consist of clusters of tiny blisters filled with a clear liquid, which then fester, open, dried, and finally disappear. These blisters are contagious until completely cured, a process that usually requires a week. Usually, the virus is transmitted by contact from person to person by kissing or using the same toothbrush or sharing utensils. Many people have the herpes virus. Once infected with the virus, we can not get rid of it; remains dormant until certain factors, such as stress or other diseases, decrease our resistance facilitating the attack. Most we developed antibodies to keep the virus under control. The rágades disappear on their own after about a week. If you feel that will appear (usually a tingling sensation or irritation), starts using an antiviral cream like Zovirax, immediately. With it is possible to shorten the duration of the attack, or even stop it altogether. Applying yourself Zovirax follows according to the manufacturer’s instructions. You can also take ibuprofen to reduce inflammation and place an ice cube on the affected area to feel fast relief area.

Go to your doctor if you show any new, unexplained symptoms, or if the rágades are unusually frequent and are accompanied by fever, headache or muscle, or if the vesicles contain pus instead of clear liquid. Bad breath Most of us worry about bad breath or halitosis. In fact, we spend hundreds of millions of euros annually in mouthwashes and oral solutions that refresh the mouth. Spicy foods, snuff and caffeine are common causes of halitosis. Also continuous intake of large amounts of certain foods, such as garlic or onion. Digestive problems (hiatal hernia, esophagitis, ulcers, liver problems . . ) are a common cause of this problem. However, any condition that causes bacterial growth, can cause bad breath, such as: Colds and flu Throat infections and sinus Decayed teeth

Often, it is simply the result of not properly clean the teeth by brushing and flossing. The dieting or skipping meals can also be a cause. Do not eat regularly causes bad odor because not eating no saliva secretion is stimulated, which helps keep the mouth clean and fresh. To combat bad breath is recommended to clean the teeth with brushing and flossing at least twice a day, preferably after every meal. It can also help clean the tongue with a brush. If you suspect your diet is the cause of bad breath, try to eat less spicy or spicy foods and drinking coffee reduces. If the problem persists, see your dentist to check your mouth you or your doctor to rule out the existence of a digestive problem. Barbas, languages ​​and aftershave lotions Beards, mustaches and pierced tongues -piercing- can harbor bacteria. Be sure to regularly wash your beard with your regular shampoo or soap and brushing the tongue around the ball or ring, if you have it drilled. Both stubble as aftershave lotion can irritate the skin of others, so try to be clean-shaven and not miss you too much lotion. contagious kisses With kisses can be transmitted infections different from those which produce a simple cough, cold or rágades, to more serious diseases such as infectious mononucleosis, also called glandular fever or HIV infection.

Can I get HIV by kissing? There are four body fluids that can carry and transmit HIV: blood, semen, vaginal fluids, and breast milk. Saliva, by itself, is not transmitting. However, it is theoretically possible for HIV to have besarse. si or your partner / a has cuts or sores in the mouth or bleeding gums (eg brushing teeth after brushing or flossing), for an exchange may occur infected blood. This fact is, however, extremely unlikely. As in all practice safe sex, kissing must anticipate risks. If you have cuts or sores in the mouth or on the lips, it is better not kiss anyone until they have disappeared. Do you really glandular fever is transmitted by kissing? Infectious mononucleosis or glandular fever ( “kissing disease”) is a disease caused by the Epstein-Barr virus. This is an extremely common virus, which spreads through saliva. In fact, most middle-aged people have been infected by this virus, although many have no symptoms. However, when infection occurs during adolescence, often through kissing, the symptoms of infectious mononucleosis occur most virulence.

