TRIPASS XR تري باس

 

Hope VD et al. Prevalence and estimation of hepatitis B and C infections in the WHO European Region: a

review of data focusing on the countries outside the European Union and the European Free Trade Association.

Epidemiol Infect. 2014;142:270–286.

Williams IT et al. Incidence and transmission patterns of acute hepatitis C in the United States, 1982–2006. Arch

Intern Med. 2011;171:242.

Wilkins T et al. Hepatitis C: diagnosis and treatment. Am Fam Physician. 2010;81:1351.

Bartenschlager R et al. Hepatitis C virus replication cycle. J Hepatol. 2010;53:583.

Smith BD et al. Hepatitis C virus antibody prevalence, correlates and predictors among persons born from 1945

through 1965, United States, 1999–2008 [Abstract]. American Association for the Study of Liver Disease,

November 6, 2011. San Francisco, CA 2011.

Rein DB et al. The cost-effectiveness of birth-cohort screening for hepatitis C antibody in U.S. primary care

settings. Ann Intern Med. 2012;156:263–270.

Armstrong GL et al. The prevalence of hepatitis C virus infection in the United States, 1999 through 2002. Ann

Intern Med. 2006;144:705–714.

AASLD/IDSA/IAS-USA. Recommendations for testing, managing, and treating hepatitis C. HCV testing and

linkage to care. Accessed July 15, 2017.

Hepatitis C: Screening. U.S. Preventive Services Task Force. September 2016.

https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/hepatitis-c-screening.

Chung RT. Acute hepatitis C virus infection. Clin Infect Dis. 2005;41 Suppl 1:S14–S17.

Maheshwari A et al. Acute hepatitis C. Lancet. 2008;372:321–332.

Gerlach JT et al. Acute hepatitis C: high rate of both spontaneous and treatment-induced viral clearance.

Gastroenterology. 2003;125:80–88.

Hajarizadeh B et al. Case definitions for acute hepatitis C virus infection: a systematic review. J Hepatol.

2012;57:1349–1360.

Thomas DL et al. The natural history of hepatitis C virus infection: host, viral, and environmental factors.

JAMA. 2000;284:450–456.

Missiha SB et al. Disease progression in chronic hepatitis C: modifiable and nonmodifiable factors.

Gastroenterology. 2008;134;1699–1714.

Poynard T et al. Rates and risk factors of liver fibrosis progression in patients with chronic hepatitis C. J

Hepatol. 2001;34:730–739.

Ryder SD et al. Trent Hepatitis C Study Group. Progression of hepatic fibrosis in patients with hepatitis C: a

prospective repeat liver biopsy study. Gut. 2004;53:451–455.

Thomas DL, Seeff LB. Natural history of hepatitis C. Clin Liver Dis. 2005;9:383–398.

Micallef JM et al. Spontaneous viral clearance following acute hepatitis C infection: a systematic review of

longitudinalstudies. J Viral Hepat. 2006;13:34–41.

Thomas DL et al. Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature.

2009;461:798–801.

Friedman SL. Evolving challenges in hepatic fibrosis. Nat Rev Gastroenterol Hepatol. 2010;425–436.

Hernandez-Gea V, Friedman SL. Pathogenesis of liver fibrosis. Annu Rev Pathol. 2011;6:425–456.

Hui JM et al. Insulin resistance is associated with chronic hepatitis C virus infection and fibrosis progression.

Gastroenterology. 2003;125:1695–1704.

Ishida JH et al. Influence of cannabis use on severity of hepatitis C disease. Clin Gastroenterol Hepatol.

2008;6:69–75.

Jamma S et al. Current concepts of HBV/HCV coinfection: Coexistence, but not necessarily in harmony. Curr

Hepat Rep. 2010;9:260–269.

Hezode C et al. Daily cannabis use: a novel risk factor of steatosis severity in patietns with chronic hepatitis C.

Gastroenterology. 2008;134:432–439.

