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Cervical intraepithelial neoplasia
ICD-10 D06, N87
ICD-9 233.1, 622.10
MedlinePlus 001491
MeSH D018290


Pap Smear

Cervical dysplasia that is seen on a Pap smear is called squamous intraepithelial lesion (SIL). These changes may be graded as:

  • Low-grade (LSIL)
  • High-grade (HSIL)
  • Possibly cancerous (malignant)

If a Pap smear shows abnormal cells or cervical dysplasia, further testing or monitoring will be recommended:

  • Follow-up Pap smears may be recommended for mild cases
  • Colposcopy-directed biopsy can confirm the condition
  • Cone biopsy may be done after colposcopy

Dysplasia that is seen on a biopsy of the cervix is called cervical intraepithelial neoplasia (CIN). It is grouped into three categories:

  • CIN I -- mild dysplasia
  • CIN II -- moderate to marked dysplasia
  • CIN III -- severe dysplasia to carcinoma in situ

Some strains of human papillomavirus (HPV) are known to cause cervical cancer. An HPV DNA test can identify the high-risk types of HPV linked to such cancer. This may be done:

  • As a screening test for women over age 30
  • For women of any age who have a slightly abnormal Pap test result








HPV subtypes 16 and 18 deregulate the genes E6 and E7 which code for proteins that inhibit p53 and Retinoblastoma protein (Rb), which are two important tumor suppressor genes in humans. The p53 gene product is involved in regulation of apoptosis (cell suicide), and Rb is responsible for halting the cell cycle at the G1-phase. When Rb function is impaired, the cell is allowed to progress to S-phase and complete mitosis, resulting in proliferation and hence neoplastic transformation.

Hysterectomy

Microinvasive cancer (stage IA) is usually treated by hysterectomy (removal of the whole uterus including part of the vagina). For stage IA2, the lymph nodes are removed as well. An alternative for patients who desire to remain fertile is a local surgical procedure such as a loop electrical excision procedure (LEEP) or cone biopsy.

Trachelectomy

  • If a cone biopsy does not produce clear margins,[1] one more possible treatment option for patients who want to preserve their fertility is a trachelectomy.[2]
  • This attempts to surgically remove the cancer while preserving the ovaries and uterus, providing for a more conservative operation than a hysterectomy.
  • It is a viable option for those in stage I cervical cancer which has not spread; however, it is not yet considered a standard of care,[3] as few doctors are skilled in this procedure.
  • Even the most experienced surgeon cannot promise that a trachelectomy can be performed until after surgical microscopic examination, as the extent of the spread of cancer is unknown.
  • If the surgeon is not able to microscopically confirm clear margins of cervical tissue once the patient is under general anesthesia in the operating room, a hysterectomy may still be needed. This can only be done during the same operation if the patient has given prior consent.
  • Due to the possible risk of cancer spread to the lymph nodes in stage 1b cancers and some stage 1a cancers, the surgeon may also need to remove some lymph nodes from around the womb for pathologic evaluation.

Radical Trachelectomy

A radical trachelectomy can be performed abdominally[4] or vaginally[5] and there are conflicting opinions as to which is better.[6] A radical abdominal trachelectomy with lymphadenectomy usually only requires a two to three day hospital stay, and most women recover very quickly (approximately six weeks). Complications are uncommon, although women who are able to conceive after surgery are susceptible to preterm labor and possible late miscarriage.[7] It is generally recommended to wait at least one year before attempting to become pregnant after surgery.[8] Recurrence in the residual cervix is very rare if the cancer has been cleared with the trachelectomy.[9] Yet, it is recommended for patients to practice vigilant prevention and follow up care including pap screenings/colposcopy, with biopsies of the remaining lower uterine segment as needed (every 3-4 months for at least 5 years) to monitor for any recurrence in addition to minimizing any new exposures to HPV through safe sex practices until one is actively trying to conceive.

Radical Hysterectomy

Early stages (IB1 and IIA less than 4 cm) can be treated with radical hysterectomy with removal of the lymph nodes or radiation therapy. Radiation therapy is given as external beam radiotherapy to the pelvis and brachytherapy (internal radiation). Patients treated with surgery who have high risk features found on pathologic examination are given radiation therapy with or without chemotherapy in order to reduce the risk of relapse.



  • Precancerous changes of the cervix and early stage cervical cancer,physical examination findings can be normal. Special tests and tools are needed to spot such conditions:
  • A Pap smear is used for screening precancers and cervical cancer, but final diagnosis cannot be made.
  • The human papillomavirus (HPV) DNA test may be done along with a pap test. Or it may be used after a woman has had an abnormal Pap test result. It may also be used as a main test.
  • If abnormal changes are found, the cervix is usually examined using colposcope.cervical biopsy can be taken form tissue and examined.

Radiation and Chemotherapy

Larger early stage tumors (IB2 and IIA more than 4 cm) may be treated with radiation therapy and cisplatin-based chemotherapy, hysterectomy (which then usually requires adjuvant radiation therapy), or cisplatin chemotherapy followed by hysterectomy.

Advanced stage tumors (IIB-IVA) are treated with radiation therapy and cisplatin-based chemotherapy.

On June 15, 2006, the US Food and Drug Administration approved the use of a combination of two chemotherapy drugs, hycamtin and cisplatin for women with late-stage (IVB) cervical cancer treatment.[10] Combination treatment has significant risk of neutropenia, anemia, and thrombocytopenia side effects. Hycamtin is manufactured by GlaxoSmithKline.

Contraindicated medications

Invasive cervical carcinoma is considered a relative contraindication to the use of the following medications:


According to the International Federation of Gynecology and Obstetrics, survival improves when radiotherapy is combined with cisplatin-based chemotherapy.[11]

As the cancer metastasizes to other parts of the body, prognosis drops dramatically because treatment of local lesions is generally more effective than whole body treatments such as chemotherapy. Regular screening has meant that pre cancerous changes and early stage cervical cancers have been detected and treated early. Figures suggest that cervical screening is saving 5,000 lives each year in the UK by preventing cervical cancer.[12] Interval evaluation of the patient after therapy is imperative. Recurrent cervical cancer detected at its earliest stages might be successfully treated with surgery, radiation, chemotherapy, or a combination of the three. Thirty-five percent of patients with invasive cervical cancer have persistent or recurrent disease after treatment.[13]In screening a general or low-risk population, most Pap results are normal.


In the United States, about 2–3 million abnormal Pap smear results are found each year.[14] Most abnormal results are mildly abnormal (ASC-US (typically 2–5% of Pap results) or low-grade squamous intraepithelial lesion (LSIL) (about 2% of results)), indicating HPV infection.[citation needed] Although most low-grade cervical dysplasias spontaneously regress without ever leading to cervical cancer, dysplasia can serve as an indication that increased vigilance is needed.