Therefore: yes, infectious mononucleosis or glandular fever can be transmitted by kissing. Translated, adapted and expanded by www. sanitas. es under the medical supervision of Dr. Ignacio Orive.

equine viral rhinopneumonitis – EcuRed

equine viral rhinopneumonitis Equine viral rhinopneumonitis: infectious disease. It affects the respiratory system in foals and causes abortions in pregnant mares. Are susceptible horses, donkey and zebra. It is seasonal, and has an incubation period of 2 to 10 days for the respiratory form and 1 to 3 months for abortive form. It is not a zoonosis. epizootiology Equine rhinopneumonitis is an enzootic disease in equine populations worldwide and often appears in frequently despite not incorporated new animals to the rodeo. The causative agent is equi herpesvirus type 1 (EHV-1), responsible for causing abortions, perinatal death, respiratory problems and Neurolytic, the equi herpesvirus type 4 (EHV-4), which affects the airways with rinofaringitis and traquebronquitis. The virus can induce latent infections in some horses, form through which self-perpetuating. It is argued that a high percentage of animals over one year old are latent carriers. Overcrowding, poor diet, transfer, some diseases and all those stressful situations can trigger the multiplication of the virus so far latent and affect susceptible horses by direct contact. Horses, zebras and donkeys are the only receptive to the disease under natural conditions animals.

The respiratory and digestive tract rhinopneumonitis transmitted through aborted fetuses and contaminated with nasal secretions elements. They are susceptible to infection foals between 6 months and 2-3 years of age and pregnant mares, resulting in these abortions after 5 months of gestation, but most often happen between 7 and 11 great weakness, pneumonia and severe liver damage. Death inevitably occurs within a few days of life. Weanling foals have respiratory symptoms. The foals that come from free establishments rhinopneumonitis spread from animals exposed to the virus during training in equestrian venues, exhibitions, etc. The rhinopneumonitis provides immunity for about 3- 4 months. The adult horses reinfected have mild symptoms. EHV-1 is widely disseminated in high density area of ​​equines, infecting susceptible hosts. The existing humoral response to respiratory infections does not protect from all the animals, since they can reinfect despite the presence of neutralizing antibodies. Perhaps this is due to the short time of the aforementioned immunity, so effective protection need reinfection or several of many vaccinations. HEV-1 and EHV-4 are genetically and antigenically very similar. Each virus exists as a single neutralizing serotype. Both viruses have managed to evolve to persist latently in those horses who have suffered from illness.

Hence the suspicion that the reservoir is about half of the total population of horses, latent carriers capable of spreading EHV-1 and EHV-4 intermittently. EHV-1 is held responsible for abortions, birth of sick infants and paralytics tables in adult animals, since it has some affinity for the nervous system. EHV-1 can cause respiratory symptoms simultaneous or abortion of the mare at the end of her pregnancy myeloencephalopathy. The neurological condition may occur in pregnant horses, not pregnant, castrated or integers. There ataxias in the hindlimbs of varying degrees and can be mild or severe enough to prevent the normal movement of the animal, which remains supine. In addition, patients are febrile, with runny nose and edema in the limbs. The anamnesis can raise horses prior contact with aborting or suffered respiratory signs accompanied by fevers. Animals with mild ataxia usually recover within 15 to 30 days. Those who lie supine are reserved prognoses, therapy and prolonged support stricter still needed. EHV-4 is responsible for respiratory symptoms in foals and very rarely get to cause abortions. Other herpes viruses that affect horses are Herpesvirus equi type 2 (EHV-2), isolated frequently and without further clinical relevance, and equi herpesvirus type 3 (EHV-3) causing the rash Genital, venereal disease that affects the penis stallion and the mare’s vulva. Virology Herpesvirus belongs to the Herpesviridae family.

Icosahedral shaped, the nucleic acid is DNA and measures 130-200nm. They can be easily isolated through crushed lung or liver and then infected brain inoculated suckling mice or primary cells of rabbit kidney. They have the ability to remain latent in the host organism after primary infection, reinfection or causing new infections in susceptible animals. Both EHV-1 and EHV-4 have one serotype neutralizer, whereby no antigenic changes that does have Influenzavirus. pathogenesis EHV-1 and EHV-4 cause destruction and nasopharyngeal epithelial exfoliation, trachea and bronchi, which brings about severe inflammation and increased removal of glandular secretions. After replication, the viral agents are transported by macrophages to regional lymph nodes. EHV-1 is usually spread to other organs where endothelia cells affected vessel. It is so vasculitis generated results sequels in the uterus production of abortions, or the central nervous system with neurological conditions. The abortion occurs following anoxia suffering the fetus after rapid separation of the placenta and the endometrium. The broodmare no signs that it will abort. Expels the fetus to the placenta and uterus regresses normally. Le aborted fetus contains a high viral load.