Chen CM et al. Alcohol and hepatitis C mortality among males and females in the United States: a life table

analysis. Alcohol Clin Exp Res. 2007;31:285–292.

Fartoux L et al. Impact of steatosis on progression of fibrosis in patients with mild hepatitis C. Hepatology.

2005;41:82–87.

.

.

.

.

.

.

.

.

169.

170.

.

.

.

.

.

.

.

.

179.

.

.

.

.

184.

185.

186.

187.

188.

189.

Benvegnu L et al. Natural history of compensated viral cirrhosis: a prospective study on the incidence and

hierarchy of major complications. Gut. 2004;53:744–749.

Centers for Disease Control and Prevention. National Notifiable Diseases Surveillance System (NNDSS).

Hepatitis C, acute: 2012 case definition.

Dustin LB. Too low to measure, infectious nonetheless. Blood. 2012;119:6181–6182.

McGovern BH et al. Improving the diagnosis of acute hepatitis C virus infection with expanded viral load

criteria. Clin Infect Dis. 2009;49:1051–1060.

Glynn SA et al. Dynamics of viremia in early hepatitis C virus infection. Transfusion. 2005;45:994–1002.

Mondelli MU et al. Acute hepatitis C: diagnosis and management. J Hepatol. 2005;42(Suppl 1):S108–S114.

Ghany MG et al. American Association for the Study of Liver Diseases. An update on treatment of genotype 1

chronic hepatitis C virus infection: 2011 practice guideline by the American Associaton for the Study of Liver

Diseases. Hepatology. 2011;54:1433–1444.

Boursier J et al. Comparison of eight diagnostic algorithms for liver fibrosis in hepatitis C: new algorithms are

more precise and entirely noninvasive. Hepatology. 2012;55:58–67.

Castera L. Noninvasive methods to assess liver disease in patients with hepatitis B or C. Gastroenterology.

2012;142:1293–1302.e4.

Duarte-Rojo A et al. Noninvasive markers of fibrosis: key concepts for improving accuracy in daily clinical

practice. Ann Hepatol. 2012;11:426–439.

Holmberg SD et al. Non-invasive serum fibrosis markers for screening and staging chronic hepatitis C virus

(HCV) patients in a large U.S. cohort. Clin Infect Dis. 2013;57:240–246.

Vallet-Pichard A et al. FIB-4: an inexpensive and accurate marker of fibrosis in HCV infection. Comparison

with liver biopsy and fibrotest. Hepatology. 2007;46:32–36.

Koda M et al. FibroIndex, a practical index for predicting significant fibrosis in patients with chronic hepatitis C.

Hepatology. 2007;45:297–306.

Forns X et al. Identification of chronic hepatitis C patietns without hepatic fibrosis by a simple predictive model.

Hepatology. 2002;36:986–992.

Becker L et al. Validation of hepascore, compared with simple indices of fibrosis, in patients with chronic

hepatitis C virus infection in United States. Clin Gastroenterol Hepatol. 2009;7:696–701.

Patel K et al. An independent and prospective comparison of two commercial fibrosis marker panels (HCV

FibroSURE and FIBROSpect II) during interferon alfa-2b combination therapy for chronic hepatitis C. J Viral

Hepat. 2009;16:178–186.

Zaman A et al. Assessment of FIBROSpect II to detect hepatic fibrosis in chronic hepatitis C patients. Am J

Med. 2007;120:280.e9–e14.

Rockey DC et al. American Association for the Study of Liver Diseases. Liver biopsy. Hepatology.

2009;49:1017–1044.

Lefkowitch JH. Liver biopsy assessment in chronic hepatitis. Arch Med Res. 2007;38:634–643.

Theise ND. Liver biopsy assessment in chronic viral hepatitis: a personal, practical approach. Mod Pathol.

2007;20(Suppl 1):S3–S14.

Moghaddam SM et al. Hepatitis C and renal transplantation: a review on historical aspects and current issues.

