Files veterinary medicine – Rhodococcus equi pneumonia and colitis in a foal: First report in

First case described in Chile of pneumonia and colitis Rhodococcus equi in a potrillo Rhodococcus equi pneumonia and colitis in a foal: First report in Chile E. Paredes1, M. V. , Dr. med. vet . ; R. GALLEGO2, M. V .

; A. M. Channel3, M. V. , M. Sc . ; O. ARAYA4, M. V. , Ph. D . ; E.

CHAHUÁN5, T. M . ; P. THOMAS5, T. M . ; J. ZAMORA5, M. V. 1Institute of Animal Pathology, Fac. Veterinary Science, Universidad Austral de Chile. Military 2Criadero Riñihue, Chilean Army. Animal 3Patología. Fac.

Of Agriculture and Veterinary. Universidad Nacional del Litoral, P. Kreder 2805, 3080 Esperanza, Santa Fe, Argentina. 4Instituto of Veterinary Clinical Sciences, Fac. Veterinary Science. 5Instituto of Microbiology, Faculty of Sciences, Universidad Austral de Chile. ; Casilla 567, Valdivia, Chile. SUMMARY Rhodococcus equi was isolated for the first time in Chile from lung sample, bronchial lymph node and mesenteric lymph node Obtained from a 3 month chronic enteritis and foal With pneumonia. Gross lesions Were Characterised by pneumonia pyogranulomatous multiple abscesses varying size. Multiple well-defined necrotic foci, 1 to 3 cm in diameter, in the mucosal surface Were of the colon, and mesenteric lymph nodes Were enlarged. Due to the infectious disease condition, it is Necessary to carry out further studies to determine STI epidemiological relevance in Chile.

Keywords: pneumonia, colitis, Rhodococcus equi foal. Key Words: pneumonia, enterocolitis, Rhodococcus equi foal. INTRODUCTION Rhodococcus equi (R. equi), formerly classified in the genus Corynebacterium as C. equi, is an important pathogen of foals being pyogranulomatous etiologic agent of bronchiolitis and ulcerative enteritis, preferably less than 6 months old young horses (Burks, 1996; Nay, 1996; Fernandez, 1997; Castagna Vargas, 1998) with abscess formation of thoracic and mesenteric lymph nodes (Knottenbelt, 1993; Lopez 1995; Van Kruiningen, 1995) also may occur joint injuries, skin, bone , eye and various viscera (Fernandez et al. , 1995; Van Kruiningen, 1995; Burks, 1996; Nay 1996). R. equi has also been isolated from healthy and diseased animals of other species, such as pigs, cattle, sheep and also in free-living animals (Bern and Lämmler, 1994; Soedarmanto et al, 1997, 1998. ). In man is gaining importance as an emerging disease, particularly in immunosuppressed individuals (Prescott, 1991; Bern and Lämmler, 1994; Fernandez et al. , 1995; Takai et al. , 1995; and Lämmler Fuhrmann, 1997).

This article aims to communicate the first isolation in the country of R. equi, describe the typical injuries and cultural characteristics and antibiotic sensitivity of germ found in a dead foal pneumonia in the Tenth Region, Chile. MATERIAL AND METHOD In a stud farm 10 cases of diarrhea as the only symptom in foals of different breeds of 20-45 days old were detected in mid-November 1995, which did not respond to therapy potentiated sulfa (sulfa + trimethoprim) for 5 days and supportive therapy (oral rehydration salts, ringer lactate serum EV, bismuth subnitrate Flumixin oral Meglumine, EV); due to inclement weather, the offspring had remained confined stabling night with their mothers in a shed for three days, without spare bed. At the end of November totaled 40 cases detected (80% of total offspring), when Salmonella sp is isolated. E. coli and from faecal samples, starting specific treatment according to antibiogram sensitivity (Advocin® and Baytril) for 4 days, with no clinical improvement in most of them. In January 1996, 14 offspring remain with diarrhea (35% of affected), 9 of which had also respiratory compromise, which were treated with gentamicin and sodium penicillin E. V. (3 times a day for 10 days), with no remission of the symptoms. It was decided to leave without antibiotic treatment to a colt race Selle Français, 90 days old, being sacrificed later. necropsy according to the technique described by Walls and Cubillos (1995) was performed, taking samples in neutral formalin 10% of affected tissues (lungs and large colon) and samples of lung, lymph node bronchial and mesenteric lymph node for microbiological examinations. To this effect it was plated on sheep blood agar and chocolate agar, later to make morphological, physiological and biochemical isolates according to described by Holt et al exam.

(1994) and Fuhrmann and Lämmler (1997). In addition, isolates were determined sensitivity to different antibiotics by conventional methods. RESULTS AND DISCUSSION a) Clinical manifestations and laboratory tests. The clinical symptomatology was characterized by watery diarrhea began at 36 days of age, with no initial respiratory compromise or alteration of physiological constants situation is described by Yager (1987) and Burks (1996), who argue that infection R . equi, diarrhea this may be the only sign. At 75 days of age, respiratory symptoms (mild cough, crackles and hissing noises cranioventral level of both lungs) and fever, similar to that described by Prescott (1991), Vivrette (1992) and Burks (1996) are detected. During the course of the disease he continued suckling foal. After initiation of respiratory symptoms blood count was performed, finding neutrofilia (10. 0 mil / microliter) with deviation to the left (N. baciliform 1. 5 mil / ul) and increased plasma fibrinogen concentration 10 g / l). The insidious presentation of the disease in this colt, characterized first by diarrhea and later by bronchopneumonia tending to chronicity and the history of other respiratory symptoms sporadically presented earlier in the stud farm, became suspicious of R.

