Sandbox m ex
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- Imiquimod (Aldara) a topical immune response cream, applied to the affected area
- A 20% podophyllin anti-mitotic solution, applied to the affected area and later washed off
- A 0.5% podofilox solution, applied to the affected area but not to be washed off
- A 5% 5-fluorouracil (5-FU) cream
- Trichloroacetic acid (TCA)
- Pulsed dye laser
- Liquid nitrogen cryosurgery
- Electric or laser cauterization
- Condylox
- Sinecatechins (Veregen) also Polyphenon E: ointment made of several green-tea-extracted catechines and other components. Mode of action is undetermined.[1] It is FDA-approved but very expensive
- Podophyllin and podofilox should not be used during pregnancy, as they are absorbed by the skin and may cause birth defects in the fetus. 5-fluorouracil cream should not be used while trying to become pregnant or if there is a possibility of pregnancy.
Some doctors inject the antiviral drug interferon-alpha directly into the warts, to treat warts that have returned after removal by traditional means. The drug is expensive, and does not reduce the rate that the warts return.
- In general, warts located on moist surfaces or in intertriginous areas respond best to topical treatment.
- Patients should be warned that persistent hypopigmentation or hyperpigmentation occurs commonly with ablative modalities and has also been described with immune modulating therapies (imiquimod).
HSV=====Antiviral Drugs=
Acyclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valacyclovir and famciclovir. During the acute phase, oral acyclovir should be given. Use of acylovir is most effective in moderating the progress of the symptoms, and in preventing post-herpetic neuralgia, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. Immunocompromised patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective. It is also reported that the amino acid lysine inhibits the replication of herpes zoster.[2]
Analgesics
People with mild to moderate pain can be treated with over-the-counter analgesics. Topical lotions containing calamine can be used on the rash or blisters and may be soothing. Occasionally, severe pain may require an opioid medication, such as morphine. Once the lesions have crusted over, capsaicin cream (Zostrix) can be used. Topical lidocaine and nerve blocks may also reduce pain.[3] Administering gabapentin along with antivirals may offer relief of postherpetic neuralgia[4].
Steroids
Orally administered corticosteroids are frequently used in treatment of the infection, despite clinical trials of this treatment being unconvincing. Nevertheless, one trial studying immunocompetent patients older than 50 years of age with localized herpes zoster, suggested that administration of prednisone with aciclovir improved healing time and quality of life.[5] Upon one-month evaluation, aciclovir with prednisone increased the likelihood of crusting and healing of lesions by about twofold, when compared to placebo. This trial also evaluated the effects of this drug combination on quality of life at one month, showing that patients had less pain, and were more likely to stop the use of analgesic agents, return to usual activities and have uninterrupted sleep. However, when comparing cessation of herpes zoster-associated pain or post herpetic neuralgia, there was no difference between aciclovir plus prednisone and simply aciclovir alone. Because of the risks of corticosteroid treatment, it is recommended that this combination of drugs only be used in people more than 50 years of age, due to their greater risk of postherpetic neuralgia.[5]
Other Drugs
Cimetidine, a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.[6][7][8] This usage is considered an off-label use of the drug. In addition, cimetidine and probenecid have been shown to reduce the renal clearance of aciclovir. [9] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.
==VZV==
Complementary Therapies
Digestive Enzymes are available on prescription and in some over the counter preparations. Before the availability of antivirals, oral pancreatic enzyme therapy in shingles was used in some countries and later subjected to clinical and scientific research. A large scale multi-centre clinical study, using an oral preparation of such enzymes, has shown promising results.[10] [11] The results of another clinical study support the concept that oral enzyme therapy is beneficial in diseases characterized in part by TGF-beta overproduction that included shingles patients. [12] TGF-β has also been found to be elevated in instances of VZV infection. [13] [14]
Anti-viral medication
Nucleoside analogs
Treatment is available in the form of antiviral medications such as nucleoside analogs, which reduce the duration of symptoms of a herpex simplex virus outbreak and accelerate healing. Nucleoside analogs are molecules which possess a similarity to natural nucleotides - the building-blocks of DNA and RNA. Active herpes simplex virus will replicate; a virus replicating in the presence of these analogs will incorporate them into its DNA, so that its genetic material will contain defects and mutations. As a result, the next generation of virus will be damaged and reduced in number.
Nucleoside analogs are typically used at the first symptoms of an viral outbreak to reduce the duration of the outbreak and improve healing of the lesion. Treatment taken prior to the appearance of lesions may avert or reduce the symptoms of the outbreak. Occasionally nucleoside analogs are used as a daily suppressive therapy, and taken daily for several years. Suppressive therapy reduces frequency of symptoms and recurrence of outbreaks. In addition, suppressive therapy reduces subclinical viral shedding, lowering the risk of transmission through sexual contact or kissing.
Common nucleoside analogs are listed in the table above. Of these, Ganciclovir is known to have cytotoxic effects on infected cells but Acyclovir is not known to have this effect.[15]
Oral Prodrug |
Drug | Analog of Nucleoside | Nucleoside Family |
---|---|---|---|
Famciclovir[16] (bioavailability: 75% oral) (trade names: Famvir) |
Penciclovir (1.5% oral, IV, locally topical) (Denavir, Fenistil) |
<math>\Bigg\}</math>guanosine | purine |
Valaciclovir (55% oral) (Valtrex) |
Aciclovir (10-20% oral) (Zovirax, Zovir) | ||
Valganciclovir (60% oral) (Valcyte) |
Ganciclovir (5% oral, IV, locally intraocular) (Cytovene, Cymevene) | ||
Brivudine[17] (BVDU) | thymidine | pyrimidine |
Fusion inhibitors
Fusion inhibitors prevent "fusion" of the viral envelope with the cell membrane. This prevents viral entry to the cell.