Rev Med Virol. 2008;18:375.

Gane E, Pilmore H. Management of chronic viral hepatitis before and after renal transplantation.

Transplantation. 2002;74:427.

Dal Maso L, Franceschi S. Hepatitis C virus and risk of lymphoma and other lymphoid neoplasms: a metaanalysis of epidemiologic studies. Cancer Epidemiol Biomarkers Prev. 2006;15:2078–2085.

Dalrymple LS et al. Hepatitis C virus infection and the prevalence of renal insufficiency. Clin J Am Soc

Nephrol. 2007;2:715–721.

Gisbert JP et al. Prevalence of hepatitis C virus infection in porphyria cutanea tarda: systematic review and

meta-analysis. J Hepatol. 2003;39:620–627.

Hanouneh IA et al. Clinical significance of metabolic syndrome in the setting of chronic hepatitis C virus

infection. Clin Gastroenterol Hepatol. 2008;6584–6589.

Hartridge-Lambert SK et al. Hepatitis C and non-Hodgkin lymphoma: the clinical perspective. Hepatology.

2012;55:634–641.

Iannuzella F et al. Management of hepatitis C virus-related mixed cryoglobulinemia. Am J Med. 2010;123:400–

408.

Kamar N et al. Treatment of hepatitis C virus-related glomerulonephritis. Kidney Int. 2006;69:436–439.

.

.

.

193.

.

.

.

.

.

.

.

.

.

203.

.

.

.

.

.

.

.

.

.

.

.

.

.

Zignego AL et al. Italian Association of the Study of Liver Commission on Extrahepatic Manifestations of HCV

infection. Extrahepatic manifestations of hepatitis C virus infection: a general overview and guidelines for a

clinical approach. Dig Liver Dis. 2007;39:2–17.

Burgess SV et al. Concordance of sustained virologic response at weeks 4, 12 and 24 post-treatment of hepatitis

C in the era of new oral direct-acting antivirals: a concise review. Ann Hepatol. 2016;15:154–159.

George SL et al. Clinical, virologic, histologic, and biochemical outcomes after successful HCV therapy: a 5-year

follow-up of 150 patients. Hepatology. 2009;49:729–738.

Maylin S et al. Eradication of hepatitis C virus in patients successfully treated for chronic hepatitis C.

Gastroenterology. 2008;135:821–829.

Morisco F et al. Sustained virological response: a milestone in the treatment of chronic hepatitis C. World J

Gastroenterol. 2013;19:2793–2798.

Pockros PJ et al. Histologic outcomes in hepatitis C-infected patients with varying degrees of virologic response

to interferon-based treatments. Hepatology. 2010;52:1193–1200.

Toccaceli F et al. Long-term liver histology improvement in patients with chronic hepatitis C and sustained

response to interferon. J Viral Hepat. 2003;10:126–133.

Veldt BJ et al. Sustained virologic response and clinical outcomes in patients with chronic hepatitis C and

advanced fibrosis. Ann Intern Med. 2007;147:677–684.

Simmons B et al. Long-term treatment outcomes of patients infected with hepatitis C virus: a systematic review

and meta-analysis of the survival benefit of achieving a sustained virological response. Clin Infect Dis.

2015;61:730–740.

Arase Y et al. Sustained virological response reduces incidence of onset of type 2 diabetes in chronic hepatitis

C. Hepatology. 2009;49:739–744.

Conjeevaram HS et al. Changes in insulin sensitivity and body weight during and after peginterferon and ribavirin

therapy for hepatitis C. Gastroenterology. 2010;140:469–477.

Butt AA et al. Effect of hepatitis C virus and its treatment on survival. Hepatology. 2009;50:387–392.

Fried MW et al. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection. N Engl J Med.

2002;347:975–982.

Hadziyannis SJ et al. Peginterferon alfa-2a and ribavirin combination therapy in chronic hepatitis C: a

randomized study of treatment duration and ribavirin dose. Ann Intern Med. 2004;140:346–355.