equi infection , since the clinical characteristics coincided fully with those described in the literature (Vivrette, 1992; Knottenbelt. , 1993; Fernandez et al, 1995; Lopez, 1995; Van Kruiningen, 1995, Burks, 1996; Nay, 1996; Fernandez et al . , 1997; Vargas Castagna, 1998). b) Findings anatomical and histopathological. Necropsy performed the animal accentuated suspicion, since the postmortem examination revealed that serious injuries were confined to lungs and large colon. Both lungs were observed without collapsing, irregularly firm, with the presence of multiple nodules of varying sizes scattered all lobes and protuían into the pleural surface. When cutting the lung tissue, these nodules were observed as multiple focal and confluent areas of yellowish white color, completely replacing the lung tissue (Figure 1) and corresponding to areas of chronic inflammation, central necrosis and discrete purulent exudate. Bronchial lymph nodes were enlarged, hyperemic and exudative. Figure 1. Lung (cutting surface): confluent foci of necrosis and purulent inflammatory reaction. Lung (cut surface): large and confluent granulomas caseated. In addition, the lining of the colon showed greater number of circular ulcers, up to 3 cm in diameter, with a thick border of cream and a depressed with traces of necrotic tissue (Figure 2) center. Mesenteric lymph nodes were increased volume and had a cutting surface with great whitish exudates.

Figure 2. greater Colon: Circular mucosal ulcerations. Mucosal surface of the colon: well defined necrotic foci. Furthermore, histopathology found in the lungs the presence of large areas of necrosis with severe inflammatory reaction neutrohistiocitaria type, finding some giant cells. In turn, the more severe inflammatory bowel exhibited neutrohistiocitaria reaction type with large areas of necrosis, covering mucosa and submucosa. c) Microbiology. All lesions observed, and that characterize a disorder caused by this bacterium box, were confirmed with isolation lung, bronchial lymph nodes and mesenteric pure culture of a Gram positive bacteria and weakly acid resistant Ziehl – Neelsen modified, pleomorphic aspect cocoide (0,71,4 microns), distributed in cuneiform palisades or encapsulated. Colonies were small, 2 to 3 mm in diameter, smooth, shiny, pale mucous salmon acquired after March 4 days of culture and development in gelatin presented a strong orange. Other features are included in Table 1. TABLE 1. biochemical and physiological characteristics of R. equi strains isolated. Biochemical and physiological properties of the isolated strains.

biochemical and physiological characteristics Motility catalase gelatinase lipase urease Nitrate reduction CAMP Glucose acid Acid Lactose Acid Mannitol – +

– + + + + – – – According to the stated characteristics, it was identified as Rhodococcus equi strain, being sensitive to different antibiotics that are included in Table 2. TABLE 2. Antibiograms of the R. equi isolates. Antibiogram of the isolated R.

equi strains. Antibiotic Sensitivity Penicilinaaa Cloxacilinaa Erythromycin Lincospectin Bipencilaaa Baytrilaaaa Advocinaaa Ceftiofuraaa Resistant Resistant

Sensitive Sensitive Sensitive Sensitive Sensitive Sensitive Although considered to R. equi has a cosmopolitan distribution, they had not described in Chile infections in foals by this agent. The table causes this microorganism is generally sporadic in enzootic areas, but also outbreaks have been reported responsible for great economic losses in the stud farm, although the most common is that the infection goes unnoticed (Knottenbelt, 1993, Burks, 1996; Soedarmanto , 1998). R. equi, causing a suppurative bronchopneumonia Subacute to chronic, associated with purulent lymphadenitis, pneumonic infections that 50% are complicated by intestinal infection (Yager, 1987), especially in foals under 6 months of age and particularly those of January 3 months of life, in which it has not yet fully matured their immune system being immunocompromised adults also particularly susceptible to infection (Burks, 1996). You can not ignore that, in addition, on some occasions it is believed that viral infections may be predisposing factors, such as with equine herpesvirus type 2 (EHV-2) (Nordengrahn et al. , 1996).

Treatment of the disease is difficult, not by the resistance R. equi may have antibacterial, but rather the facultative intracellular bacteria property, a factor that probably concurred in failure of therapy instituted in previous cases, since the isolated strain was sensitive to several antibiotics (table 2), including employees at the farm, although it must be remembered that in vitro conditions are different from those in vivo, which does not allow the conclusion that the antimicrobial susceptibility test result can be the same in the animal. Also, it should be recalled that the organism quickly becomes resistant when the antibiotic is used alone, hence it is necessary to use simultaneously more than one drug in prolonged, being recommended the primary application of erythromycin and rifampin, reinforced therapy support such as dimethylsulfoxide, aminophylline and even ranitidine (Fernandez et al. , 1995; Burks, 1996). However, Gustafsson et al. (1997) report that erythromycin may induce severe colitis in horses associated with large changes in intestinal microbiota of these animals. The discovery of R. equi in the country to presume that the infection is quite widespread, causing serious problems, given the survival and development of the agent in the external environment (especially where there is overcrowding, agglomeration of fecal material and dusty environments), the different routes of transmission, the difficulty of achieving an early diagnosis by the characteristic insidious disease development and the progressive increase in the incidence denouncing the literature, are a set of attributes that make R. equi one of the most problematic pathogens, refractory to treatment and causes a high rate of mortality in foals (Higuchi et al. , 1998). It is therefore high convenience continue studies on the subject to determine the epidemiological importance in the country, not only for its role in the health of the horses, but also because it is considered an important agent of emerging infections the human species, especially in immunosuppressed people. SUMMARY Described for the first time in the country, isolation of Rhodococcus equi from an infection in a colt of 3 months old, who suffered from chronic enteritis and pneumonia.