Helicase-primase inhibitors
One of three key protein structures involved in HSV DNA replication is the Helicase-Primase structure. New research compounds which bind to this megamolecule show remarkable effectiveness against HSV. In particular, BAY 57-1293 has shown positive results in animal models of HSV infection.[18]
Dietary supplements
The amino acid lysine has demonstrated the ability to reduce the duration of infection through inhibiting the replication of the HSV. When foods high in lysine (such as lentils) are consumed in preference to foods high in arginine, HSV replication may be inhibited; conversely, consuming foods high in arginine (such as nuts or peanuts) may interfere with the therapeutic use of lysine.[19] However, according to the American Social Health Association: "While some studies have suggested that lysine supplements can reduce the frequency of recurrences or healing time, other trials have been unable to replicate those results. Therefore, there is not sufficient information to discern how effective it may be, in addition to what the effective dosages or frequency of L-lysine may be."[16]
Other anti-viral medication
Undecylenic acid (Castor oil derivative) is proven to have anti-bacterial and anti-viral properties that are effective on viral skin infections such as the herpes simplex virus (HSV).
Butylated hydroxytoluene (BHT), commonly available as a food preservative, has been shown in vitro to inactivate enveloped viruses including herpes.[20][21] In-vivo studies of topical application to animals confirmed the anti-viral activity of BHT during outbreaks.[22] BHT has not been clinically tested and approved to treat herpes in humans.
Drug Resistance
Resistance of HSVes in cell culture has been reported for nucleosides in the range of 10-2 to 10-4 and for Helicase-Primase inhibitors in the range of 10-4 to 10-6. However, in the clinic roughly 1-2% of the patients are infected by nucleoside-resistant HSVes. In the immunocompromised patient population such as transplant, AIDS or cancer patients the resistance rate can reach up to 10%.
Chlamydia
Chlamydia is a genus of obligate intracellular bacteria in the family Chlamydiaceae, order Chlamydiales, class and phylum Chlamydiae. Several species of Chlamydia are pathogenic to humans causing pneumonia, eye infections, and sexually transmitted disease, which is called Chlamydia
C. trachomatis infection can be effectively cured with antibiotics once it is detected. Current Centers for Disease Control guidelines provide for the following treatments:
- Azithromycin 1 gram oral as a single dose, or
- Doxycycline 100 milligrams twice daily for seven days.
- Tetracycline
- Erythromycin
Untested Treatments
- Ciprofloxacin 500 milligrams twice daily for 3 days. (Although this is not an approved method of treatment, as it is shown to be ineffective and may simply delay symptoms.)
β-lactams are not suitable drugs for the treatment of chlamydia. While they have the ability to halt growth of the organism (i.e. are microbistatic), these antibiotics do not eliminate the bacteria. Once treatment is stopped, the bacteria will begin to grow once more. (See below for Persistence.)
The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a breathing machine for weeks, plus intensive medical and nursing care. After several weeks, the paralysis slowly improves. If diagnosed early, foodborne and wound botulism can be treated by inducing passive immunity with a horse-derived antitoxin, which blocks the action of toxin circulating in the blood.[23] This can prevent patients from worsening, but recovery still takes many weeks. Physicians may try to remove contaminated food still in the gut by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism.
Besides supportive care, infant botulism can be treated with human botulism immune globulin (BabyBIG), when available. Supply is extremely limited, but is available through the California Department of Health Services. This dramatically decreases the length of illness for most infants. Paradoxically, antibiotics (especially aminoglycosides or clindamycin) may cause dramatic acceleration of paralysis as the affected bacteria release toxin. Visual stimulation should be performed during the time the infant is paralyzed as well, in order to promote the normal development of visual pathways in the brain during this critical developmental period.
Furthermore each case of food-borne botulism is a potential public health emergency in that it is necessary to identify the source of the outbreak and ensure that all persons who have been exposed to the toxin have been identified, and that no contaminated food remains.
There are two primary Botulinum Antitoxins available for treatment of wound and foodborne botulism. Trivalent (A,B,E) Botulinum Antitoxin is derived from equine sources utilizing whole antibodies (Fab & Fc portions). This antitoxin is available from the local health department via the CDC. The second antitoxin is heptavalent (A,B,C,D,E,F,G) Botulinum Antitoxin which is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This is a less immunogenic antitoxin that is effective against all known strains of botulism where not contraindicated. This is available from the US Army. On June 1, 2006 the US Department of Health and Human Services awarded a $363 million contract with Cangene Corporation for 200,000 doses of Heptavalent Botulinum Antitoxin over five years for delivery into the Strategic National Stockpile beginning in 2007.[24]
Antimicrobial regimen
- 1. Antibiotics
- Antibiotics are not recommended in gastrointestinal botulism due to the risk of worsening of neurological symptoms caused by the lysis of the bacteria. For wound botulism antibiotics are indicated with surgical treatment as followed:
- Preferred regimen: Metronidazole 500 mg IV q8h
- Alternative regimen: Penicillin G 3 million units IV q4h
- 2. Antitoxin [25]
- Preferred regimen: Trivalent antitoxin (A 7,500 IU, B 5,000 IU, and E 5,000 IU) 1 vial diluted 1:10, IV infusion over 30 min
- Alternative regimen: Equine antitoxin
- 3. General Therapy
- Preferred regimen: Mechanical ventilation; IV hydration; tube feedings
- 1. Antibiotics
- Antibiotics are not recommended in gastrointestinal botulism due to the risk of worsening of neurological symptoms caused by the lysis of the bacteria. For wound botulism antibiotics are indicated with surgical treatment as followed:
- Preferred regimen: Metronidazole 500 mg IV q8h
- Alternative regimen: Penicillin G 3 million units IV q4h
- 2. Antitoxin [26]
- Preferred regimen: Trivalent antitoxin (A 7,500 IU, B 5,000 IU, and E 5,000 IU) 1 vial diluted 1:10, IV infusion over 30 min
- Alternative regimen: Equine antitoxin
- 3. General Therapy
- Preferred regimen: Mechanical ventilation; IV hydration; tube feedings
Pharmacotherapy brucella
Acute Pharmacotherapies
The gold standard treatment for adults is daily intramuscular injections of streptomycin 1 g for 14 days and oral doxycycline 100 mg twice daily for 45 days (concurrently). Gentamicin 5 mg/kg by intramuscular injection once daily for 7 days is an acceptable substitute when streptomycin is not available or difficult to obtain.[27] Another widely used regimen is doxycycline plus rifampin twice daily for at least 6 weeks. This regimen has the advantage of oral administration. A triple therapy of doxycycline, together with rifampin and cotrimoxazole has been used succefully to treat neurobrucellosis. [28] Doxycycline is able to cross the blood-brain barrier, but requires the addition of two other drugs to prevent relapse. Ciprofloxacin and co-trimoxazole therapy is associated with an unacceptably high rate of relapse.