In a typical scenario, about 0.5% of Pap results are high-grade SIL (HSIL), and less than 0.5% of results indicate cancer; 0.2 to 0.8% of results indicate Atypical Glandular Cells of Undetermined Significance (AGC-NOS).

As liquid based preparations (LBPs) become a common medium for testing, atypical result rates have increased. The median rate for all preparations with low-grade squamous intraepithelial lesions using LBPs was 2.9% compared with a 2003 median rate of 2.1%. Rates for high-grade squamous intraepithelial lesions (median, 0.5%) and atypical squamous cells have changed little.[15]


It's important for you to take care of yourself by eating well and staying as active as you can during the sometimes rough treatment of cervical cancer. You need the right amount of calories to maintain a good weight. You also need enough protein to keep up your strength. Eating well may help you feel better and have more energy. However, you may not feel like eating during or soon after treatment. You may be uncomfortable or tired. You may find that foods don't taste as good as they used to. In addition, the side effects of treatment (such as poor appetite, nausea, vomiting, or mouth sores) can make it hard to eat well. Your doctor, a registered dietitian, or another health care provider can suggest ways to cope with these problems. Research shows that people with cancer feel better when they stay active. Walking, yoga, swimming, and other activities can keep you strong and increase your energy. Exercise may reduce nausea and pain and make treatment easier to handle. It also can help relieve stress. Whatever physical activity you choose, be sure to talk to your doctor before you start.

You'll need regular checkups after treatment for cervical cancer. Checkups help ensure that any changes in your health are noted and treated if needed. If you have any health problems between checkups, you should contact your doctor. Your doctor will check for the return of cancer. Even when the cancer seems to have been completely removed or destroyed, the disease sometimes returns because undetected cancer cells remained somewhere in the body after treatment. Checkups may include a physical exam, Pap tests, and chest x-rays.



It is often located in the chest area. Most malignant teratomas can spread throughout the body, and have spread by the time of diagnosis.

A number of other cancers are often associated with these tumors, including:




Editor-In-Chief: C. Michael Gibson, M.S., M.D. [11]

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Overview

DiseasesDB = 3604 |

 DiseasesDB_mult  = Template:DiseasesDB2 Template:DiseasesDB2 |
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 ICDO           = 9080 |
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Pathology classification of individual teratomas

Teratomas commonly are classified using the Gonzalez-Crussi grading system: 0 or mature (benign); 1 or immature, probably benign; 2 or immature, possibly malignant (cancerous); and 3 or frankly malignant. See also cancer staging. Teratomas are also classified by their content: a solid teratoma contains only tissues (perhaps including more complex structures); a cystic teratoma contain only pockets of fluid or semi-fluid such as cerebrospinal fluid, sebum, or fat; a mixed teratoma contains both solid and cystic parts. Cystic teratomas usually are grade 0 and, conversely, grade 0 teratomas usually are cystic.

Grade 0, 1 and 2 pure teratomas have the potential to become malignant (grade 3), and malignant pure teratomas have the potential to metastasize. These rare forms of teratoma with malignant transformation may contain elements of somatic (non germ cell) malignancy such as leukemia, carcinoma or sarcoma.[16] A teratoma may contain elements of other germ cell tumors, in which case it is not a pure teratoma but rather is a mixed germ cell tumor and is malignant. In infants and young children, these elements usually are endodermal sinus tumor, followed by choriocarcinoma. Finally, a teratoma can be pure and not malignant yet highly aggressive: this is exemplified by growing teratoma syndrome, in which chemotherapy eliminates the malignant elements of a mixed tumor, leaving pure teratoma which paradoxically begins to grow very rapidly.

"Benign" teratoma may prove to be malignant

A "benign" grade 0 (mature) teratoma nonetheless has a non-zero risk of malignancy. Recurrence with malignant endodermal sinus tumor has been reported in cases of formerly benign mature teratoma,[17] even in fetiform teratoma and fetus in fetu.[18][19] A grade 1 immature teratoma that appears to be benign (e.g., because AFP is not elevated) has a much higher risk of malignancy, and requires adequate follow-up.[20][21][22][23]

Teratoma with malignant transformation

A teratoma with malignant transformation or TMT is a very rare form of teratoma that may contain elements of somatic (non germ cell) malignant tumors such as leukemia, carcinoma or sarcoma.[16] Of 641 children with pure teratoma, 9 developed TMT[24]: 5 carcinoma, 2 glioma, and 2 embryonal (here, these last are classified among germ cell tumors).

Extraspinal ependymoma

Extraspinal ependymoma, usually considered to be a glioma (a type of non-germ cell tumor), may be an unusual form of mature teratoma.[25]

References

  1. [1]
  2. [2]
  3. [3]
  4. [4]
  5. [5]
  6. [6]
  7. [7]
  8. [8]
  9. [9]
  10. [10]
  11. Committee on Practice Bulletins-Gynecology (2002). "ACOG practice bulletin. Diagnosis and treatment of cervical carcinomas, number 35, May 2002". Obstetrics and gynecology. 99 (5 Pt 1): 855–67. PMID 11978302.
  12. "Cervical cancer statistics and prognosis". Cancer Research UK. Retrieved 2007-03-24.
  13. "Cervical Cancer". Cervical Cancer: Pathology, Symptoms and Signs, Diagnosis, Prognosis and Treatment. Armenian Health Network, Health.am.
  14. "Pap Smear". Retrieved 2008-12-27.
  15. Eversole, GM; Moriarty, AT; Schwartz, MR; Clayton, AC; Souers, R; Fatheree, LA; Chmara, BA; Tench, WD; Henry, MR (2010). "Practices of participants in the college of american pathologists interlaboratory comparison program in cervicovaginal cytology, 2006". Archives of pathology & laboratory medicine. 134 (3): 331–5. doi:10.1043/1543-2165-134.3.331. PMID 20196659.
  16. 16.0 16.1 Harms D, Zahn S, Göbel U, Schneider DT (2006). "Pathology and molecular biology of teratomas in childhood and adolescence". Klinische Pädiatrie. 218 (6): 296–302. doi:10.1055/s-2006-942271. PMID 17080330.
  17. Ohno Y, Kanematsu T (1998). "An endodermal sinus tumor arising from a mature cystic teratoma in the retroperitoneum in a child: is a mature teratoma a premalignant condition?". Hum. Pathol. 29 (10): 1167–9. PMID 9781660.
  18. Chen YH, Chang CH, Chen KC, Diau GY, Loh IW, Chu CC (2007). "Malignant transformation of a well-organized sacrococcygeal fetiform teratoma in a newborn male". J. Formos. Med. Assoc. 106 (5): 400–2. PMID 17561476. (publisher offers free full text PDF to registered users)
  19. Hopkins KL, Dickson PK, Ball TI, Ricketts RR, O'Shea PA, Abramowsky CR (1997). "Fetus-in-fetu with malignant recurrence". J. Pediatr. Surg. 32 (10): 1476–9. PMID 9349774.
  20. Muscatello L, Giudice M, Feltri M (2005). "Malignant cervical teratoma: report of a case in a newborn". European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery. 262 (11): 899–904. doi:10.1007/s00405-005-0917-2. PMID 15895292.
  21. Ukiyama E, Endo M, Yoshida F, Tezuka T, Kudo K, Sato S, Akatsuka S, Hata J (2005). "Recurrent yolk sac tumor following resection of a neonatal immature gastric teratoma". Pediatr. Surg. Int. 21 (7): 585–8. doi:10.1007/s00383-005-1404-y. PMID 15928937.
  22. Bilik R, Shandling B, Pope M, Thorner P, Weitzman S, Ein SH (1993). "Malignant benign neonatal sacrococcygeal teratoma". J. Pediatr. Surg. 28 (9): 1158–60. PMID 7508500.
  23. Hawkins E, Issacs H, Cushing B, Rogers P (1993). "Occult malignancy in neonatal sacrococcygeal teratomas. A report from a Combined Pediatric Oncology Group and Children's Cancer Group study". The American journal of pediatric hematology/oncology. 15 (4): 406–9. PMID 7692755.
  24. Biskup W, Calaminus G, Schneider DT, Leuschner I, Göbel U (2006). "Teratoma with malignant transformation: experiences of the cooperative GPOH protocols MAKEI 83/86/89/96". Klinische Pädiatrie. 218 (6): 303–8. doi:10.1055/s-2006-942272. PMID 17080331.
  25. Aktuğ T, Hakgüder G, Sarioğlu S, Akgür FM, Olguner M, Pabuçcuoğlu U. (2000) Sacrococcygeal extraspinal ependymomas: the role of coccygectomy. J Pediatr Surg. 35(3):515-518. PubMed