Also, they disclosed the lesions observed in the postmortem and histopathological examination consisting of multiple pulmonary nodules with areas of chronic inflammation, central necrosis with purulent exudate and bronchial lymph nodes increased in size: hyperaemic and exudative. In addition, the large colon showed ulcerations with necrotic tissue and mesenteric lymph nodes were enlarged with great exudation, lesions which show typical features that characterize this pyogranulomatous infection of foals. As this is an emerging infectious disease, it is necessary to continue studies, in order to determine its epidemiological relevance in Chile. _________________________________ Accepted: 05/02/2000. BIBLIOGRAPHY BERN, D. , CH. Lämmler. 1994. Biochemical and serological Characteristics of Rhodococcus equi isolates from animals and humans. J. Vet.

B Med. 41: 161165. [Links] Burks, B. 1996. Managing Rhodococcus equi infections in foals. Vet. Med. 91: 656662. [Links] CASTAGNA VARGAS, A. 1998. Infecçâo Rhodococcus equi.

Quoted in RIET-CORREA, F. , A. L. Schild, M. C. MENDEZ (Eds. ). Doenças of ruminants and equines. Edit. University, Pelotas, Brazil. [Links] FERNÁNDEZ, A. S.

, S. M. Estein, P. SOTO. 1995. Rhodococcus equi: a model of immunopathology. Arch. Med. Vet. 27: 512. [Links] FERNÁNDEZ, A. S.

, J. F. PRESCOTT, V. M. NICHOLSON. Protective effect 1997. Against Rhodococcus equi infection in mice of purified IgG from horses Vaccinated With virulance associated protein (VAP) enriched antigen. Vet. Microbiol. 56: 187-192. [Links] Fuhrmann, C. , C.

Lämmler. 1997. Characterisierung von Rhodococcus equi Mensch und Pferd von isolaten. Berliner Münch. Tierarztliche Wochenschr. 110: 5459. [Links] Gustafsson, A. , V. BAVERUD, A. GUNNARSSON, M. H. Rantzien A.

Lindholm, A. , FRANKLIN, M. HORN-Rantzien. 1997. The association of erythromycin ethylsuccinatte With acute colitis in horses in Sweden. Equine Vet. J. 29: 314318. [Links] Higuchi, T. , S. TAHARAGUCHI, A. HASHIKURA, S.

Hagiwara, C. GOJO, S. Satoh M. Yoshida, S. TAKAI. 1998. Physical and serological examinations of foals at 30 and 45 days of age for early diagnosis of Rhodococcus equi infection on endemically infected farms. JAVMA 212: 776 781. [Links] HOLT, J. G. , N. R.

KRIEG, P. H. A. Sneath, J. T. Staley, S. T. WILLIAMS. 1994. Bergey’s Manual of Determinative Bacteriology. 9th Edit. Williams \x26amp; Wilkins, Baltimore, USA. [Links]

Knottenbelt, D. C. 1993. Rhodococcus equi infection in foals: a report of an outbreak on a thoroughbred stud in Zimbabwe. Vet. 132 Rec. 7985. [Links] LOPEZ, A. 1995. Respiratory System. Quoted in: CARLTON, W. W.

and M. D. Mc GAVIN. Thomson’s Special Veterinary Pathology. 2nd Edit. Mosby, St. Louis. [Links] NAY, T. S. 1996. Extra-pulmonary Rhodococcus equi in a foal throroughbred. Dog.

Vet. J. 37: 623624. [Links] NORDENGRAHN, A. , M. RUSVAI, M. MERZA, J. EKSTROM, B. Morein, S. Belak. Equine herpesvirus 1996. Type 2 (EHV-2) as a predisposing factor for Rhodococcus equi pneumonia in foals: prevention of the disease bifactorial With EHV-2 immunostimulating complexes.

Vet. Microbiol. 51: 5568. [Links] WALLS, E. , V. CUBILLOS. 1995. Manual of Necropsy in Domestic Animals. Faculty of Veterinary Science, Universidad Austral de Chile, Valdivia. [Links] PRESCOTT, J. F.

Rhodococcus equi 1991: an Animal and human pathogen. Clinical Microbiology Reviews 4: 20-34. [Links] SOEDARMANTO, I. , R. OLIVEIRA, CH. Lämmler, H. DURRLING. 1997. Identification and epidemiological relationship of Rhodococcus equi isolated from cases of lymphadenitis in cattle. Zbl. Bak. 286: 457467.

[Links] SOEDARMANTO, I. , W. Zhicai, A. SETYAMAHANANI, CH. Lämmler. 1998. Pheno- and genotyping of Rhodococcus equi isolated from faeces of healthy horses and cattle. Res. Vet. Sci. 64: 181185. [Links]

Takai S. , Y. IMAI, N. Fukunaga, Y. UCHIDA, KAMISARA K. , Y. Sasaki, S. TSUBAKI, T. Sekizaki. 1995. Identification of virulence-associated antigens and plasmids from Rhodococcus equi in Patients With AIDS. J. Infect.