In brucellic endocarditis surgery is required for an optimal outcome.
Even with optimal antibrucellic therapy relapses still occur in 5-10 percent of patients with Malta fever. Experiments have shown that cotrimoxyzol and rifampin are both safe drugs to use in treatment of pregnant women who have Brucellosis.
Acute Pharmacotherapies gonorrhea
-
Gonorrhea treatment advertisement from 1944, when penicillin became widely available due to mass production.
Several antibiotics can successfully cure gonorrhea in adolescents and adults. However, drug-resistant strains of gonorrhea are increasing in many areas of the world, including the United States, and successful treatment of gonorrhea is becoming more difficult. Because many people with gonorrhea also have chlamydia, another sexually transmitted disease, antibiotics for both infections are usually given together. Persons with gonorrhea should be tested for other STDs.
It is important to take all of the medication prescribed to cure gonorrhea. Although medication will stop the infection, it will not repair any permanent damage done by the disease. People who have had gonorrhea and have been treated can get the disease again if they have sexual contact with persons infected with gonorrhea. If a person's symptoms continue even after receiving treatment, he or she should return to a doctor to be reevaluated.
The mainstay of treatment is the appropriate use of antibiotics. While penicillin was the most common antibiotic used to treat gonorrhea up until the 1970s, an increase in antibiotic resistance has led to a decline in its use. Recommendations for first choice treatment of gonorrhea must depend on local information on resistance patterns and it is not possible to make treatment recommendations that are applicable to all parts of the world.
The Centers for Disease Control and Prevention (CDC) released a report on Thursday, April 12, 2007 officially adding gonorrhea to a list of super bugs that are now resistant to common antibiotics according to CDC.
Antibiotics that may be used to treat gonorrhea include:
- Amoxycillin 2 g plus probenecid 1 g orally
- Ampicillin 2 to 3 g plus probenecid 1 g orally
- Azithromycin 2 g orally
- Cefixime 400 mg orally
- Cefotaxime 500 mg by intramuscular injection
- Cefoxitin 2 g by intramuscular injection, plus probenecid 1 g orally
- Cefpodoxime (Vantin) 400 mg orally
- Ceftriaxone (Rocephin) 125 to 250 mg by intramuscular injection
- Ciprofloxacin 500 mg orally
- Levofloxacin 250 mg orally
- Ofloxacin 400 mg orally
- Spectinomycin 2 g by intramuscular injection
These drugs are all given as a single dose.
The level of tetracycline resistance in Neisseria gonorrheae is now so high as to make it completely ineffective in most parts of the world.
The fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin) cannot be used in pregnancy. It is important to refer all sexual partners to be checked for gonorrhea to prevent spread of the disease and to prevent the patient from becoming re-infected with gonorrhea. Patients should also be offered screening for other sexually transmitted infections. In areas where co-infection with chlamydia is common, doctors may prescribe a combination of antibiotics, such as ceftriaxone with doxycycline or azithromycin, to treat both diseases.
Penicillin is ineffective at treating rectal gonorrhea: this is because other bacteria within the rectum produce β-lactamases that destroy penicillin. All current treatments are less effective at treating gonorrhea of the throat, so the patient must be rechecked by throat swab 72 hours or more after being given treatment, and then retreated if the throat swab is still positive.
Although gonorrhea usually does not require follow-up (with the exception of rectal or pharyngeal disease), patients are usually advised to phone for results five to seven days after diagnosis to confirm that the antibiotic they received was likely to be effective. Patients are advised to abstain from sex during this time.
Drug resistant strains are known to exist.
United States recommendations
The United States does not have a federal system of sexual health clinics, and the majority of infections are treated in family practices. A third-generation cephalosporin antibiotic such as ceftriaxone is recommended for use in most areas. Since some areas such as Hawaii and California have very high levels of resistance to fluoroquinolone antibiotics (ciprofloxacin, ofloxacin, levofloxacin) they are no longer used empirically to treat infections originating in these areas.
United Kingdom recommendations
In the United Kingdom, the majority of patients with gonorrhea are treated in dedicated sexual health clinics. The current recommendation is for ceftriaxone or cefixime as first line therapy; no resistance to either drug has yet been reported in the UK. Levels of spectinomycin resistance in the UK are less than 1%, which would make it a good choice in theory, but intramuscular spectinomycin injection is very painful.