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See Ben Underwood for a case who compensated for the resulting blindness by developing human echolocation.

In October 2007, researchers have identified the specific cell that causes retinoblastoma.[12]old daughter had the condition. Fisher missed Game 1 and half of Game 2 of the 2007 NBA playoff series versus the Golden State Warriors to be with his daughter for her surgery in New York City

Retinoblastoma is a cancer of the retina. Development of this tumor is initiated by mutations[1] that inactivate both copies of the RB1 gene, which codes for the retinoblastoma protein.[2]

It occurs mostly in children younger than 5 years and accounts for about 3% of the cancers occurring in children younger than 15 years. Adult cases have also been clinically recorded.[3] The estimated annual incidence is approximately 4 per million children.[4] It begins with white blotches in one or both eyes (leukocoria) which can be seen in photographs (this is distinct from the red-eye effect which is normal); or when light reflects off the eye, as when watching television



The term uterine cancer may refer to one of several different types of cancer which occur in the uterus. These include:

  • Endometrial carcinomas originate from cells in the glands of the endometrium (uterine lining). These include the common and readily treatable well-differentiated endometrioid adenocarcinoma, as well as the more aggressive uterine papillary serous carcinoma and uterine clear-cell carcinoma.
  • Endometrial stromal sarcomas originate from the connective tissues of the endometrium, and are far less common than endometrial carcinomas
  • Malignant mixed müllerian tumors are rare endometrial tumors which show both glandular (carcinomatous) and stromal (sarcomatous) differentiation - their true cell of origin is unknown.
  • Cervical cancer arises from the transitional zone of the cervix, the lower portion of the uterus which lies at the upper aspect of the vagina


A procedure that makes a series of detailed pictures of areas inside the body, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography.


A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI).

Treatment

There is no specific treatment for infectious mononucleosis, other than treating the symptoms. No antiviral drugs or vaccines are available. Some physicians have prescribed a 5-day course of steroids to control the swelling of the throat and tonsils. The use of steroids has also been reported to decrease the overall length and severity of illness, but these reports have not been published.

Prevention & Treatment

  • Epstein-Barr Virus (EBV) [5]
  • There is no vaccine to protect against EBV infection. You can help protect yourself by not kissing or sharing drinks, food, or personal items, like toothbrushes, with people who have EBV infection.
  • There is no specific treatment for EBV. However, some things can be done to help relieve symptoms, including
  • Drinking fluids to stay hydrated
  • Getting plenty of rest
  • Taking over-the-counter medications for pain and fever



Gas gangrene

Preferred regimen: Penicillin G 3-4 million units IV q4h AND (Clindamycin 900 mg IV q8h OR Tetracycline 500 mg IV q6h)[78]



Antibiotics are used if an infection is suspected. Fluoroquinolones are an option, although resistance of N. gonorrhoeae may limit their use. A cephalosporin (such as ceftriaxone) combined with doxycycline is an alternative. Azithromycin can be used for susceptible strains. In children, quinolones and doxycycline are best avoided. Since bacteria that cause urinary tract infections are often the cause of epididymitis in children, co-trimoxazole or suited penicillins (for example, cephalexin) can be used. If there is a sexually transmitted disease, the partner should also be treated.

Household remedies such as elevation of the scrotum and cold compresses applied regularly to the scrotum may relieve the pain. Painkillers or anti-inflammatory drugs are often necessary. Hospitalisation is indicated for severe cases, and check-ups can ensure the infection has cleared up.


  • Preferred regimen: Doxycycline 100 mg IV q12h for 7-14 days
  • Alternative regimen (1): Chloramphenicol
  • Alternative regimen (2): Rifampin
  • Pediatric regimen: Doxycycline 2.2 mg/kg PO bid (Children under 45 kg (100 lbs)) for 7-14 days
  • Note: Patients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement


Febrile Neutropenia

Template:Seealso

Exception may be made for neutropenic patients in which delayed treatment could lead to serious complications.

After samples for cultures are obtained, febrile neutropenia should be aggressively treated with broad-spectrum antipseudomonal antibiotics. The antimicrobial regimen should be modified in accordance with the culture results.[6][7][8]

HIV/AIDS patients

HIV-infected persons with pyrexia and hypoxia, should be placed on therapy for Pneumocystis jirovecii infection and adjusted once the diagnosis is confirmed.[8]

Giant Cell Arteritis

Empiric corticosteroids may be considered in patients with suspected giant cell arteritis to prevent vascular complications such as stroke and blindness. Giant cell arteritis should be suspected in a patient over the age of 50 with the following symptoms:


Premenopausal, Nonpregnant Women

No screening or treatment recommended for healthy, bacteriuric women.
Although asymptomatic bacteriuria increases the risk of urinary tract infection but has no effect on the long term adverse outcomes like CKD, genitourinary cancer or overall survival.[9] [10] Studies' results indicated that the treatment wouldn't decrease the frequency for asymptomatic bacteriuria or the risk of developing symptomatic urinary tract infection.[11]

Pregnant Women

Pregnant women
Regimen:3-7 day for any of the following
Amoxicillin 250 mg–1 gm po tid
OR
Oral cephalosporins
Cefaclor500 mg po q8h or 500 mg extended release q12h
Cefdinir 300 mg po q12h or 600 mg po q24h
Cefditoren 200 mg tabs—2 tabs bid
Cefixime 400 mg po q24h
Cefpodoxime proxetil 200 mg po q12h
Cefprozil 500 mg po q12h
Ceftibuten 400 mg po q24h
Cefuroxime axetil 250 or 500 mg q12h
Loracarbef 400 mg po q12h

OR
TMP-SMX DS 1 tab bid
OR
Trimethoprim 100 mg po q12h or 200 mg po q24h.