Manns MP et al. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial

treatment of chronic hepatitis C: a randomised trial. Lancet. 2001;358:958–965.

Zeuzem S et al. Optimized threashold for serum HCV RNA to predict treatment outcomes in hepatitis C patients

receiving peginterferon alfa-2a/ribavirin. J Viral Hepat. 2012;19:766–774.

Kowdley KV et al. Ledipasvir and sofosbuvir for 8 or 12 weeks for chronic HCV without cirrhosis. N Engl J

Med. 2014;370:1879–1888.

Ge D et al. Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance. Nature.

2009;462:399–401.

Charlton M et al. Ledipasvir and sofosbuvir plus ribavirin for treatment of HCV infection in patients with

advanced liver disease. Gastroenterology. 2015;149:649–659.

Poordad F, Dieterich D. Treating hepatitis C: current standard of care and emerging direct-acting antiviral

agents. J Viral Hepat. 2012;19:449–464.

American Association for the Study of Liver Diseases and the Infectious Diseases Society of America.

Recommendations for testing, management, and treating hepatitis C. When and in whom to initiate HCV

therapy. AASLD/IDSA; 2016

Feld JJ et al. Ribavirin revisited in the era of direct-acting antiviral therapy for hepatitis C virus infection. Liver

Int. 2017;37:5–18.

Roberts SS et al. The ribavirin pregnancy registry: Findings after 5 years of enrollment, 2003–2009. Birth

Defects Res A Clin Mol Teratol. 2010;88:551–559.

Pockros PJ. New direct-acting antivirals in the development for hepatitis C virus infection. Therap Adv

Gastroenterol. 2010;3:191–202.

Hunt D, Pockros P. What are the promising new therapies in the field of chronic hepatitis C after the firstgeneration direct-acting antivirals? Curr Gastroenterol Rep. 2013;15:303–313.

Olysio (simeprevir). US FDA approved [product information]. Titusville, NJ: Janssen Therapeutics, Division of

Janssen Products, LP,; November 2013.

Lenz O et al. Resistance analyses of HCV isolates from patients treated with simeprevir in phase 2b/3 studies.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

Presented at the 64th annual meeting of the American Association for the Study of Liver Diseases,

Washington, DC, November 1–5, 2013. Abstract #1101.

Jacobson IM et al. Simeprevir (TMC435) with peginterferon/ribavirin for chronic HCV genotype 1 infection in

treatment-naïve patients: results from QUEST-1, a phase III trial. Presented at the 48th annual meeting of the

European Association for the Study of the Liver, Amsterdam, The Netherlands, April 24–28, 2013. Abstract

1425.

Manns M et al. Simeprevir (TMC435) with peginterferon/ribavirin for treatment of chronic HCV genotype 1

infection in treatment-naïve patients: results from QUEST-2, a phase III trial. Presented at the 48th annual

meeting of the European Association for the Study of the Liver, Amsterdam, The Netherlands, April 24–28,

2013. Abstract 1413.

Williams JA et al. Comparative metabolic capabilities of CYP3A4, CYP3A5, and CYP3A7. Drug Metab

Dispos. 2002;30:883–891.

Lawitz E et al. Simeprevir plus sofosbuvir, with or without ribavirin, to treat chronic infection with hepatitis C

virus genotype 1 in non-responders to pegylated interferon and ribavirin and treatment-naïve patients: the

COSMOS randomized study. Lancet. 2014;384:1756–1765.

Evans MJ et al. Phosphorylation of hepatitis C virus nonstructural protein 5A modulates its protein interactions

and viral RNA replication. Proc Natl Acad Sci USA. 2004;101:13038–13043.

Tellinghuisen TL et al. Regulation of hepatitis C virion production via phosphorylation of the NS5A protein. PLoS

Pathol. 2008;4:e1000032.

Gao M et al. Chemical genetics strategy identifies an HCV NS5A inhibitor with a potent clinical effect. Nature.