Azithromycin (given as a single dose of 2 g) is recommended if there is concurrent infection with chlamydia. A single dose of oral ciprofloxacin 500 mg is effective if the organism is known to be sensitive, but fluoroquinolones were removed from the UK recommendations for empirical therapy in 2003 because of increasing resistance rates. In 2005, resistance rates for ciprofloxacin were 22% for the whole of the UK (42% for London, 10% for the rest of the UK).[29]
antrax
Bacillus anthracis | ||||||||||||||
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Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain). Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain).
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Scientific classification | ||||||||||||||
| ||||||||||||||
Binomial name | ||||||||||||||
Bacillus anthracis Cohn 1872 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2]
Overview
Bacillus anthracis is a Gram-positive, facultatively anaerobic, rod-shaped bacterium of the genus Bacillus. An endospore forming bacterium, B. anthracis is a natural soil-dwelling organism, as well as the causative agent of anthrax.[30]
Each cell is about 1 by 6 μm in size.
Historical background
B. anthracis was the first bacterium conclusively demonstrated to cause disease, by Robert Koch in 1877.[31] The species name anthracis is from the Greek anthrakis (ἄνθραξ), meaning coal and referring to the most common form of the disease, cutaneous anthrax, in which large black skin lesions are formed.
Pathogenicity
Under conditions of environmental stress, B. anthracis bacteria naturally produce endospores which rest in the soil and can survive for decades in this state. When ingested by a cattle, sheep, or other herbivores, the bacteria begin to reproduce inside the animal and eventually kill it, then continue to reproduce in its carcass. Once the nutrients are exhausted, new endospores are produced and the cycle repeats.[32]
B. anthracis has at least 89 known strains, ranging from highly virulent strains with biological warfare and bioterrorism applications (Ames and Vollum) to benign strains used for inoculations (Sterne). The strains differ in presence and activity of various genes, determining their virulence and production of antigens and toxins. The form associated with the 2001 anthrax attacks produced both toxin (consisting of three proteins: the protective antigen, the edema factor and the lethal factor) and a capsule (consisting of a polymer of glutamic acid). Infection with anthrax requires the presence of all three of these exotoxins.[33]
The bacterium can be cultivated in ordinary nutrient medium under aerobic or anaerobic conditions.
Treatment
Infections with B. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against Gram-positive bacteria.[34]
References
- ↑ "Veragen package insert" (PDF). Retrieved 2008-08-18.
- ↑ Griffith, RS (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183–190. PMID 3115841. Unknown parameter
|coauthors=
ignored (help) - ↑ Baron R (2004). "Post-herpetic neuralgia case study: optimizing pain control". Eur. J. Neurol. 11 Suppl 1: 3–11. doi:10.1111/j.1471-0552.2004.00794.x. PMID 15061819.
- ↑ Tyring SK (2007). "Management of herpes zoster and postherpetic neuralgia". J Am Acad Dermatol. 57 (6 Suppl): S136–42. doi:10.1016/j.jaad.2007.09.016. PMID 18021865.
- ↑ 5.0 5.1 Whitley RJ, Weiss H, Gnann JW, Tyring S, Mertz GJ, Pappas PG, Schleupner CJ, Hayden F, Wolf J, Soong SJ (1996). "Acyclovir with and without prednisone for the treatment of herpes zoster. A randomized, placebo-controlled trial. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group". Ann. Intern. Med. 125 (5): 376–83. PMID 8702088.
- ↑ Kapinska-Mrowiecka M, &Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation". Pol Tyg Lek. 51 (23–26): 338–339. PMID 9273526. Check date values in:
|year=
(help) - ↑ Hayne ST, & Mercer JB (1983). "Herpes zoster: treatment with cemetidine". Canadian Medical Association Journal. 129 (12): 1284–1285. PMID 6652595.
- ↑ Notmann J, Arieli J, Hart J, Levinsky H, Halbrecht I, & Sendovsky U (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine". Asian Pacific Journal Allergy and Immunology. 12 (1): 51–58. PMID 7872992.
- ↑ De Bony F, Tod M, Bidault R, On NT, Posner J, & Rolan P (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir". Antimicrobial Agents and Chemotherapy. 46 (2): 458–463. PMID 11796358.
- ↑ Billigmann P (1995). "[Enzyme therapy--an alternative in treatment of herpes zoster. A controlled study of 192 patients]". Fortschr. Med. (in German). 113 (4): 43–8. PMID 7713467.
- ↑ Roxas M (2006). "Herpes zoster and postherpetic neuralgia: diagnosis and therapeutic considerations". Alternative medicine review : a journal of clinical therapeutic. 11 (2): 102–13. PMID 16813460.
- ↑ Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I (2001). "Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood". Cancer Chemother. Pharmacol. 47 Suppl: S10–5. PMID 11561866.
- ↑ Kaygusuz I, Gödekmerdan A, Keleş E; et al. (2004). "The role of viruses in idiopathic peripheral facial palsy and cellular immune response". American journal of otolaryngology. 25 (6): 401–6. PMID 15547808.
- ↑ Sato M, Abe T, Tamai M (2000). "Expression of the Varicella Zoster Virus Thymidine Kinase and Cytokines in Patients with Acute Retinal Necrosis Syndrome". 44 (6): 693. PMID 11094200.
- ↑ Rubsam LZ, Davidson BL, Shewach DS (1998). "Superior cytotoxicity with ganciclovir compared with acyclovir and 1-beta-D-arabinofuranosylthymine in herpes simplex virus-thymidine kinase-expressing cells: a novel paradigm for cell killing". Cancer Res. 58 (17): 3873–82. PMID 9731497.
- ↑ 16.0 16.1 "Learn About Herpes: Treatment". American Social Health Association. Retrieved 2007-07-09.