Dis. 172: 13061311. [Links] VAN Kruiningen, H. 1995. Gastrointestinal System. Quoted in: CARLTON, W. W. and M. D. Mc GAVIN. Thomson’s Special Veterinary Pathology. 2nd Edit.

Mosby, St. Louis. [Links] VIVRETTE, S. 1992. The diagnosis, treatment, and prevention of Rhodococcus equi pneumonia in foals. Vet. Med. 87: 144-149. [Links] YAGER, J. A. 1987.

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PTA forum online: neuropathy: nerve in need

neuropathy Nerve in need itch By Susanne Poth / permanent and tingling toes and legs, as if an ant colony darüberkrabbelt. This nightmare scenario many people must endure with neuropathy daily. What causes this insidious disease, which treatment options are there, and what recommendations can PTA or pharmacist Pronounce? display When neuropathy is a disease of the central or peripheral nervous. Unlike the classic pain with an injury, inflammation or irritation of the healthy tissue has an important function as a warning signal, when the neuropathy pain-conducting system itself is damaged. By hyperexcitability of damaged nerves leads to the described irritation phenomena. In the industrialized nations, the number of people affected should be 2 to 4 percent and increases with age up to 8 percent. It seems regardless of gender, to be racial and socio-economic status. Many neuropathy patients suffer from itching and tingling of the legs and feet. To prevent damages, especially diabetics should inspect their feet daily for changes.

Photo: Lilly Pharma Holding GmbH Many sufferers suffer from constant itching or tingling of the legs and feet, sometimes with burning the soles, also called “burning feet”. In addition, irritation of touch, and motor functions, reduction in reflection, for example, paralysis of the eye muscles, muscle cramps and a decreased touch, temperature and pain. Typical of some neuropathic pain syndromes like trigeminal neuralgia or zoster neuralgia are spontaneous stabbing pain attacks. The nerve pain usually take in the disease process continuously and spread gradually throughout the nervous system (polyneuropathy). High risk for diabetics The most common cause of neuropathy is diabetes mellitus. Both type 1 and type 2 diabetes, it occurs as a result of sustained high blood sugar levels, because this damage in addition to the blood vessels and nerves. So about half of people with diabetes is affected by this disease, which can affect both the peripheral nerves and the autonomic nervous system. Later in this autonomic neuropathy organs damaged: So come incontinence, gastroparesis, or erectile dysfunction, and cardiac arrhythmias in the risk of cardiac arrest. Another cause of the damage to the nerves of chronic alcohol abuse or neurotoxins are eligible. Moreover neuropathies are often accompanying symptom of infections such as shingles, HIV or Lyme disease. Also permanent pressure on a nerve can cause malfunctions, such as the herniated disc or carpal tunnel syndrome.

If the nerve damage, an atypical activity and sensitization of afferent pain-sensitive nerve fibers is usually the result. Thus, the function of ion channels and pro-inflammatory substances changes are propagated released. Difficult diagnosis Asking the diagnosis of neuropathy, is difficult and requires a thorough history of the doctor expected. It is based on specific questionnaires, a neurological examination and sensitivity tests of vibration, shock and temperature perception. When indicated, the physician performs cardiovascular examinations and tests the function of the autonomic nervous system. As further diagnostics measuring the nerve conduction and electromyography come by the neurologist into consideration. Depending verdächtigtem trigger examine physicians whether a tumor or toxins cause discomfort. Causes of neuropathy Metabolic diseases such as diabetes Viral diseases such as shingles (herpes zoster), HIV infection Mechanical nerve injuries caused by trauma, herniated disc, carpal tunnel syndrome Taking neurotoxic substances or poisons such as cytostatics, heavy metals or alcohol abuse

Inflammatory changes in the blood vessels (vasculitis), or of the nervous system Degenerative diseases such as multiple sclerosis, Alzheimer’s, Parkinson’s or stroke Approximately 40 percent of all patients in pain clinics and pain clinics suffer from neuropathic pain. Standard analgesics not help most. By careful selection of the active ingredient and optionally a combination of various substances with other treatment options, however, can significantly alleviate by 30 to 50 percent of the pain. Therapeutic goal is to maintain or restore the sleep and quality of life and the working capacity of the patient. Symptoms of peripheral neuropathy light touch results in disproportionately severe pain (allodynia) Pain is perceived differently, such as tingling or pinprick (dysesthesia, paresthesia) pain sensitivity is either increased (hyperalgesia) or decreased (hypoalgesia) Pain remains after the releases consist (Hyperpathy) Is polyneuropathy result of another disease, such as diabetes mellitus, alcohol abuse or poisoning is the causal therapy in the first place, which means a good glycemic control and abstinence from alcohol or detoxification. The most common drug classes of symptomatic therapy include tricyclic antidepressants such as amitriptyline and imipramine, newer antidepressants from the group of serotonin-norepinephrine reuptake inhibitors such as duloxetine and venlafaxine and acting on neuronal calcium channels anticonvulsant pregabalin.