2010;465:96–100.

Sulkowski MS et al. Daclatasvir plus sofosbuvir for previously treated or untreated chronic HCV infection. N

EnglJ Med. 2014;370:211–221.

Nelson DR et al. All-oral 12-week treatment with daclatasvir plus sofosbuvir in patients with hepatitis C virus

genotype 3 infection: ALLY-3 phase III study. Hepatology. 2015;61:1127–1135.

Sovaldi (sofosbuvir). US FDA approved product information; Foster City, CA: Gilead Sciences; December 2013.

Lawitz E et al. Sofosbuvir for previously untreated chronic hepatitis C infection. N EnglJ Med. 2013;368:1878–

1887.

Lawitz E et al. Sofosbuvir in combination with peginterferon alfa-2a and ribavirin for non-cirrhotic, treatmentnaïve patients with genotypes 1, 2, and 3 hepatitis C infection: a randomised, double-blind, phase 2 trial. Lancet

Infect Dis. 2013;13:401–408.

FDA Hepatitis Update—Important safety information: Harvoni and Sovaldi. March 21, 2015.

http://content.govdelivery.com/accounts/USFDA/bulletins/f97c71. Accessed on July 16, 2017.

Renet S et al. Extreme bradycardia after first doses of sofosbuvir and daclatasvir in patients receiving

amiodarone: 2 cases including a rechallenge. Gastroenterology. 2015;149:1378–1380.

Au JS, Pockros PJ. Novel therapeutic approaches for hepatitis C. Clin Pharmacol Ther. 2014;95:78–88.

Zepatier (elbasvir and grazoprevir). US FDA approved product information; Whitehouse Station, NJ: Merck and

Co, Inc; January 2016.

Zeuzem S et al. Grazoprevir-elbasvir combination therapy for treatment-naïve cirrhotic and noncirrhotic patients

with chronic hepatitis C virus genotype 1, 4, or 6 infection: a randomized trial. Ann Intern Med. 2015;163:1–13.

Lawitz E et al. Efficacy and safety of 12 weeks versus 18 weeks of treatment with grazoprevir (MK–5172) and

elbasvir (MK-8742) with or without ribavirin for hepatitis C virus genotype 1 infection in previously untreated

patients with cirrhosis and patients with previous null response with or without cirrhosis (C-WORTHY): a

randomized, open-label phase 2 trial. Lancet. 2015;185:1075–1086.

Wyles D et al. Post-treatment resistance analysis of hepatitis C virus from phase II and III clinical trials of

ledispasvir/sofosbuvir. J Hepatol. 2017;66:703–710.

Jacobson IM et al. The tolerability of sofosbuvir/velpatasvir for 12 Weeks in > 1000 patients treated in the

ASTRAL-1, ASTRAL-2, and ASTRAL-3 studies: An integrated safety analysis. Presented at the 51

st Annual

Meeting of the European Association for the Study of the Liver (EASL), Barcelona, Spain, April 13–17, 2016.

Viekira Pak Product Information: oral extended-release tablets, dasabuvir, ombitasvir, paritaprevir, ritonavir oral

extended-release tablets. AbbVie Inc (per FDA), North Chicago, IL, 2016.

FDA Drug Safety Communication: FDA warns of serious liver injury risk with hepatitis C treatments Viekira

Pak and Technivie. October 22, 2015. http://www.fda.gov/Drugs/DrugSafety/ucm468634.htm. Accessed on

July 16, 2017.

Feld JJ et al. Treatment of HCV with ABT-450/r-ombitasvir and dasabuvir with ribavirin. N Engl J Med.

.

241.

.

.

.

245.

.

.

.

.

.

.

252.

.

.

.

.

.

.

.

.

.

.

.

2014;370:1594–1603.

Zeuzem S et al. Retreatment of HCV with ABT-450/r-ombitasvir and dasabuvir with ribavirin. N Engl J Med.