- ↑ Ciucci A, Lafrate EM, Manzini S, Giachetti A (1997). "Mechanism of antiviral action of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) : direct evidence with 14-C-BVDU in herpes simplex virus-infected cells". Antiviral Chemistry & Chemotherapy. 8: 565&ndash, 71.
- ↑ Crumpacker CS, Schaffer PA (2002). "New anti-HSV therapeutics target the helicase-primase complex". Nat. Med. 8 (4): 327–8. doi:10.1038/nm0402-327. PMID 11927930.
- ↑ "Cold Sores". Healthnotes. Retrieved 2007-07-09.
- ↑ Snipes W, Person S, Keith A, Cupp J (1975). "Butylated hydroxytoluene inactivated lipid-containing viruses". Science. 188 (4183): 64–6. PMID 163494.
- ↑ Coohill TP, Babich M, Taylor WD, Snipes W (1980). "A comparison of herpes simplex virus plaque development after viral treatment with anti-DNA or antilipid agents". Biophys. J. 30 (3): 517–21. PMID 6266532.
- ↑ Richards JT, Katz ME, Kern ER (1985). "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs". Antiviral Res. 5 (5): 281–90. PMID 2998276.
- ↑ Shapiro, Roger L. MD; Charles Hatheway, PhD; and David L. Swerdlow, MD Botulism in the United States: A Clinical and Epidemiologic Review Annals of Internal Medicine. 1 August 1998 Volume 129 Issue 3 Pages 221-228
- ↑ http://mmrs.fema.gov/news/publichealth/2006/aug/nph2006-08-03a.aspx
- ↑ Bartlett, John (2012). Johns Hopkins ABX guide : diagnosis and treatment of infectious diseases. Burlington, MA: Jones and Bartlett Learning. ISBN 978-1449625580.
- ↑ Bartlett, John (2012). Johns Hopkins ABX guide : diagnosis and treatment of infectious diseases. Burlington, MA: Jones and Bartlett Learning. ISBN 978-1449625580.
- ↑ Roushan MRH, Mohraz M, Hajiahmadi M, Ramzani A, Valayati AA (2006). "Efficacy of gentamicin plus doxycycline versus streptomycin plus doxycycline in the treatment of brucellosis in humans". Clin Infect Dis. 42 (8): 1075&ndash, 80.
- ↑ McLean DR, Russell N, Khan MY (1992). "Neurobrucellosis: Clinical and therapeutic features". Clin Infect Dis. 15: 582&ndash, 90.
- ↑ Health Protection Agency. "The gonococcal resistance to antimicrobials surveillance programme: Annual report 2005" (PDF). Retrieved 2006-10-28.
- ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
- ↑ Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed. ed.). Prentice Hall. ISBN 0-13-144329-1.
- ↑ Turnbull PCB (1996). Bacillus. In: Barron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
- ↑ Dixon TC, Meselson M, Guillemin J, Hanna PC (1999). "Anthrax". N. Engl. J. Med. 341 (11): 815–26. PMID 10477781.
- ↑ Barnes JM (1947). "Penicillin and B. anthracis". J Path Bacteriol. 194: 113.
Gallery
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
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Bacillus anthracis. From Public Health Image Library (PHIL). [1]
References
Antibiotic Treatment
Cutaneous Anthrax without Systemic Involvement
Choice of Antibiotics
- Uncomplicated cutaneous anthrax has been successfully treated with a single oral antimicrobial drug.
- Oral fluoroquinolones (ciprofloxacin, levofloxacin, and moxifloxacin) and doxycycline are equivalent first-line agents.
- Clindamycin is an alternative option if fluoroquinolones and doxycycline are contraindicated or unavailable.
- Given the long history of successful treatment of localized uncomplicated cutaneous anthrax with penicillin, amoxicillin and penicillin VK are also alternative therapeutic options if the isolate is known to be susceptible to penicillin. However, adequate dosages must be used because of the potential for development of drug resistance during treatment with subtherapeutic dosing.[1]
Duration of Treatment
- Duration of treatment for localized or uncomplicated cutaneous disease depends on the B. anthracis exposure source:[1]
- Naturally acquired (e.g., animals with anthrax, products such as hides from animals with anthrax): 7–10-day course
- Bioterrorism-related exposure or an aerosol exposure is suspected: 60 days (because the patient is likely to have also inhaled spores.)