Diabetics should be tested regularly served by a podiatric specialist in foot care. Photo: Super Image Some patients received tramadol as the drug does not only affect the opioid, but also to the serotonergic and noradrenergic receptors. Depending on the intensity of pain doctors combine a opioid with a psychotropic drug. Only mild pain they cause a temporary therapy experiment with painkillers such as paracetamol or metamizol. If the neuropathic pain syndrome associated with an inflammatory component, but not in diabetic polyneuropathy, the patient can also take NSAIDs (NSAIDs) in addition. Based on the findings of the molecular and biochemical mechanisms in neuropathies develop scientists currently taking medication with other mechanisms of action, for example in the direction of a blockade of sodium and calcium channels. In recent years came with active substance patches containing local anesthetics, new therapeutic options on the market. So a lidocaine patch (Versatis®) was developed for the relief of neuropathic pain after healing of herpes zoster infection. After the skin symptoms have healed, the patient should apply the patch about six weeks. In parallel, researchers observed that the active substance capsaicin on vanilloid receptor initially triggers a burning sensation, but after repeated use affects pain relieving effect. From this they developed a prescription high dose capsaicin patch (Qutenza®), which is on the market since of 2010. The patch is suitable for HIV-associated neuropathies and neuralgia after herpes zoster infection, always has the skin intact.

For painful diabetic polyneuropathy, but the two patches according to the treatment guidelines are not suitable. substitution controversial For other ways to support the drug therapy, there are no clearly documented evidence of efficacy. With proven vitamin deficiency but a substitution therapy is helpful, alcoholics lacks example most vitamin B1. Patients with sensory loss can help the intake of alpha-lipoic acid. The substance is not a vitamin, but a coenzyme. In vitro and animal studies indicate an antioxidant protective function of lipoic acid against oxidative nerve damage. Also be first placebo-controlled human studies suggest that alpha-lipoic acid at least temporarily improve symptoms and individual parameters of nerve functions. In the current guideline neuropathy in diabetes, the use of the substance is not recommended due to lack of available data. In the future, earlier diagnosis The damage to the nerve pathways to recognize even before the first symptoms, to take early therapeutic countermeasures, is the goal of a new diagnostic method. A working group of the University of Rostock succeeded using a special microscope method to detect changes in the nerve center of the cornea of ​​the eye. From the image obtained is possible to draw conclusions on the extent of diabetic neuropathy.

Many patients turn to non-drug therapies, their action is not always clearly established. The effect depends on the type of neuropathic disease. For example, two-chamber baths stimulate circulation of the feet and thus contribute to pain relief. Physiotherapy and orthopedic aids that facilitate walking, and in particular the right shoes to reduce the risk of injury in patients with diabetic neuropathy. For the effectiveness of electrical nerve stimulation are effectiveness evidence justifying a therapeutic trial. These include transcutaneous electrical nerve stimulation (TENS), the frequency-modulated electromagnetic nerve stimulation (FREMS), a special form of TENS, and the high tone (nerve stimulation at higher frequencies). advice needed Complains a customer about sensory loss, numbness or canted pain, should recommend him to visit a doctor or neurologist PTA or pharmacist. This can clarify possible causes and prevent, for example, in infectious polyneuropathy through early causal therapy, the disease becomes chronic. Diabetics should be made aware of the increased risk of neuropathy and also noted that the optimum adjustment of blood glucose levels can slow the progression of the disease, especially in younger patients. Often, the nerves of the lower legs of the first affected, and it comes to diabetic foot ulcers. Patients complain of burning feet, drilling, stabbing or cramping pain that worsens at rest, be improved while running on the other hand. As a result of the discomfort of legs and feet sufferers often feel not when her feet were injured, for example by pressing shoes and pedicures.

Unnoticed infections are spreading, at the same time favoring existing circulatory problems yet. Not infrequently necrosis develop. According to the German Diabetes Center at the University of Dusseldorf in Germany lose therefore approximately 25,000 diabetics each year a foot or part of a leg. Maintain feet properly The advice to all diabetics is this: In order to prevent the development of diabetic neuropathy, they should – maintain their weight and blood pressure in the normal range, do not smoke and only drink alcohol excessively – besides the near normal control of blood sugar levels. Annually they should checked the neurological functions in their diabetologists. Particular attention is the feet. To prevent diabetic foot syndrome, the shoes should fit well and not cause bruising. Walking barefoot can lead to foot injuries. Diabetics should inspect their feet daily to changes and maintain the feet gently, is best supported by a specialist in medical pedicure. Podiatrists treat warts, calluses, corns or ingrown toenails. Cave: If the foot of a diabetic injured, there is always an emergency and must be treated urgently. /

Vitamin C high dose therapy – Alternative Therapy Rolf Pauli

This form of therapy has been successfully used in acute therapy (infection, inflammation), chronic disease and allergies. The need for vitamin C is higher in many diseases, as it could take on the gastrointestinal tract. In addition, possibly may be reduced for recording illness in their ability to intestinal mucosa. In these cases, necessary therapeutic vitamin C levels can be achieved only with high-dose intravenous vitamin C infusions. What can a vitamin C cause high-dose therapy? Boost Immune System Strong antioxidant activity Degradation and excretion of histamine Promoting iron absorption Enables the breakdown of cholesterol in the liver Reduces exposure to environmental toxins and other toxins Stimulates the synthesis of prostaglandins, so inflammation are rapidly degraded Stimulates the synthesis of interferon – viral infections such as herpes zoster (shingles)

Protective function for the vitamins A, E and B vitamins Vitamin C in the treatment of cancer In moderate doses of vitamin C acts as an antioxidant. In high doses vitamin C changes its role and is pro-oxidantisch, so the free radical and produces toxic hydrogen peroxide. A possible mechanism of action, we could run this: Tumor cells have a relative deficiency of catalase, an enzyme protection, which is necessary to convert the harmful hydrogen peroxide into water and oxygen and thus to defuse. is a ten- to hundred-fold discrepancy in the catalase concentration between normal cells and tumor cells. Without the protective catalase the toxic hydrogen peroxide accumulates together with aldehydes (toxic by-products) in the cancer cells, which increases the malignant cells in cell death. The healthy cell remains unaffected. Frequently, alpha lipoic acid, Vitamin B 12, Vitamin C, selenium, vitamin B3, as resveratrol additionally infused, so as to increase the Vitamin C in its effect.