2014;370:1604–1614.

Ferenci P et al. ABT-450/r-ombitasvir and dasabuvir with or without ribavirin for HCV. N Engl J Med.

2014;370:1983–1992.

Andreone P et al. ABT-450, ritonavir, ombitasvir, and dasabuvir achieves 97% and 100% sustained virologic

response with or without ribavirin in treatment-experienced patients with HCV genotype 1b infection.

Gastroenterology. 2014;147:359–365.

Schaefer EA, Chung RT. Anti-hepatitis C virus drugs in development. Gasteroenterology. 2012;142:1340.

Taylor JM. Hepatitis delta virus. Virology. 2006;344:71.

Rizzetto M. Hepatitis D: thirty years after. J Heptol. 2009;50:1043.

Pascarella S, Negro F. Hepatitis D virus: an update. Liver Int. 2011;31:7.

Rizzetto M. Hepatitis D: clinical features and therapy. Dig Dis. 2010;28:139.

GrabowskiJ, Wedemeyer H. Hepatitis delta: immunopathogenesis and clinical challenges. Dig Dis. 2010;28:133.

Yurdaydin C et al. Natural history and treatment of chronic delta hepatitis. J Viral Hepat. 2010;17:749.

Farci P et al. Treatment of chronic hepatitis D. J Viral Hepat. 2007;14(Suppl 1):58.

Castelnau C et al. Efficacy of peginterferon alpha-2b in chronic hepatitis delta: relevance of quantitative RTPCR for follow-up. Hepatology. 2006;44:728.

Niro GA et al. Pegylated interferon alpha-2b as monotherapy or in combination with ribavirin in chronic hepatitis

delta. Hepatology. 2006;44:713.

Wedemeyer H et al. Peginteferon plus adefovir versus either drug alone for hepatitis delta. N Engl J Med.

2011;264:322.

Mansour W et al. Resolution of chronic hepatitis delta after 1 year of combined therapy with pegylated

interferon, tenofovir and emtricitabin. J Clin Virol 2010;47:97.

Aggarwal R. Hepatitis E: historical, contemporary and future perspectives. J Gastroenterol Hepatol.

2011;26(Suppl 1):72.

Aggarwal R, Naik S. Epidemiology of hepatitis E: current status. J Gastroenterol Hepatol. 2009;24:1484.

Khuroo MS. Hepatitis E virus. Curr Opin Infect Dis. 2008;21:539.

Bihl F, Negro F. Hepatitis E virus: a zoonosis adapting to humans. J Antimicrob Chemother. 2010;65:817.

Mushahwar IK. Hepatitis E virus: molecular virology, clinical features, diagnosis, transmission, epidemiology, and

prevention. J Med Virol. 2008;80:646.

Teshale EH et al. The two faces of hepatitis E virus. Clin Infect Dis. 2010;51:328.

Mahtab MA et al. Hepatitis E virus is a leading cause of acute and chronic liver disease: experience from a

tertiary centre in Bangladesh. Hepatobiliary Pancreat Dis Ing. 2009;8:50.

Mahtab MA et al. HEV infection as an etiologic factor for acute hepatitis: experience from a tertiary hospital in

Bangladesh. J Health Popul Nutr. 2009;27:14.

Navaneethan U et al. Hepatitis E and pregnancy: understanding the pathogenesis. Liver Int. 2008;28:1190.

p. 1692

MALARIA

Malaria in humans is caused by protozoan parasites of the genus

Plasmodium: Plasmodium falciparum, P. vivax, P. ovale, or P. malariae.

Early symptoms of malaria are nonspecific with fever present in the

majority of patients, and approximately two-thirds of infected persons

may experience symptoms such as headache, muscle aches and pains,

and malaise.