Systemic Anthrax When Meningitis Has Been Excluded
Choice of Antibiotics
- The initial treatment should include ≥2 antimicrobial drugs with activity against B. anthracis:[1]
- ≥1 should have bactericidal activity, and
- ≥1 should be a protein synthesis inhibitor
- Intravenous ciprofloxacin is preferred as the primary bactericidal component in the treatment of systemic disease. Linezolid or clindamycin are the preferred as the first-line protein synthesis inhibitor.[1]
- If the B. anthracis strain is susceptible to penicillin, then penicillin G is considered equivalent to the fluoroquinolone options for primary bactericidal treatment.[1]
- Treatment with antimicrobial drugs that have good central nervous system (CNS) penetration is not a crucial factor. Thus, meropenem is recommended as an acceptable alternative option than as a first-line antimicrobial drug, and vancomycin is also an acceptable alternative. Clindamycin and linezolid are considered equivalent first-line choices for protein synthesis inhibitors. Doxycycline is added as an alternative protein synthesis inhibitor option if linezolid or clindamycin are contraindicated or unavailable.[1]
Duration of Treatment
- Initial intravenous combination treatment should be given for ≥2 weeks or until the patient is clinically stable, whichever is longer.[1]
Follow–up Oral Treatment for Systemic Disease
Once patients with systemic illness who were exposed to aerosolized spores have completed initial combination treatment, they should be transitioned to single-agent oral treatment to prevent relapse from surviving B. anthracis spores.[1]
Systemic Anthrax with Possible/Confirmed Meningitis
Choice of Antibiotics
- Empiric treatment for anthrax in which anthrax meningitis is suspected or cannot be ruled out should include ≥3 antimicrobial drugs with activity against B. anthracis:[1]
- ≥1 drug should have bactericidal activity
- ≥1 should be a protein synthesis inhibitor
- All should have good CNS penetration
- Hospitalized patients for systemic anthrax should be immediately treated with a combination of broad-spectrum intravenous antibiotic drug treatment pending confirmatory test results because any delay may prove fatal. Because meningitis and hemorrhagic brain parenchymal infection was observed in ≤50% of cases, meningitis must be considered in all cases of systemic anthrax. Therefore antibiotics to treat possible meningitis must have good penetration of the central nervous system (CNS).[1]
- Intravenous ciprofloxacin is preferred as the primary bactericidal component in the treatment of systemic disease on the basis of efficacy in non-human primates (NHP) infection models and recent use for anthrax cases. Levofloxacin and moxifloxacin are considered equivalent alternatives to ciprofloxacin. The fluoroquinolones have adequate CNS penetration and there are no reports of natural resistance.[1]
- The carbapenem class of antimicrobial drugs is highly resistant to β-lactamases and provides good CNS penetration. Meropenem is preferred as the second antimicrobial drug in the combination antimicrobial drug regimen for anthrax meningitis. If meropenem is unavailable, doripenem and imipenem/cilastatin are considered equivalent alternatives. Imipenem/cilastatin is associated with increased seizure risk and should be used with caution in patients with suspected meningitis. If the B. anthracis strain is susceptible to penicillin (MIC <0.125 µg/mL), penicillin G or ampicillin are acceptable alternatives to carbapenems.[1]
- At least 1 antimicrobial drug that inhibits protein synthesis should be used to reduce exotoxin production. Linezolid is preferred as the first-line protein synthesis inhibitor. It is preferred over clindamycin because it is likely to provide better CNS penetration, although randomized controlled trials on treatment for CNS infections with either agent are lacking. However, linezolid toxicity issues must be taken into consideration. Myelosuppression, peripheral and optic neuropathies, and serotonin syndrome have been reported in patients receiving linezolid. Linezolid should be used cautiously in patients with pre-existing myelosuppression. In patients receiving monoamine oxidase inhibitors or serotonin reuptake inhibitors, the benefit of linezolid treatment should be weighed against the risk for serotonin toxicity and an alternative should be considered. If patients experience visual impairment, prompt ophthalmic evaluation is recommended. If patients have contraindications to linezolid use or it is unavailable, clindamycin is an acceptable alternative. Rifampin, although not a protein synthesis inhibitor, has been widely used for its synergistic effect with a primary drug and could also be used in this capacity if linezolid or clindamycin are unavailable. The protein synthesis inhibitor chloramphenicol has good CNS penetration and has historically been used to successfully treat anthrax. Where available, it could be an acceptable alternative if linezolid, clindamycin, and rifampin are unavailable. Doxycycline should not be used if meningitis is suspected because it does not adequately penetrate the CNS.[1]
Duration of Treatment
- Intravenous combination treatment for systemic anthrax with possible meningitis should be provided for ≥2 weeks or until the patient is clinically stable, whichever is longer.
- Given the high mortality rate associated with meningitis, some expert panelists favored 3 weeks of treatment for patients in whom meningitis could not be ruled out.[1]
Follow–up Oral Treatment for Systemic Disease
Once patients with systemic illness who were exposed to aerosolized spores have completed initial combination treatment, they should be transitioned to single-agent oral treatment to prevent relapse from surviving B. anthracis spores.
Dosage of Antibiotics
▸ Click on the following categories to expand treatment regimens.[2][3][4]
Cutaneous Anthrax Without Systemic Involvement ▸ Adult Patients ▸ Pediatric Patients ▸ Pregnant Patients Systemic Anthrax with Possible/Confirmed Meningitis ▸ Adult Patients ▸ Pediatric Patients ▸ Pregnant Patients Systemic Anthrax Without Meningitis ▸ Adult Patients ▸ Pediatric Patients ▸ Pregnant Patients |
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piss
Psittacosis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Sandbox m ex On the Web |
American Roentgen Ray Society Images of Sandbox m ex |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [4]
Overview
Psittacosis is an infection caused by the obligatory intracellular bacterium Chlamydia psittaci. It is apparently acquired from the birds (parrots).
Causes
Psittacosis is an infection caused by the obligatory intracellular bacterium Chlamydia psittaci. It is apparently acquired from the birds (parrots). Ornithosis is infection from any kind bird.
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 "Centers for Disease Control and Prevention Expert Panel Meetings on Prevention and Treatment of Anthrax in Adults".
- ↑ Hendricks, Katherine A. (2014-02). "Centers for disease control and prevention expert panel meetings on prevention and treatment of anthrax in adults". Emerging Infectious Diseases. 20 (2). doi:10.3201/eid2002.130687. ISSN 1080-6059. PMC 3901462. PMID 24447897. Unknown parameter
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(help) - ↑ Bradley, John S. (2014-04-28). "Pediatric Anthrax Clinical Management". Pediatrics. doi:10.1542/peds.2014-0563. ISSN 1098-4275. PMID 24777226. Unknown parameter
|coauthors=
ignored (help) - ↑ Meaney-Delman, Dana (2014-02). "Special considerations for prophylaxis for and treatment of anthrax in pregnant and postpartum women". Emerging Infectious Diseases. 20 (2). doi:10.3201/eid2002.130611. ISSN 1080-6059. PMC 3901460. PMID 24457117. Unknown parameter
|coauthors=
ignored (help); Check date values in:|date=
(help)
plam
Malaria Microchapters |
Diagnosis |
---|
Treatment |
Case studies |
Sandbox m ex On the Web |
American Roentgen Ray Society Images of Sandbox m ex |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-In-Chief: Yazan Daaboul, Serge Korjian, Alison Leibowitz [6]
Overview
Malaria is a vector-borne infectious disease caused by protozoan parasites. P. vivax is the most common cause of infection, responsible for about 80% of all malaria cases. P. falciparum, the most significant cause of disease, is responsible for about 15% of infections and 90% of deaths.[1][2]
Causes
P. vivax is the most common cause of infection, responsible for about 80% of all malaria cases. P. falciparum, the most significant cause of disease, is responsible for about 15% of infections and 90% of deaths.[3] The remainder of human malaria infections are caused by P. ovale, P. malariae, and P. knowlesi.