BIOTURM Natural Cosmetics – Foot Deocreme No.80

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free from perfume The main active ingredients: Usnea (beard lichen) Usnea Barbata Extract The old man’s beard belongs to the family of lichens (Parmeliaceae), these are symbiotic organisms from a fungus and green algae or cyanobacteria (blue-green algae). They can be found on trees and shrubs in areas with high humidity. The assertion usnic the Bartflechte has a strong anti-bacterial and also has anti-inflammatory, anti-proliferative and deodorizing properties. salicylic Salicylic Acid The salicylic acid is obtained from oil of wintergreen (Gaultheria procumbens) – a traditional medicinal plant that has been used by Native Americans for various ailments. Salicylic acid has antibacterial and keratolytic properties. Lacto-intensive active complex Lac

Fresh Biomolke is fermented by a special procedure. The basis of almost all BIOTURM products fermented Biomolke caused by the contained ingredients normalization of skin flora and the acid mantle. The natural lactic acid, essential amino acids, trace elements, etc. , are well absorbed by the skin and normalize the moisture content. More information can be found in our extended drug Description: lacto-intensive active complex.

Infectious diseases

Source: Wikipedia. Pages: 182. Chapters: List of infectious diseases, prion, Pneumonia, zoonosis, Infectious disease in the 20th century, vaccines, encephalitis, Dysentery, urethritis, infection, Urinary tract infection, common cold, Quarantine, rotavirus, Koch’s postulates, sepsis, periodontitis, Foodborne illness, AIDS, Smallpox, Anaerobic infection, History of emerging infectious diseases, community-acquired pneumonia, wound licking, Refugee health, food microbiology, gastroenteritis, Globalization and disease, Ascending cholangitis, Nosocomial infection, Molecular mimicry, traveler’s diarrhea, Tropical disease, co-receptor, Lower respiratory tract infection, vaccinia, subclinical infection, Buruli ulcer, Neglected diseases, Upper respiratory tract infection, Bartonella, pharyngitis, transmission, Sweating sickness, herpes gladiatorum, astrovirus, Infectious Diseases Society of America, Fever of unknown origin, Tropical eosinophilia, Pasteurellaceae, multidrug tolerance, Anorectal abscess, hospital-acquired pneumonia, non-gonococcal urethritis, TORCH complex, Tropical ulcer, Tick-borne disease, notifiable disease, Protothecosis, Galveston National Laboratory, National Hotel Disease, cholera Hospital ‘list of clinically important bacteria, phlegmon, Peritonsillar abscess, Chest photofluorography, Foot rot, Statesville Penitentiary malaria Study, Chandipura virus, Coinfection, clostridial necrotizing enteritis, Fecal-oral route, retropharyngeal abscess, Cuban fever, antibiogram, Blood-borne disease, Negative room pressure, Global Infectious Disease Epidemiology Network, Scarlet fever serum, discitis, UK statutory notification system, Infectious Disease Pharmacokinetics Laboratory, Kennel cough, Opportunistic infection, extra-Terrestrial exposure Law, Ocular citrosis, orbital cellulitis, Contagious disease, AIDS-associated Kaposi sarcoma, Picardy sweat, Freshers’ Flu, Natural reservoir, National emerging Infectious Diseases Laboratories, skin and skin structure infection, Treponema denticola, South Texas Center for emerging Infectious Diseases, Barcoo fever, Winterbottom’s sign, adenitis, alastrim, Vertical transmission, Asymptomatic carrier, Centre for Infectious Disease Research in Zambia, Maxwell Finland Award, list of infections of the central nervous system, genitourinary tuberculosis, Severe fever with thrombocytopenia syndrome, Bill of health, Riggs’ disease, HIV set point, horizontal transmission, list of infectious diseases Causing flu-like syndrome, immunization Active, auto Infection, Synthetic vaccine, Infectious dose, Preventorium, Global Public Health Intelligence Network, Pathogenicity, Crysodavarious, Hutchinson’s triad, intra-amniotic infection, Complicated skin and skin structure infection, BCG-oma, retrograde infection, Epidemic polyarthritis, Paget’s abscess, Cryptic infection. Excerpt: Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system Caused by the human immunodeficiency virus (HIV). This condition progressively Reduces the effectiveness of the immune system and leaves worth individuals susceptible to opportunistic infections and tumors. HIV is trans mitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid Containing HIV,: such as blood, semen, vaginal fluid, preseminal fluid, and breast milk. This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and . . . product details product details Publisher: Books LLC, Reference Series Number of pages: 184

2011 English Dimensions: 246mm x 189mm x 10mm ISBN-13: 9781156152546 ISBN-10: 1156152542 Best. Nr . : 33628162

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EUROIMMUN: Products – Borrelia