Case 81-1 (Question 1)

Travelers with symptoms of malaria should seek medical evaluation as

soon as possible. Falciparum malaria is the most severe form of malaria

and has the highest mortality. Mortality is higher in those with no

immunity such as travelers from non-endemic areas, while adults living

permanently in the country and exposed to malaria do develop semiimmunity. Suspected or confirmed malaria, especially P. falciparum, is a

medical emergency necessitating early intervention. In instances when

the traveler develops a febrile illness consistent with malaria and access

to medical care is not readily available, a reliable supply of malaria

treatment can be self-administered presumptively as a temporary

measure.

Case 81-1 (Questions 1, 2, 3,

5)

Travelers to malaria-endemic areas need to understand the risk of

malaria and know how to best prevent it with mosquito-avoidance

measures and chemoprophylaxis (where appropriate). Pregnant women

are at greater risk for malaria and its associated complications. Women

who are pregnant or likely to become pregnant should be advised to

avoid travel to endemic areas if possible. If travel cannot be deferred,

use of an effective chemoprophylaxis regimen is essential.

Case 81-1 (Question 4),

Case 81-2 (Questions 1–3),

Case 81-3 (Question 1),

Tables 81-1 and 81-2

Several factors must be considered when selecting a chemoprophylactic

drug regimen, including drug resistance, patient-specific factors, adverse

effects, precautions, and contraindications.

Case 81-1 (Question 4),

Case 81-2 (Questions 1–3),

Case 81-3 (Question 1),

Tables 81-1 and 81-2

AMEBIASIS

Amebiasis is caused by Entamoeba histolytica and implicated in amebic

dysentery and hepatic abscesses. Diagnosis of amebic dysentery may

Case 81-4 (Questions 1, 2),

Case 81-5 (Questions 1, 2),

include the following information: history of travel, stool and biopsy

specimens, and ultrasound to exclude liver abscesses. Treatment for

amebiasis calls for a combination of agents with both luminal-acting and

extraintestinal effects. Amebic cyst passers and pregnant women must

be treated to avoid invasive disease and transmission of the infection.

Case 81-6 (Question 1),

Case 81-7 (Question 1),

Table 81-3

GIARDIASIS

The signs and symptoms of giardiasis could be insidious and vague, but

patients usually present with diarrhea and bulky, foul-smelling stools

along with laboratory confirmation of Giardia lamblia.

Case 81-8 (Question 1)

The major treatments for giardiasis are metronidazole and tinidazole or

nitazoxanide.

Case 81-8 (Question 2),

Table 81-3

p. 1693

p. 1694

ENTEROBIASIS

The signs and symptoms of the infection may be subtle, but the specific

diagnostic test for Enterobius vermicularis is the cellophane tape swab.

Therapy for enterobiasis includes the antihelminthic agents: albendazole,

pyrantel pamoate, or mebendazole (not available in the United States).

Household measures to eradicate the infection need to be addressed.

Case 81-9 (Questions 1, 2),

Table 81-3

CESTODIASIS

Primarily this includes Taenia saginata and Taenia solium, and symptoms

of infections are nonspecific. It is critical to differentiate these two

infections from other cestode infections. Praziquantel remains an

effective agent for allspecies of Cestodes. Cysticercosis, a

complication caused by the larval cysts of T. solium that may be

associated with central nervous system infection (neurocysticercosis), is

serious and requires separate diagnostic testing and controversial

therapy. Praziquantel, which is indicated for most cestodiasis, is well

tolerated.

Case 81-10 (Questions 1, 2),

Table 81-3

PEDICULOSIS

Head and body lice are associated with dermatologic reactions, which

can be treated with a number of agents: permethrin, pyrethrin,

malathion, and ivermectin. Special attention needs to be focused on

correct application procedures, drug resistance, and lice

decontamination measures.

Case 81-11 (Questions 1, 2),

Table 81-3 and 81-4

SCABIES

Scabies produces pruritic rash and excoriations of the interdigital area of

the upper and lower limbs. Treatment includes lindane, permethrin, and

crotamiton. Clothes and personal items of the infected person and

family members need to laundered (>50°C) to avoid reinfection.