The following table distinguishes between the different strains of Plasmodium species, all of which are causative agents of malarial infection.
Strain | Clinical Significance |
---|---|
P. falciparum | Tertian/subtertian fever (every 48 hours), causes severe malaria in up to 24% of cases, and is frequently drug resistant. |
P. vivax |
Tertian fever (every 48 hours), results in severe malaria in up to 22% of cases, and is frequently drug resistant. Relapse is common due to the dormant liver phase. |
P. ovale | Tertian fever (every 48 hours), rarely causes severe malaria or drug resistance. Relapse is common due to dormant liver phase. |
P. malariae | Quartan fever (every 72 hrs), rarely results in severe malaria or drug resistance. Although dormant liver phase is uncommon, infection persistence is frequently demonstrated. |
P. knowlesi | Daily fevers, may result in severe malaria in up to 10% of cases, although resistance is rare. |
References
- ↑ Mendis K, Sina B, Marchesini P, Carter R (2001). "The neglected burden of Plasmodium vivax malaria" (PDF). Am J Trop Med Hyg. 64 (1-2 Suppl): 97–106. PMID 11425182.
- ↑ Mendis K, Sina B, Marchesini P, Carter R (2001). "The neglected burden of Plasmodium vivax malaria" (PDF). Am J Trop Med Hyg. 64 (1-2 Suppl): 97–106. PMID 11425182.
- ↑ Mendis K, Sina B, Marchesini P, Carter R (2001). "The neglected burden of Plasmodium vivax malaria" (PDF). Am J Trop Med Hyg. 64 (1-2 Suppl): 97–106. PMID 11425182.
q fever microb
Coxiella burnetii | ||||||||||||||
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C. burnetii, the causative agent of Q fever C. burnetii, the causative agent of Q fever
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Scientific classification | ||||||||||||||
| ||||||||||||||
Binomial name | ||||||||||||||
Coxiella burnetii (Derrick 1939) Philip 1948 |
Coxiella burnetii is a species of intracellular, pathogenic bacteria, and is the causative agent of Q fever. The genus Coxiella is morphologically similar to the rickettsia, but with a variety of genetic and physiological differences. C. burnetii are small Gram negative bacteria with two growth phases, as well as a spore form which lies idle in soil.[1] It can survive standard disinfectants, and is resistant to many other environmental changes.[2]
Pathogenesis
The ID50 (the dose needed to infect 50% of experimental subjects) is one via inhalation— i.e. inhalation of one organism will yield disease in 50% of the population. Disease occurs in two states: An acute state presents with headaches, chills, and respiratory symptoms, and an insidious chronic stage.
While most infections clear up spontaneously, treatment with tetracycline or doxycycline appears to reduce the symptomatic duration and reduce the likelihood of chronic infection. A combination of erythromycin and rifampin is highly effective in curing and prevention of disease and so is vaccination with Q-vax vaccine (CSL).
References
- ↑ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
- ↑ Sankaran, Neeraja (2000). "Coxiella burnetii". Microbes and people : an A-Z of microorganisms in our lives. Phoenix, Arizona: The Oryx Press. p. 72. ISBN 1-57356-217-3. "In contrast to other rickettsiae, which are highly sensitive and easily killed by chemical disinfectants and changes in their surroundings, C. burnetii is highly resistant" & "Q fever". Centers for Disease Control and Prevention; National Center for Infectious Diseases; Division of Viral and Rickettsial Diseases; Viral and Rickettsial Zoonoses Branch. 2003-02013. Retrieved 2006-05-24. Check date values in:
|date=
(help) "The organisms are resistant to heat, drying, and many common disinfectants."