EI 2132-9601 M Borrelia incl. IgG / RF absorbent whole antigen, detergent extracts of Borrelia burgdorferi sensu stricto, Borrelia garinii and Borrelia afzelii IgM 2/20/200 RU / ml 96 x 01 EI 2132-9601-1 G Borrelia burgdorferi VisE

recombinant VisE from Borrelia burgdorferi sensu stricto IgG 2/20/200 RU / ml 96 x 01 EI 2132-9601-2 G Borrelia plus VisE whole antigen, detergent extracts of Borrelia burgdorferi sensu stricto, Borrelia garinii and Borrelia afzelii plus recombinant VisE from Borrelia burgdorferi sensu stricto

IgG 2/20/200 RU / ml 96 x 01 EI 2132-9601-24 O Lyme ELISA recombinant VisE from Borrelia burgdorferi sensu stricto and Borrelia OspC IgG M qualitative 96 x 01 EI 2132-9601-5 G Borrelia Select

mixture of specific recombinant Borrelia antigens incl. VisE IgG 2/20/200 RU / ml 96 x 01 EI 2132-9601-5 M Borrelia Select mixture of specific recombinant Borrelia antigens IgM 2/20/200 RU / ml 96 x 01

EI 2132-9601-L M Borrelia antibody determination in CSF whole antigen, detergent extracts of Borrelia burgdorferi sensu stricto, Borrelia garinii and Borrelia afzelii IgM 5/25/50/100/175 U 96 x 01 EI 2132-9601-G L Borrelia PLUS VisE antibody determination in CSF whole antigen, detergent extracts of

Borrelia burgdorferi sensu stricto, Borrelia garinii and Borrelia afzelii PLUS recombinant VisE from Borrelia burgdorferi sensu stricto IgG 5-230 U 96 x 01 DN G 2131-24001 DN 2131-3201 G Borrelia EUROLINE-RN-AT (P18, p19, p20, p21, p58, OspC (p25), p39, p83, LBb LBa VisE Bg, VisE Bb, Ba VisE separately)

IgG membrane strip with antigens (EURO LINE) 240 strips 32 strips DN 2131-24001 M DN 2131-3201 M Borrelia EUROLINE-RN-AT (OspC Bg native OspC Bb native, OspC Ba native, p39, VisE Bb separately) IgM membrane strip with antigens (EURO LINE)

240 strips 32 strips DN 2131-24001-2 M DN 2131-3201-2 M EUROLINE Borrelia-RN-AT-adv (OspC adv eg, OspC adv Bg, OspC adv Bb OspC adv Ba, p39, VisE Bb separately) IgM membrane strip with antigens (EURO LINE) 240 strips 32 strips FI 2131-1005-1 G

EUROPLUS Borrelia afzelii VisE antigen IgG 2 BIOCHIPs per field: bacterial smear VisE BIOCHIPs B. afzelii recombinant 10 x 05 (test system) FI 2131-1005-2 M EUROPLUS

Borrelia afzelii OspC antigen IgM 2 BIOCHIPs per field: bacterial smear OspC BIOCHIPs B. afzelii B. burgdorferi 10 x 05 (test system) FI 2132-1005 G FI 2132-1010 G

FI 2132-1005 M FI 2132-1010 M FK 2132-1005 FK 2132-1010 Borrelia burgdorferi (CH) IgG IgM bacterial smear verification BIOCHIP (2 BIOCHIPs per field)

Borrelia burgdorferi (CH) 10 x 05 (test system) 10 x 10 (test system) 10 x 05 (test system) 10 x 10 (test system) 10 x 05 (single slides) 10 x 10 (single slides) FI 2136-1005-1 G FI 2136-1010-1 G FI 2136-1005-1 M FI 2136-1010-1 M

EUROPLUS Borrelia afzelii Borrelia burgdorferi (USA) OspC antigen VisE antigen IgG IgM 4 BIOCHIPs per field: bacterial smear bacterial smear OspC BIOCHIPs VisE BIOCHIPs B.

afzelii B. burgd. (USA) B. burgdorferi recombinant 10 x 05 (test system) 10 x 10 (test system) 10 x 05 (test system) 10 x 10 (test system) FI 2138-1005-2 G FI 2138-1005-2 M

Borrelia afzelii Borrelia burgdorferi (CH) Borrelia burgdorferi (USA) Borrelia garinii IgG IgM bacterial smears (4 BIOCHIPs per field) B. afzelii B. burgdorferi (CH)

B. burgdorferi (USA) B. garinii 10 x 05 (test system) 10 x 05 (test system) FI 2822-1001-1 G FI 2822-1002-1 G FI 2822-1001-1 M * FI 2822-1002-1 M * “Exanthema Profile 1” (Consisting of 21 different substrate) IgG

IgM A field: verification BIOCHIP, HHV-6, Rubella virus *, Measles virus, mumps virus field B: VZV, EBV-CA, EBV-EA, Treponema pallidum field C: HSV-1 and -2, Coxsackie virus type B1 and A9 field D: Echo virus type 7, Borrelia afzelii, burgdorferi (CH), garinii field E: CMV, Candida albicans, krusei *, tropicalis * 10 x 01 (test system)

10 x 02 (test system) 10 x 01 (test system) 10 x 02 (test system) FI 2824-1001-1 G FI 2824-1002-1 G FI 2824-1001-1 M * FI 2824-1002-1 M * “Central Nervous System Profile 1” (Consisting of 21 different substrate) IgG IgM A field: verification BIOCHIP, Rubella virus *, Measles virus,