It is noteworthy that abortions occurred beyond 6 months of gestation are not autolysed, unlike what happens in cases of Salmonella abortus equi infection. The horses who have endured several exposures to EHV-1 or EHV-4 have no detectable respiratory signs before a new reinfection. When the mare than the disease, neutralizing antibodies protect it until the 4th -5th month, when it can be reinfected. The fetus is better protected when the female has passed several infections. symptomatology Foals are feverish, a situation that usually maintained for 5 to 7 days. No congestion of the nasal mucosa and serous discharge, as pharyngitis and mandibular lymph edema in. The larynx is somewhat inflamed and the animal has a productive cough. There may be enteritis with diarrhea and edema in the limbs. The disease returns in 10 days of no secondary complications. In mares, the infection is spread very quickly. In general, no clinical symptoms. They can get to give birth to their foals, but infected and weak, dying within a few hours of birth.


complications Secondary bacterial infections commonly occur with purulent pharyngitis and adenitis. EHV-1, besides affecting the respiratory system, is responsible for causing invasion to other organs. The consequence of which is the occurrence of sequelae below: If the fetus of pregnant mare becomes infected during the late pregnancy, it is likely to be born alive. However, it has signs of disease or present them within a few hours of birth. The infant does not suck, have extreme weakness, fever, hypoxia and pneumonia. They are also very susceptible to bacterial invasion, and so the prognosis is always very serious with a case fatality rate of almost 100%. Although isolated situations have been detected mieloencefalíticos animals with respiratory disorders such as sequelae of conditions EHV-1. The event appears between 5 to 10 days appeared respiratory signs, incoordination and paraplegics with pictures. Aborting mares may also manifest signs of ataxia. Since the virus has been isolated from nervous tissue, it is supposed to be due to paraplegia vasculitis in small vessels CNS motivated by metabolic changes, with a consequent disorder in the blood supply. To the extent that the sequel does not cause recumbency prognosis is favorable, as this disorder usually returns within a few days.

Animals lying on the floor for more than 2-3 days are more committed. Another sequel of respiratory infections EHV-1 usually has a seat on the eyeball, uveitis and / or chorioretinitis. Even, the situation may worsen with retinal detachment and irreversible blindness in extreme cases. Diagnosis The clinical diagnosis is presumptive because it confused with other respiratory symptoms. The disease occurs in animals up to 2 to 3 years of age and at any time of year. The appearance of abortions in foals makes suspect the presence of Rhinopneumonitis. Moreover, as already noted, the aborted fetus before the 6th month of pregnancy is autolysed, while the reverse is true if the expulsion occurs from the 7th month onwards. The viral phase may go unnoticed, signs appearing before secondary bacterial invasion. Herpesvirus infections show a characteristic decrease of leukocytes with neutropenia at 48 hours after the start viremia. The diagnosis of equine rhinopneumonitis is confirmed by the presence of EHV-1 or EHV-2 in respiratory secretions. From 48 hours of onset of the disease, nasopharyngeal samples serous secretions through a sterile swab taken. The material obtained was placed in a fluid medium with antibiotics refrigerated transport and sent to the laboratory to maintain the viability of the agent.

Another way of shaming Herpesvirus is from white blood cells of the venous blood of horses affected. Within 5-10 days of the onset of infection 20-30 milliliters of blood without anticoagulant are extracted. The sample is sent to the laboratory refrigerated. The increase in titers between paired sera taken in the acute course of illness and convalescence also confirms the diagnosis by complement fixation or Elisa. This last test uses the G glycoprotein as antigen, being highly sensitive and specific for detecting EHV-1 and EHV-4 in infected horses (Kirisawa et al. ). The result is positive as there is an increase of four or more dilutions title of specific antibodies against EHV-1 or EHV-4 between the two samples. Sending the fetus by the placenta to a specialized laboratory allows us to demonstrate acidophilic intranuclear inclusions in hepatocytes and respiratory epithelial cells, pathological lesions typical of herpesvirus. The fluorescent antibody test performed in liver or lungs cutting confirm the diagnosis of Rhinopneumonitis. Differential Necropsy Young animals have edema of lungs with necrotic areas in bronchial and alveolar epithelium. fibrinous exudates in the alveoli and widespread atelectasis, with lungs adopting a purple coloration are observed.