Anti-malarial Agents
Anti-malarial Agent | Indication | Dosing |
Chloroquine phosphate | P. falciparum from chloroquine-sensitive areas P. vivax from chloroquine-sensitive areas All P. ovale All P. malariae |
1g oral load, followed by 500 mg orally at 6, 24, and 48 h |
Hydroxychloroquine | Same as chloroquine (second line agent) | 800 mg oral load, followed by 400 mg orally at 6, 24, and 48 h |
Atovaquone-Proguanil | P. falciparum from chloroquine-resistant areas | 250 mg atovaquone/100 mg proguanil (1 tab) orally 4 times daily for 3 days |
Primaquine phosphate | Cure of P. vivax and P. ovale (to eliminate hypnozoites) | 30 mg orally once daily for 14 days |
Clindamycin* | P. falciparum or P. vivax from chloroquine-resistant areas | 20 mg/kg/day orally for 3 days or 10 mg/kg IV load, followed by 5 mg/kg IV every 8 hours |
Doxycycline* | P. falciparum or P. vivax from chloroquine-resistant areas | 100 mg orally twice daily for 7 days or 100 mg IV every 12 hours for 7 days (can switch from IV to PO) |
Tertacycline* | P. falciparum or P. vivax from chloroquine-resistant areas | 250 mg orally 4 times daily for 7 days or 250 mg IV 4 times daily for 7 days (can switch from IV to PO) |
Mefloquine | P. falciparum or P. vivax from chloroquine-resistant areas except Thailand-Burmese and Thailand-Cambodian border regions | 750 mg oral load, followed by 500 mg orally 6-12 hours after initial dose |
Quinine sulfate | P. falciparum or P. vivax from chloroquine-resistant areas | 650 mg orally 3 times daily for 3 days or 7 days if acquired from Southeast Asia |
Quinidine gluconate | Severe malaria (all species Unable to tolerate oral agents Parasitemia>10% |
10 mg/kg IV load over 1-2 hours, then 0.02 mg/kg/min continuous infusion for at least 24 hours |
Artemether-lumefantrine | All P. falciparum (outside USA) | 1.5 mg/kg - 9 mg/kg orally twice daily for 3 days |
Dihydroartemisinin–piperaquine | All P. falciparum (outside USA) | 2·5 mg/kg – 20 mg/kg orally once daily for 3 days |
Artesunate | All P. falciparum (outside USA) First line IV agent for severe malaria (outside USA) |
In severe malaria: 2.4 mg/kg IV or IM load, followed by 2.4 mg/kg at 12 h and 24 h; continue injection once daily if necessary In uncomplicated malaria: Monotherapy not recommended, 4mg/kg orally once daily for 3 days combined with a single oral dose of sulfadoxine–pyrimethamine 25/1.25 mg/kg or mefloquine 8 mg/kg orally daily for 3 days |
*Used in combination with quinine or quinidine
mx
The treatment approach in patients with suspected or confirmed malaria varies according to several factors namely travel history, species of Plasmodium, severity of presentation, and availability of certain therapeutic agents.
Initial Assessment & Severe Malaria
The first step in the management of patients with malaria is to conduct a clinical assessment of status and disease severity, as well as determination of the degree of parasitemia. Signs of severe malarial disease include any of the following: Prostration, impaired consciousness/coma, respiratory distress, convulsions, shock, pulmonary edema, acute respiratory distress syndrome (ARDS), jaundice, abnormal bleeding, severe anemia, hemolysis, hemoglobinuria, acute kidney injury, metabolic acidosis, disseminated intravascular coagulopathy, parasitemia >5%. Patients with severe disease require rapid resuscitation and medical therapy. The most vital step in the management is immediate initiation of appropriate parenteral treatment. Unlike patients who appear stable clinically, patients with severe malaria do not require speciation prior to initiation of medical therapy.
The therapeutic regimen in patients with severe malaria consists of intravenous quinidine gluconate plus either tetracycline, doxycycline, or clindamycin.[1] Other supportive measures include admission to the intensive care unit, continuous monitoring of cardiac function, glycemia, parasitemia, hemoglobin and electrolytes. Exchange transfusions may also be considered in patients with a degree of parasitemia >10%.
Uncomplicated Malaria
In patients with clinically and bacteriologically uncomplicated malaria, speciation is required to tailor medical therapy. For most non-falciparum species, chloroquine remains the first line therapeutic agent. It is important to add primaquine to the treatment regimen in patients with documented P. vivax and P. ovale infections to eradicate liver hypnozoites (dormant liver spores that are responsible for recurrence). Care should be taken in patients with G6PD deficiency as large doses of primaquine can cause significant hemolysis. Patients infected with P. malaria do not require primaquine as the species is not capable of forming hypnozoites.[2] Patients diagnosed with P. falciparum malaria require hospitalization given the risk of progression to severe malaria. These patients have to be monitored on daily basis with a blood film and a full physical exam. The choice of drug in these patients depends on two main factors: the area of acquisition of the parasite, and the center at which the patient is being treated.[1]
Despite being the mainstay of therapy since its introduction, empiric treatment with chloroquine in patients with P. falciparum is no longer recommended due to a sharp increase in resistance. A detailed travel history is important to determine where the infection was acquired. Most malaria endemic countries have reported chloroquine resistant strains, with the exception of Central America west of Panama Canal, Mexico, Hispaniola, certain parts of China, and the Middle East (see figure below). If acquired in any of the latter sites then treatment with chloroquine is adequate. Acquisition from all other endemic countries requires other therapeutic regimens such as oral quinine with either tetracycline, doxycycline, or clindamycin as a first line therapy in the United States, otherwise atovaquone-proguanil or mefloquine if the primary regimen is unavailable.
Worldwide, the treatment of both complicated and uncomplicated P. falciparum malaria requires a combination therapy that includes artemisinin derivatives. According to the 2010 WHO guidelines on the treatment of malaria, the following regimens are first line for the treatment of uncomplicated P. falciparum: artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine, and artesunate plus sulfadoxine-pyrimethamin. It is important to note that artemisin monotherapy in not recommended due to increasing resistance. For patients with severe P. falciparum malaria, artesunate IV or IM is first line followed by IV quinidine. The artemisinin derivatives clear parasites very rapidly have been shown to reduce mortality in severe malaria compared with parenteral quinine. Artemisins are not widely available in the United States and their use is not common practice. Only oral artemether plus lumefantrine is available, while IV atresunate can be obtained through the CDC part of an investigational drug protocol. [3]
- ↑ 1.0 1.1 Griffith KS, Lewis LS, Mali S, Parise ME (2007). "Treatment of malaria in the United States: a systematic review". JAMA. 297 (20): 2264–77. doi:10.1001/jama.297.20.2264. PMID 17519416.
- ↑ White NJ, Pukrittayakamee S, Hien TT, Faiz MA, Mokuolu OA, Dondorp AM (2014). "Malaria". Lancet. 383 (9918): 723–35. doi:10.1016/S0140-6736(13)60024-0. PMID 23953767.
- ↑ Template:Cite website
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