In early pregnancy, both screening for asymptomatic bacteriuria by urine culture and treatment of positive results are recommended.

  • Single screening with urine culture[12]in the first trimester[13]proved to be effective.[14]
  • Antibiotics treatment has shown a significant decrease in the risk of subsequent pyelonephritis(from 25-30% to 1-4%).[15] They also reduce the frequency of preterm deliveries and low birth weight.[16] [17]
  • The duration of antimicrobial therapy is 3-7 days.
  • After therapy of recurrent bacteriuria, periodic screening should be considered.

Diabetic Women

Asymptomatic bacteriuria screening or treatment is not recommended for diabetic women.

  • No change in the rate of symptomatic urinary tract infection, diabetes progression and complication or overall mortality in diabetic women[18] [19], in addition to the adverse effects of antimicrobial therapy.[20]

Older Persons Residing in the Community

Routine screening and treatment for asymptomatic bacteriuria is not indicated.

  • Treatment has no effect on decreasing symptomatic urinary tract infections,[21] adverse outcomes or survival.[22] [23]

Elderly Institutionalized Subjects

No recommendation for screening for or treatment of asymptomatic bacteriuria.

  • No reduction in rates of symptomatic infections or survival.[24] [25]
  • Instead, treatment has increased the risk of adverse effects and reinfections with resistant strains.[24]

Subjects with Spinal Cord Injuries

No benefit from screening for or treatment of asymptomatic bacteriuria Although the high prevalence of asymptomatic bacteriuria in patients with spinal cord injuries[26], but antimicrobial therapy harm outweigh benefit because of recurrent infections with more resistant strains.[27]

Patients with Indwelling Urethral Catheters

It is not recommended to screen for or treat asymptomatic bacteriuria or fungiuria for short or long term catheters,[28] but antimicrobial therapy can be used for women with persistent bacteriuria 48 hours after removal of the urethral catheter.

  • No benefit of therapy of asymptomatic bacteriuria due to similar recurrence rates with more resistance to antibiotics.[29][30]
  • Significant improvement has been shown with women treated for bacteriuria that existed 48 hours after removal of indwelling urethral catheters.[31]

Urologic Interventions

Urologic Intervention
Regimen
TMP-SMX DS 1 tab bid x 3 days


Due to high risk of bacteremia (60%) and sepsis(6-10%) because of traumatic genitourinary procedures,[32] and the effectiveness of antimicrobials to prevent these complications;[33] [32] [34] screening for bacteriuria and antimicrobial therapy is recommended before the initiation of invasive urologic procedures like transurethral resection of prostate.[33][34]

  • Antibiotic therapy usually discontinued after the procedure, unless there is an indwelling urethral catheter until removed. [32][33]

Immunocompromised Patients and Other Patients

Poor transplant prognosis and complications hasn't been associated with asymptomatic bacteriuria,[35][36]so there is no benefit from screening[37][38] for or treatment of asymptomatic bacteriuria in renal transplant or other solid organ[39] transplant patients.[40]

There is no vaccine against the bacteria. LGV can be treated with three weeks of antibiotics. CDC STD Treatment Guidelines recommend the use of doxycyline, twice a day for 21 days. An alternative treatment is erythromycin base or azithromycin. The health care provider will determine which is best.

Medical Therapy

Acute Pharmacotherapy

Treatment involves antibiotics and may involve drainage of the buboes or abscesses by needle aspiration or incision. Further supportive measure may need to be taken: dilatation of the rectal stricture, repair ofrectovaginal fistulae, or colostomy for rectal obstruction. Common antibiotic treatments include: tetracycline, doxycycline (all tetracyclines, including doxycycline, are contraindicated during pregnancy and in children due to effects on bone development and tooth discoloration), and erythromycin.

If a patient has been treated for LGV, he/she should notify any sex partners they had sex with within 60 days of the symptom onset so they can be evaluated and treated. This will reduce the risk that their partners will develop symptoms and/or serious complications of LGV. It will reducetheir risk of becoming re-infected as well as reduce the risk of ongoing transmission in the community. The patient and all of his/her sex partners should avoid sex until the patient has completed treatment for the infection and symptoms of both the patient and their partners have disappeared.

Note: Doxycycline is not recommended for use in pregnant women. Pregnant and lactating women should be treated with erythromycin. Azythromycin may prove useful for treatment of LGV in pregnancy, but no published data are available regarding its safety and efficacy. A health care provider (like a doctor or nurse) can discuss treatment options with patients.

Persons with both LGV and HIV infection should receive the same LGV treatment as those who are HIV-negative. Prolonged therapy may be required, and delay in resolution of symptoms may occur among persons with HIV.

As with all STD's sex partners of patients who have LGV should be examined and tested for urethral or cervical chlamydial infection. After a positive culture for chlamydia, clinical suspicion should be confirmed with testing to distinguish serotype. Antibiotic treatment should be started if they had sexual contact with the patient during the 30 days preceding onset of symptoms in the patient. Patients with a sexually transmitted disease need to be tested for other STD's. Antibiotics are not without risks and prophylaxtic broad antibiotic coverage is not recommended.[1]

Overview

Genital warts may disappear without treatment, but sometimes eventually develop a fleshy, small raised growth. There is no way to predict whether they will grow or disappear.