There fluids in the pleural cavity and liver necrosis, hemorrhage in previous airways and laryngeal edema. Aborted fetuses towards the end of gestation not show large lung injury although in certain cases may also exist lungs atelectasis and purple. petechiae are noted in mucous membranes, splenomegaly and jaundice. No separation between allantochorion and endometrium of the mare and edema of the uterine wall. It is believed to be due to reactions that produce cytotoxic substances originating between the virus and the sensitized lymphocytes endometrium. Treatment Implement therapy is individual and depends on a lot of clinical signs of each patient. It is necessary to reduce the febrile and severe inflammation of the respiratory tract. The application of anti-inflammatory analgesics fulfills this function, phenylbutazone can be used in dose 4mg / kg intravenously every 24 hours or flunixin meglumine at a rate of 1mg / kg intramuscularly every 12-24 hours. As prevention of secondary bacterial contaminants one antibiotic therapy is administered broad spectrum. It is useful to use trimethoprim-sulfadiazine in doses of 15 mg / kg intramuscularly or 30 mg / kg, cda 24 hours for 10 days. They are also indicated benzatínicas penicillins or intramuscularly procaínicas penicillins or the sodium or potassium intramuscular or intravenous routes, in all cases at a rate of 20000 IU / kg. other antibiotics used are ticarcilina, in doses of 45 mg / kg intramuscularly every 8 hours or amikacin 20 mg / kg intramuscularly every 24 hours.

In particular cases minor tranquilizers and electrolyte solutions are used to correct water imbalances. The aftermath caused by rhinopneumonitis resolve symptomatically. Infants with severe respiratory disorders require oxygen therapy. Foals with disorders in the nervous system that are recumbent need constant attention. The bed should be soft and avoid remaining wet with urine. You need to change the patient’s position every 3-4hours to minimize complications that occur from prolonged recumbency, as myositis and ulcerations. Gentle massage in areas exposed to pressure, made two or three times a day, usually very helpful. Prophylaxis The eradication of equine rhinopneumonitis rodeos is virtually impossible because of the existence of carrier animals. However, by vaccinations to all groups of animals and effective management practices can reduce largely the onset of this disease, thus reducing the negative economic impact it generates. In foals, maternal antibodies against EHV-1 and EHV-4 decay around 3-4 months of age, which become seronegative and susceptible to Rhinopneumonitis. Therefore, the first vaccination to prevent respiratory form is made at the foot of the mother at the age of 3 months, then revaccinated at weaning and at one year of age. That way, future protection is achieved when the foal must face stressful situation weaning coexistence in new social groups, transport, training and competitions.

Pregnant mares are immunized in the 5th, 7th and 9th month of pregnancy, along with the rest of the horses from the property. sick animals or mares with gestations of more than 9 months not vaccinated. In areas where the disease is endemic, four months vaccination should be performed per year. As already mentioned, the herpesvirus may be stationed in the host after a primary infection and intensify in stressful situations. For that reason, it is very important to the isolation of all animals entering an establishment at least for three to four weeks to recover from stress and as a prevention of any disease. The mares that have aborted must be separated from the challenges of horses. If the abortion was a field, animals will avoid incorporating this sector for at least 30 days. Fetuses have to be incinerated and proceed to disinfect the stable and to remove the bed and any object that has had contact with the sick animal. In short, for effective control of equine rhinopneumonitis, it is essential to apply the following strategy: Vaccinate all horses from the property. Separate pregnant mares from other categories, especially foals. Subdivide pregnant mares for gestational age and small groups. Establish a quarantine not least 3 weeks in all mares entering or re establishment.

Avoid stress in all animals. Perform a thorough disinfection of the pits. Maintaining effective hygienic measures in facilities, utensils and clothing of personnel. Sources

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