Mumps virus, VZV field B: Adenovirus type 3, EBV-CA, Treponema pallidum, Toxoplasma gondii field C: HSV-1 and -2, Coxsackie virus type B1 and A7 field D: Echo virus type 7, Borrelia afzelii, burgdorferi (CH), garinii field E: CMV, Haemophilus influenzae *, Listeria monocytogenes 1 / 2a and 4b 10 x 01 (test system) 10 x 02 (test system) 10 x 01 (test system)

10 x 02 (test system) FI 2825-1001-1 G FI 2825-1002-1 G FI 2825-1001-1 M FI 2825-1002-1 M “Myocarditis Profile 1” (Consisting of 17 different substrate) IgG IgM A field: verification BIOCHIP, Mumps virus, adenovirus type 3, influenza virus type A (H1N1 and H3N2) field B: Influenza virus type B,

Parainfluenza virus type 1 and 2, Mycoplasma pneumoniae field C: CMV, Coxsackie virus type B1 and A16, Echo virus type 7 field D: Borrelia afzelii, burgdorferi (CH), garinii, Chlamydia pneumoniae 10 x 01 (test system) 10 x 02 (test system) 10 x 01 (test system) 10 x 02 (test system) FI 2826-1001-1 G FI 2826-1002-1 G FI 2826-1001-1 M

FI 2826-1002-1 M “Infectious arthritis Profile 1” (Consisting of 13 different substrate) IgG IgM A field: verification BIOCHIP, VZV, Influenza virus type A (H1N1 and H3N2) and B field B: Yersinia enterocolitica O: 3 *, O: 6 *, O: 9 * Toxoplasma gondii field C: Borrelia afzelii, burgdorferi (CH), garinii,

Chlamydia trachomatis 10 x 01 (test system) 10 x 02 (test system) 10 x 01 (test system) 10 x 02 (test system) CK 2132-0220-G L CSQ pair of controls anti-Borrelia (IgG) IgG 2 x 2 ml, ready for use CK 2132-0220-L M CSQ pair of controls anti-Borrelia (IgM)

IgM 2 x 2 ml, ready for use CL 2131-0107 G positive control serum: IgG, human, 50x Concentrated for Borrelia IgG 0. 1 ml for EUROBlotOne CL 2131-0107 M positive control serum: IgM, human, 50x Concentrated for Borrelia IgM 0.

1 ml for EUROBlotOne CI 2131-0101 M CI 2131-0102 M CI 2131-0105 M antibodies against Borrelia afzelii / B. burgdorferi / B. garinii / OspC IgM positive control IgM 0. 1 ml 0. 25ml

0. 5 ml CI 2131-0101 G CI 2131-0102 G CI 2131-0105 G antibodies against Borrelia afzelii / B. burgdorferi / B. garinii / VisE IgG positive control IgG 0. 1 ml 0.

25ml 0. 5 ml CI 2131-0101 Z CI 2131-0102 Z CI 2131-0105 Z Borrelia afzelii / B. burgdorferi / B. garinii negative control IgA, IgG, IgM 0. 1 ml

0. 25ml 0. 5 ml ZF 1020-0112-3 ZF 1020-0125-3 ZF 1020-0530-3 sample buffer 3 (IIFT) (Only for the anti-Borrelia IgG IIFT) 12. 0 ml 25. 0 ml

5 x 30. 0 ml (ready for use) in Euro Tank DY 2131-1601 G DY 2131-24001 G DY 2131-3001 G DY 2131-3201 G DY 2131-1601 M DY 2131-24001 M DY 2131-3001 M DY 2131-3201 M Borrelia afzelii whole antigen, SDS extract of Borrelia afzelii

IgG IgM 16 strips 240 strips 30 strips 32 strips 16 strips 240 strips 30 strips 32 strips DY 2131-1601-1 G DY 2131-24001-1 G DY 2131-3001-1 G

DY 2131-1601-1 M DY 2131-24001-1 M DY 2131-3001-1 M EUROLINE-WB Borrelia whole antigen, SDS extract of Borrelia afzelii plus VisE IgG IgM 16 strips 240 strips 30 strips 16 strips

240 strips 30 strips DY 2132-1601 G DY 2132-24001 G DY 2132-3001 G DY 2132-3201 G DY 2132-1601 M DY 2132-24001 M DY 2132-3001 M DY 2132-3201 M Borrelia burgdorferi whole antigen, SDS extract of Borrelia burgdorferi sensu stricto

IgG IgM 16 strips 240 strips 30 strips 32 strips 16 strips 240 strips 30 strips 32 strips DY 2134-1601 G DY 2134-24001 G DY 2134-3001 G

DY 2134-3201 G DY 2134-1601 M DY 2134-24001 M DY 2134-3001 M DY 2134-3201 M Borrelia garinii whole antigen, SDS extract of Borrelia garinii IgG IgM 16 strips 240 strips 30 strips

32 strips 16 strips 240 strips 30 strips 32 strips CW 2131-5001 G antibodies against Borrelia afzelii IgG positive control (Western / EUROLINE-WB) IgG 0. 1 ml CW 2131-5001 M

antibodies against Borrelia afzelii IgM positive control (Western / EUROLINE-WB) IgM 0. 1 ml CW 2132-5001 G antibodies against Borrelia burgdorferi IgG positive control IgG 0. 1 ml CW 2132-5001 M

antibodies against Borrelia burgdorferi IgM positive control IgM 0. 1 ml CW 2134-5001 G antibodies against Borrelia garinii IgG positive control IgG 0. 1 ml CW 2134-5001 M antibodies against Borrelia garinii

IgM positive control IgM 0. 1 ml