Medical Treatment

Overveiw

  • The primary reason for treating genital warts is the amelioration of symptoms (including relieving cosmetic concerns) and ultimately, removal of the warts. In most patients, treatment can induce wart-free periods.
  • If left untreated, visible genital warts can resolve on their own, remain unchanged, or increase in size or number. Available therapies for genital warts likely reduce, but probably do not eradicate, HPV infectivity.
  • Whether the reductio==Medical Treatment==n in HPV viral DNA resulting from treatment reduces future transmission remains unclear. No evidence indicates that the presence of genital warts or their treatment is associated with the development of cervical cancer.
  • Factors that influence selection of treatment include wart size, wart number, anatomic site of the wart, wart morphology, patient preference, cost of treatment, convenience, adverse effects, and provider experience.
  • The treatment modality should be changed if a patient has not improved substantially after a complete course of treatment or if side effects are severe. Most genital warts respond within 3 months of therapy.
Genital Warts Treatment
Preferred Regimen
External genital warts(Patient applied)
Podofilox (0.5% solution or gel): apply 2x/day x 3 days, 4th day no therapy, repeat cycle 4x
OR
Imiquimod 5% cream: apply once daily at bedtime 3x/week x up to 16 weeks
OR
Sinecatechins 15% ointment
External genital warts(Provider administered)
Cryotherapy with liquid nitrogen; repeat q1-2 weeks
OR
Podophyllin resin 10-25% in tincture of benzoin. Repeat weekly as needed
OR
Trichloroacetic acid(TCA): repeat weekly as needed
OR
Surgical removal
Vaginal warts
Cryotherapywith liquid nitrogen
OR
Trichloroacetic acid
Urethral warts
Cryotherapy with liquid nitrogen
OR
Podophyllin resin 10-25% in tincture of benzoin.
Anal warts
Cryotherapy with liquid nitrogen
OR
Trichloroacetic acid
OR
surgical removal.
Advise anoscopy to look for rectal warts
Skin Papillomas
Topical α-lactalbumin. Oleic acid (from human milk) applied 1x/day for 3 weeks
  • 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.[41] 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.[42]

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.[43] Administering gabapentin along with antivirals may offer relief of postherpetic neuralgia[44].

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.[45] 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.[45]

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.[46][47][48] 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. [49] 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==
Transmission electron micrograph of varicella-zoster virions
Electron micrograph of Varicella zoster virus. Approx. 150.000-fold magnification.


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.[50] [51] 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. [52] TGF-β has also been found to be elevated in instances of VZV infection. [53] [54]

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.[55]

Oral Prodrug
Drug Analog of Nucleoside Nucleoside Family
Famciclovir[56]
(bioavailability: 75% oral)
(trade names: Famvir)
Penciclovir
(1.5% oral, IV, locally topical)
(Denavir, Fenistil)
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[57] (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.[58]

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.[59] 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."[56]

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.[60][61] In-vivo studies of topical application to animals confirmed the anti-viral activity of BHT during outbreaks.[62] 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

Chlamydia trachomatis inclusion bodies (brown) in a McCoy cell culture.

C. trachomatis infection can be effectively cured with antibiotics once it is detected. Current Centers for Disease Control guidelines provide for the following treatments:

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.[63] 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.[64]

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
  • 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
  • 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.[67] 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. [68] 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

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:

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).[69]




antrax

Bacillus anthracis
Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain).
Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain).
Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Bacillaceae
Genus: Bacillus
Species: B. anthracis
Binomial name
Bacillus anthracis
Cohn 1872
File:B anthracis diagram en.png
Structure of Bacillus anthracis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [13]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [14]

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.[70]

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.[71] 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.[72]

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.[73]

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.[74]