Case 81-12 (Question 1),

Table 81-3

MALARIA

Epidemiology

According to World Health Organization (WHO) estimates, malaria was responsible

for an estimated 214 million cases of malaria in 2015 with an estimated 438,000

deaths, which reflects an overall 60% reduction in malaria mortality rates since

2000.

1 The global malaria burden continues to be disproportionately high with

approximately 89% of malaria cases and 91% of deaths in sub-Saharan Africa.

1

Within regions of high malaria transmission, children less than 5 years of age are

particularly susceptible with more than two-thirds (70%) of all malaria deaths

occurring in this age group.

1 Globally in children under the age of 5 years, the

malaria death rate fell by 65% between 2000 and 2015. While malaria is no longer

an endemic infectious disease in the industrialized countries of North America,

Europe, Australia, New Zealand, and Japan, travel to malaria-endemic regions, as

well as immigration and refugee migrations into non-endemic areas, have resulted in

increases in the numbers of imported cases of malaria in industrialized countries.

2,3

Millions of US travelers visit malaria-endemic areas each year and approximately

1,500 cases of malaria are diagnosed in the United States annually, mostly in returned

travelers.

4

Distribution of Malaria Species

Malaria in humans is caused by protozoan parasites of the genus Plasmodium:

Plasmodium falciparum, P. vivax, P. ovale, or P. malariae.

5 The distribution of the

four Plasmodium species of malaria varies worldwide. However, the vast majority

of imported cases are caused by P. falciparum or P. vivax

2

; the proportion of

imported cases caused by P. falciparum or P. vivax within a country reflects both the

destinations that travelers select and, to a larger degree, the nature of immigrant

communities.

2

In most countries, only 5% or less of malaria cases are caused by P.

ovale and P. malariae.

2

In addition, P. knowlesi, a species normally found in

monkeys, has been documented as a cause of human infections and some deaths in

forest fringe areas of Southeast Asia.

5

Life Cycle of the Malaria Parasite and Transmission

The life cycle of the malaria parasites in the human host is complex. All species are

transmitted by the bite of an infective female Anopheles mosquito that carries

malaria-causing parasites and injects the asexual forms or sporozoites into the human

bloodstream. Over a period of 5 to 16 days (depending on the species), the

sporozoites grow, divide, and produce daughter cells, or merozoites, per liver cell.

Infections caused by P. vivax and P. ovale may remain in a dormant stage for

extended periods of time within the liver (hypnozoites) and cause relapses by

invading the bloodstream for months or years later. The merozoites exit the liver

cells and reenter the bloodstream and begin a cycle of invading red blood cells and

asexual replication, thus producing and releasing newly formed merozoites from the

red blood cells. Through this process symptoms can develop 1 week after being

bitten by an infected mosquito, though in falciparum malaria this can occur up to 3

months or occasionally longer. The characteristic malarial paroxysms of chills and

fever usually coincide with the periodic release of merozoites and other pyrogens in

the blood. In P. falciparum infections, this periodicity may not always be apparent. A

subpopulation of merozoites differentiate into sexual forms of the parasite, resulting

in male and female gametocytes that circulate in the bloodstream (Fig. 81-1). If the

gametocytes in the host blood are ingested by a female Anopheles mosquito during a

blood meal, fertilization and an asexual division in the mosquito midgut occurs

where they develop into oocysts. Each oocyst grows and divides, producing

thousands of active haploid forms, called sporozoites; once mature the oocyte bursts,

releasing sporozoites, making their way to the mosquitos’s salivary glands.

Inoculation of the sporozoites into a new human host perpetuates the malaria life

cycle.

p. 1694

p. 1695

Figure 81-1 Plasmodium falciparum gametocytes.

While the majority of cases of malaria are transmitted by the bite of an infective

femal e Anopheles mosquito, occasional transmission has occurred by blood

transfusion, needle sharing, organ transplantation, or congenitally from mother to

fetus.

2