References

  1. Knudson A (1971). "Mutation and cancer: statistical study of retinoblastoma". Proc Natl Acad Sci U S A. 68 (4): 820–3. PMID 5279gadgqetqer523 Check |pmid= value (help).
  2. Friend S, Bernards R, Rogelj S, Weinberg R, Rapaport J, Albert D, Dryja T. "A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma". Nature. 323 (6089): 643–6. PMID 2877398.
  3. Takahashi T, Tamura S, Inoue M, Isayama Y, Sashikata T (1983). "Retinoblastoma in a 26-year-old adult". Ophthalmology. 90 (2): 179–83. PMID 6856254.
  4. cancer.org
  5. "Epstein-Barr Virus (EBV) center for disease control and prevention".
  6. Mandell's Principles and Practices of Infection Diseases 6th Edition (2004) by Gerald L. Mandell MD, MACP, John E. Bennett MD, Raphael Dolin MD, ISBN 0-443-06643-4 · Hardback · 4016 Pages Churchill Livingstone
  7. Harrison's Principles of Internal Medicine 16th Edition, The McGraw-Hill Companies, ISBN 0-07-140235-7
  8. 8.0 8.1 The Oxford Textbook of Medicine Edited by David A. Warrell, Timothy M. Cox and John D. Firth with Edward J. Benz, Fourth Edition (2003), Oxford University Press, ISBN 0-19-262922-0
  9. Tencer J (1988). "Asymptomatic bacteriuria--a long-term study". Scand J Urol Nephrol. 22 (1): 31–4. PMID 3387908.
  10. Bengtsson C, Bengtsson U, Björkelund C, Lincoln K, Sigurdsson JA (1998). "Bacteriuria in a population sample of women: 24-year follow-up study. Results from the prospective population-based study of women in Gothenburg, Sweden". Scand J Urol Nephrol. 32 (4): 284–9. PMID 9764457.
  11. Asscher AW, Sussman M, Waters WE, Evans JA, Campbell H, Evans KT; et al. (1969). "Asymptomatic significant bacteriuria in the non-pregnant woman. II. Response to treatment and follow-up". Br Med J. 1 (5647): 804–6. PMC 1982498. PMID 4886627.
  12. "Screening for asymptomatic bacteriuria, hematuria and proteinuria. The U.S. Preventive Services Task Force". Am Fam Physician. 42 (2): 389–95. 1990. PMID 2200247. Unknown parameter |month= ignored (help)
  13. Stenqvist, K.; Dahlén-Nilsson, I.; Lidin-Janson, G.; Lincoln, K.; Odén, A.; Rignell, S.; Svanborg-Edén, C. (1989). "Bacteriuria in pregnancy. Frequency and risk of acquisition". Am J Epidemiol. 129 (2): 372–9. PMID 2912046. Unknown parameter |month= ignored (help)
  14. Wadland, WC.; Plante, DA. (1989). "Screening for asymptomatic bacteriuria in pregnancy. A decision and cost analysis". J Fam Pract. 29 (4): 372–6. PMID 2794885. Unknown parameter |month= ignored (help)
  15. Smaill F (2001). "Antibiotics for asymptomatic bacteriuria in pregnancy". Cochrane Database Syst Rev (2): CD000490. doi:10.1002/14651858.CD000490. PMID 11405965‎ Check |pmid= value (help).
  16. Mittendorf R, Williams MA, Kass EH (1992). "Prevention of preterm delivery and low birth weight associated with asymptomatic bacteriuria". Clin Infect Dis. 14 (4): 927–32. PMID 1533541.
  17. Romero R, Oyarzun E, Mazor M, Sirtori M, Hobbins JC, Bracken M (1989). "Meta-analysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight". Obstet Gynecol. 73 (4): 576–82. PMID 2927852.
  18. Geerlings, SE.; Stolk, RP.; Camps, MJ.; Netten, PM.; Collet, JT.; Schneeberger, PM.; Hoepelman, AI. (2001). "Consequences of asymptomatic bacteriuria in women with diabetes mellitus". Arch Intern Med. 161 (11): 1421–7. PMID 11386891. Unknown parameter |month= ignored (help)
  19. Semetkowska-Jurkiewicz, E.; Horoszek-Maziarz, S.; Galiński, J.; Manitius, A.; Krupa-Wojciechowska, B. "The clinical course of untreated asymptomatic bacteriuria in diabetic patients--14-year follow-up". Mater Med Pol. 27 (3): 91–5. PMID 8935144.
  20. Harding, GK.; Zhanel, GG.; Nicolle, LE.; Cheang, M. (2002). "Antimicrobial treatment in diabetic women with asymptomatic bacteriuria". N Engl J Med. 347 (20): 1576–83. doi:10.1056/NEJMoa021042. PMID 12432044. Unknown parameter |month= ignored (help)
  21. Boscia, JA.; Kobasa, WD.; Knight, RA.; Abrutyn, E.; Levison, ME.; Kaye, D. (1987). "Therapy vs no therapy for bacteriuria in elderly ambulatory nonhospitalized women". JAMA. 257 (8): 1067–71. PMID 3806896. Unknown parameter |month= ignored (help)
  22. Nordenstam, GR.; Brandberg, CA.; Odén, AS.; Svanborg Edén, CM.; Svanborg, A. (1986). "Bacteriuria and mortality in an elderly population". N Engl J Med. 314 (18): 1152–6. doi:10.1056/NEJM198605013141804. PMID 3960089. Unknown parameter |month= ignored (help)
  23. Heinämäki, P.; Haavisto, M.; Hakulinen, T.; Mattila, K.; Rajala, S. (1986). "Mortality in relation to urinary characteristics in the very aged". Gerontology. 32 (3): 167–71. PMID 3721209.
  24. 24.0 24.1 Nicolle, LE.; Mayhew, WJ.; Bryan, L. (1987). "Prospective randomized comparison of therapy and no therapy for asymptomatic bacteriuria in institutionalized elderly women". Am J Med. 83 (1): 27–33. PMID 3300325. Unknown parameter |month= ignored (help)
  25. Abrutyn, E.; Mossey, J.; Berlin, JA.; Boscia, J.; Levison, M.; Pitsakis, P.; Kaye, D. (1994). "Does asymptomatic bacteriuria predict mortality and does antimicrobial treatment reduce mortality in elderly ambulatory women?". Ann Intern Med. 120 (10): 827–33. PMID 7818631. Unknown parameter |month= ignored (help)
  26. Erickson, RP.; Merritt, JL.; Opitz, JL.; Ilstrup, DM. (1982). "Bacteriuria during follow-up in patients with spinal cord injury: I. Rates of bacteriuria in various bladder-emptying methods". Arch Phys Med Rehabil. 63 (9): 409–12. PMID 7115037. Unknown parameter |month= ignored (help)
  27. Waites, KB.; Canupp, KC.; DeVivo, MJ. (1993). "Eradication of urinary tract infection following spinal cord injury". Paraplegia. 31 (10): 645–52. doi:10.1038/sc.1993.104. PMID 8259327. Unknown parameter |month= ignored (help)
  28. Sobel, JD.; Kauffman, CA.; McKinsey, D.; Zervos, M.; Vazquez, JA.; Karchmer, AW.; Lee, J.; Thomas, C.; Panzer, H. (2000). "Candiduria: a randomized, double-blind study of treatment with fluconazole and placebo. The National Institute of Allergy and Infectious Diseases (NIAID) Mycoses Study Group". Clin Infect Dis. 30 (1): 19–24. doi:10.1086/313580. PMID 10619727. Unknown parameter |month= ignored (help)
  29. Warren, JW.; Anthony, WC.; Hoopes, JM.; Muncie, HL. (1982). "Cephalexin for susceptible bacteriuria in afebrile, long-term catheterized patients". JAMA. 248 (4): 454–8. PMID 7045440. Unknown parameter |month= ignored (help)
  30. Alling, B.; Brandberg, A.; Seeberg, S.; Svanborg, A. (1975). "Effect of consecutive antibacterial therapy on bacteriuria in hospitalized geriatric patients". Scand J Infect Dis. 7 (3): 201–7. PMID 809837.
  31. Harding, GK.; Nicolle, LE.; Ronald, AR.; Preiksaitis, JK.; Forward, KR.; Low, DE.; Cheang, M. (1991). "How long should catheter-acquired urinary tract infection in women be treated? A randomized controlled study". Ann Intern Med. 114 (9): 713–9. PMID 2012351. Unknown parameter |month= ignored (help)
  32. 32.0 32.1 32.2 Grabe, M. (1987). "Antimicrobial agents in transurethral prostatic resection". J Urol. 138 (2): 245–52. PMID 3298693. Unknown parameter |month= ignored (help)
  33. 33.0 33.1 33.2 Cafferkey, MT.; Falkiner, FR.; Gillespie, WA.; Murphy, DM. (1982). "Antibiotics for the prevention of septicaemia in urology". J Antimicrob Chemother. 9 (6): 471–7. PMID 7107549. Unknown parameter |month= ignored (help)
  34. 34.0 34.1 Allan, WR.; Kumar, A. (1985). "Prophylactic mezlocillin for transurethral prostatectomy". Br J Urol. 57 (1): 46–9. PMID 3971104. Unknown parameter |month= ignored (help)
  35. Takai, K.; Tollemar, J.; Wilczek, HE.; Groth, CG. (1998). "Urinary tract infections following renal transplantation". Clin Transplant. 12 (1): 19–23. PMID 9541418. Unknown parameter |month= ignored (help)
  36. Lyerová, L.; Lácha, J.; Skibová, J.; Teplan, V.; Vítko, S.; Schück, O. (2001). "Urinary tract infection in patients with urological complications after renal transplantation with respect to long-term function and allograft survival". Ann Transplant. 6 (2): 19–20. PMID 11803612.
  37. Ghasemian, SM.; Guleria, AS.; Khawand, NY.; Light, JA. (1996). "Diagnosis and management of the urologic complications of renal transplantation". Clin Transplant. 10 (2): 218–23. PMID 8664523. Unknown parameter |month= ignored (help)
  38. Kasiske, BL.; Vazquez, MA.; Harmon, WE.; Brown, RS.; Danovitch, GM.; Gaston, RS.; Roth, D.; Scandling, JD.; Singer, GG. (2000). "Recommendations for the outpatient surveillance of renal transplant recipients. American Society of Transplantation". J Am Soc Nephrol. 11 Suppl 15: S1–86. PMID 11044969. Unknown parameter |month= ignored (help)
  39. "Guidelines for preventing opportunistic infections among hematopoietic stem cell transplant recipients". MMWR Recomm Rep. 49 (RR-10): 1–125, CE1–7. 2000. PMID 11718124. Unknown parameter |month= ignored (help)
  40. Nicolle LE, Bradley S, Colgan R, Rice JC, Schaeffer A, Hooton TM; et al. (2005). "Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults". Clin Infect Dis. 40 (5): 643–54. doi:10.1086/427507. PMID 15714408.
  41. "Veragen package insert" (PDF). Retrieved 2008-08-18.
  42. 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)
  43. 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.
  44. 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.
  45. 45.0 45.1 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.
  46. 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)
  47. Hayne ST, & Mercer JB (1983). "Herpes zoster: treatment with cemetidine". Canadian Medical Association Journal. 129 (12): 1284–1285. PMID 6652595.
  48. 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.
  49. 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.
  50. 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.
  51. 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.
  52. 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.
  53. 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.
  54. 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.
  55. 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.
  56. 56.0 56.1 "Learn About Herpes: Treatment". American Social Health Association. Retrieved 2007-07-09.
  57. 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.
  58. 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.
  59. "Cold Sores". Healthnotes. Retrieved 2007-07-09.
  60. Snipes W, Person S, Keith A, Cupp J (1975). "Butylated hydroxytoluene inactivated lipid-containing viruses". Science. 188 (4183): 64–6. PMID 163494.
  61. 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.
  62. 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.
  63. 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
  64. http://mmrs.fema.gov/news/publichealth/2006/aug/nph2006-08-03a.aspx
  65. Bartlett, John (2012). Johns Hopkins ABX guide : diagnosis and treatment of infectious diseases. Burlington, MA: Jones and Bartlett Learning. ISBN 978-1449625580.
  66. Bartlett, John (2012). Johns Hopkins ABX guide : diagnosis and treatment of infectious diseases. Burlington, MA: Jones and Bartlett Learning. ISBN 978-1449625580.
  67. 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.
  68. McLean DR, Russell N, Khan MY (1992). "Neurobrucellosis: Clinical and therapeutic features". Clin Infect Dis. 15: 582&ndash, 90.
  69. Health Protection Agency. "The gonococcal resistance to antimicrobials surveillance programme: Annual report 2005" (PDF). Retrieved 2006-10-28.
  70. Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
  71. Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed. ed.). Prentice Hall. ISBN 0-13-144329-1.
  72. 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.
  73. Dixon TC, Meselson M, Guillemin J, Hanna PC (1999). "Anthrax". N. Engl. J. Med. 341 (11): 815–26. PMID 10477781.
  74. Barnes JM (1947). "Penicillin and B. anthracis". J Path Bacteriol. 194: 113.

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References


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Antibiotic Treatment

Cutaneous Anthrax without Systemic Involvement

Choice of Antibiotics

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]
  • 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
  • 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]
  • 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

Cutaneous Anthrax, Adult Patients
Preferred Regimen
Ciprofloxacin 500 mg PO q12h
OR
Levofloxacin 750 mg PO q24h
OR
Moxifloxacin 400 mg PO q24h
OR
Doxycycline 100 mg PO q12h
Alternative Regimen
Clindamycin 600 mg PO q8h
OR
Penicillin VK 500 mg PO q6h
OR
Amoxicillin 1 g PO q8h
Cutaneous Anthrax, Pediatric Patients
Preferred Regimen
Ciprofloxacin 30 mg/kg/day PO q12h, max: 500 mg/dose
OR
Levofloxacin 16 mg/kg/day PO q12h, max: 250 mg/dose (<50 kg)
OR
Levofloxacin 500 mg PO q24h (≥50 kg)
OR
Doxycycline 4.4 mg/kg/day PO q12h, max: 100 mg/dose (<45 kg)
OR
Doxycycline 100 mg/dose PO q12h (≥45 kg)
Alternative Regimen
Clindamycin 30 mg/kg/day PO q8h, max: 600 mg/dose
OR
Penicillin VK 50–75 mg/kg/day PO q6–8h
OR
Amoxicillin 75 mg/kg/day PO q8h, max: 1 g/dose
Cutaneous Anthrax, Pregnant Patients
Preferred Regimen
Ciprofloxacin 500 mg PO q12h
Systemic Anthrax with Meningitis, Adult Patients
Preferred Regimen
Ciprofloxacin 400 mg IV q8h
OR
Levofloxacin 750 mg IV q24h
OR
Moxifloxacin 400 mg IV q24h
PLUS
Meropenem 2 g IV q8h
OR
Imipenem 1 g IV q6h
OR
Doripenem 500 mg IV q8h
PLUS
Linezolid 600 mg IV q12h
OR
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h
OR
Chloramphenicol 1 g IV q6–8h
Alternative Regimen
Ciprofloxacin 400 mg IV q8h
OR
Levofloxacin 750 mg IV q24h
OR
Moxifloxacin 400 mg IV q24h
PLUS
Penicillin G 4 MU IV q4h
OR
Ampicillin 3 g IV q6h
PLUS
Linezolid 600 mg IV q12h
OR
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h
OR
Chloramphenicol 1 g IV q6–8h
Systemic Anthrax with Meningitis, Pediatric Patients
Preferred Regimen
Ciprofloxacin 30 mg/kg/day IV q8h, max: 400 mg/dose
OR
Levofloxacin 20 mg/kg/day IV q12h, max: 250 mg/dose (<50 kg)
OR
Levofloxacin 500 mg IV q24h (≥50 kg)
OR
Meropenem 60 mg/kg/day IV q12h, max: 2 g/dose
OR
Imipenem/Cilastatin 100 mg/kg/day IV q6h, max: 1 g/dose
OR
Vancomycin 60 mg/kg/day IV q8h
PLUS
Clindamycin 30 mg/kg/day PO q8h, max: 600 mg/dose
OR
Linezolid 30 mg/kg/day IV q8h, max: 1 g/dose (<12 yr)
OR
Linezolid 30 mg/kg/day IV q12h, max: 600 mg/dose (≥12 yr)
OR
Doxycycline 4.4 mg/kg/day IV q12h, max: 100 mg/dose (<45 kg)
OR
Doxycycline 200 mg IV x1 then 100 mg IV q12h, max: 200 mg/dose (≥45 kg)
OR
Rifampin 20 mg/kg/day IV q12h, max: 300 mg/dose
Alternative Regimen
Penicillin G 0.4 MU/kg/day IV q4h, max: 4 MU/dose
OR
Ampicillin 200 mg/kg/day IV q6h, max: 900 mg/dose
PLUS
Clindamycin 30 mg/kg/day PO q8h, max: 600 mg/dose
OR
Linezolid 30 mg/kg/day IV q8h, max: 1 g/dose (<12 yr)
OR
Linezolid 30 mg/kg/day IV q12h, max: 600 mg/dose (≥12 yr)
OR
Doxycycline 4.4 mg/kg/day IV q12h, max: 100 mg/dose (<45 kg)
OR
Doxycycline 200 mg IV x1 then 100 mg IV q12h, max: 200 mg/dose (≥45 kg)
OR
Rifampin 20 mg/kg/day IV q12h, max: 300 mg/dose
Systemic Anthrax with Meningitis, Pregnant Patients
Preferred Regimen
Ciprofloxacin 400 mg IV q8h
PLUS
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h
Alternative Regimen
Levofloxacin 750 mg IV q24h
OR
Meropenem 2 g IV q8h
OR
Penicillin G 4 MU IV q4h
OR
Ampicillin 3 g IV q6h
PLUS
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h
Systemic Anthrax Without Meningitis, Adult Patients
Preferred Regimen
Ciprofloxacin 400 mg q8h
OR
Levofloxacin 750 mg q24h
OR
Moxifloxacin 400 mg PO q24h
OR
Meropenem 2 g q8h
OR
Imipenem 1 g IV q6h
OR
Doripenem 500 mg q8h
OR
Vancomycin 60 mg/kg/day IV q8h, trough: 15–20 μg/mL
PLUS
Clindamycin 900 mg q8h
OR
Linezolid 600 mg q12h
OR
Doxycycline 200 mg x1 then 100 mg IV q12h
OR
Rifampin 600 mg q12h
Alternative Regimen
Penicillin G 4 MU IV q4h
OR
Ampicillin 3 g IV q6h
PLUS
Clindamycin 900 mg q8h
OR
Linezolid 600 mg q12h
OR
Doxycycline 200 mg x1 then 100 mg IV q12h
OR
Rifampin 600 mg q12h
Systemic Anthrax Without Meningitis, Pediatric Patients
Preferred Regimen
Ciprofloxacin 30 mg/kg/day IV q8h, max: 400 mg/dose
OR
Levofloxacin 16 mg/kg/day IV q12h, max: 250 mg/dose (<50 kg)
OR
Levofloxacin 500 mg IV q24h (≥50 kg)
OR
Moxifloxacin 12 mg/kg/day IV q12h, max: 200 mg/dose (3 mo–2 yr)
OR
Moxifloxacin 10 mg/kg/day IV q12h, max: 200 mg/dose (2 yr–5 yr)
OR
Moxifloxacin 8 mg/kg/day IV q12h, max: 200 mg/dose (6 yr–11 yr)
OR
Moxifloxacin 8 mg/kg/day IV q12h, max: 200 mg/dose (12 yr–17 yr, <45 kg)
OR
Moxifloxacin 400 mg IV q24h (12 yr–17 yr, ≥45 kg)
PLUS
Meropenem 120 mg/kg/day IV q8h, max: 2 g/dose
OR
Imipenem/Cilastatin 100 mg/kg/day IV q6h, max: 1 g/dose
OR
Doripenem 120 mg/kg/day IV q8h, max: 1 g/dose
OR
Vancomycin 60 mg/kg/day IV q8h
PLUS
Linezolid 30 mg/kg/day IV q8h, max: 600 mg/dose (<12 yr)
OR
Linezolid 30 mg/kg/day IV q12h, max: 600 mg/dose (≥12 yr)
OR
Clindamycin 40 mg/kg/day IV q8h, max: 900 mg/dose
OR
Rifampin 20 mg/kg/day IV q12h, max: 300 mg/dose
OR
Chloramphenicol 100 mg/kg/day IV q6h
Alternative Regimen
Ciprofloxacin 30 mg/kg/day IV q8h, max: 400 mg/dose
OR
Levofloxacin 16 mg/kg/day IV q12h, max: 250 mg/dose (<50 kg)
OR
Levofloxacin 500 mg IV q24h (≥50 kg)
OR
Moxifloxacin 12 mg/kg/day IV q12h, max: 200 mg/dose (3 mo–2 yr)
OR
Moxifloxacin 10 mg/kg/day IV q12h, max: 200 mg/dose (2 yr–5 yr)
OR
Moxifloxacin 8 mg/kg/day IV q12h, max: 200 mg/dose (6 yr–11 yr)
OR
Moxifloxacin 8 mg/kg/day IV q12h, max: 200 mg/dose (12 yr–17 yr, <45 kg)
OR
Moxifloxacin 400 mg IV q24h (12 yr–17 yr, ≥45 kg)
PLUS
Penicillin G 0.4 MU/kg/day IV q4h, max: 4 MU/dose
OR
Ampicillin 400 mg/kg/day IV q6h, max: 3 g/dose
PLUS
Linezolid 30 mg/kg/day IV q8h, max: 600 mg/dose (<12 yr)
OR
Linezolid 30 mg/kg/day IV q12h, max: 600 mg/dose (≥12 yr)
OR
Clindamycin 40 mg/kg/day IV q8h, max: 900 mg/dose
OR
Rifampin 20 mg/kg/day IV q12h, max: 300 mg/dose
OR
Chloramphenicol 100 mg/kg/day IV q6h
Systemic Anthrax Without Meningitis, Pregnant Patients
Preferred Regimen
Ciprofloxacin 400 mg IV q8h
PLUS
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h
Alternative Regimen
Levofloxacin 750 mg IV q24h
OR
Meropenem 2 g IV q8h
OR
Penicillin G 4 MU IV q4h
OR
Ampicillin 3 g IV q6h
PLUS
Clindamycin 900 mg IV q8h
OR
Rifampin 600 mg IV q12h


piss

Psittacosis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [15]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [16]

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. 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".
  2. 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 |coauthors= ignored (help); Check date values in: |date= (help)
  3. 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)
  4. 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)


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plam

Malaria Microchapters

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This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Plasmodium.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [17]; Associate Editor(s)-In-Chief: Yazan Daaboul, Serge Korjian, Alison Leibowitz [18]

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.

Comparison of Plasmodium Species Implicated in Human Malaria ("Malaria". Center for Disease Control and Prevention. Center for Disease Control and Prevention (CDC). Nov. 29 2013. Retrieved Jul 24 2014. Check date values in: |accessdate=, |date= (help))
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.
Adapted from Center for Disease Control and Prevention (CDC) - Malaria

References

  1. 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.
  2. 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.
  3. 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.

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q fever microb

Coxiella burnetii
C. burnetii, the causative agent of Q fever
C. burnetii, the causative agent of Q fever
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Legionellales
Family: Coxiellaceae
Genus: Coxiella
Species: C. burnetii
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

  1. Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
  2. 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

Recommended Indications and Doses of Common 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]

Malaria management.png
  1. 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.
  2. 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.
  3. Template:Cite website