Hematologic Complications,Healthcare Utilization,and Costs in Commercially Insured Patients with Myelodysplastic Syndrome Receiving Supportive Care

Background

Myelodysplastic syndrome (MDS) is rare in people aged <50 years. Most patients with this disorder experience progressive worsening of blood cytopenias, with an increasing need for transfusion. The more advanced and severe the disorder, the greater the risk that it will progress to acute myeloid leukemia. Therapy is typically based on the patient''s risk category, age, and performance status. Supportive care alone is a major option for lower-risk, older patients with MDS or those with comorbidities. The only potentially curative treatment option is hematopoietic stem-cell transplantation, which is typically used to treat high-risk, younger patients.

Objective

To describe and compare the hematologic complications, healthcare utilization, and costs of supportive care in patients with MDS aged <50 years and in older patients aged ≥50 years.

Methods

Using the i3/Ingenix LabRx claims database, this retrospective study included patients who were continuously enrolled (ie, 6 months preindex through 1 year postindex) in the study and who had an initial claim of MDS (index date) between February 1, 2007, and July 31, 2008. Patients treated with hypomethylating agents or thalidomide analogues were excluded. Claims included information on office visits, medical procedures, hospitalizations, drug use, and tests performed. The hematologic complications, costs, and utilization analyses were stratified by age into 2 age-groups—patients aged <50 years and those aged ≥50 years. The MDS-related diagnoses, utilization, and costs were analyzed postindex. The data used in this study spanned the period from August 1, 2006, to July 31, 2009.

Results

We identified 1133 newly diagnosed patients with MDS who received supportive care only during the study period; of these, 19.5% were younger than age 50 years. These younger patients included more females (62.0% vs 52.5%; P = .011) and had fewer comorbidities (mean Charlson comorbidy index, 1.2 vs 2.4; P <.001) and physician office visits than those aged ≥50 years. Postindex, compared with the older patients, the younger patients had less use of erythropoietin therapy and fewer transfusions, anemia diagnoses, and potential complications of neutropenia and pneumonia diagnoses; however, more diagnoses of neutropenia and of decreased white blood cell counts were seen in the younger patients than in the older patients (P ≤.034 for all comparisons). Furthermore, younger patients had fewer mean office visits in the postindex period than older patients (17.5 vs 24.2, respectively; P <.001) and fewer hospitalizations (32.1% vs 44.6%, respectively; P = .004), but they had a longer (although not statistically significant) mean length of hospital stay (21 vs 14 days, respectively; P = .131). Mean total healthcare charges were $96,277 (median, $21,287) in younger patients compared with $84,102 (median, $39,402) in older patients, although this difference, too, was not significant.

Conclusions

MDS is associated with frequent and prolonged hospitalizations, frequent outpatient visits, and high costs in younger and in older patients who are receiving supportive care. Although this study shows that younger patients aged <50 years do not have significantly higher costs overall, a small proportion may have a higher healthcare utilization and cost-related burden of MDS than patients aged ≥50 years.Myelodysplastic syndrome (MDS) encompasses a heterogeneous group of clonal disorders of hematopoiesis and is characterized by dysplastic morphology of marrow and blood cells, ineffective hematopoiesis, and peripheral blood cytopenias.1,2 Most patients with MDS experience progressive worsening of blood cytopenias, with an increasing need for transfusion.2 These patients also have an increasing number of potentially fatal infections and hemorrhagic complications.2 The more advanced and severe the MDS is, the greater the risk that the disease will progress to acute myeloid leukemia (AML).3 The disease may be classified into 1 of 5 subtypes—refractory anemia, refractory anemia with ringed sideroblasts (RARS), refractory anemia with excess of blasts (RAEB), RAEB in transformation (RAEB-T), or chronic myelomonocytic leukemia.3 Approximately 5% to 15% of the relatively lower-risk patients with refractory anemia/RARS transform to AML; by contrast, 40% to 50% of the high-risk patients with RAEB/RAEB-T transform to AML.3The therapeutic options that are tailored for specific MDS subgroups are typically based on factors such as the patient''s risk category, age, and performance status.3,4 The National Comprehensive Cancer Network (NCCN) Clinical Practice Guidelines in Oncology recommend that all patients with MDS receive supportive care,3 which includes blood transfusions, erythropoietin with or without granulocyte colony-stimulating factor, iron chelation therapy, and prophylactic antibiotics.4,5 Other therapies indicated for the treatment of patients with MDS include the thalidomide analogue lenalidomide and the hypomethylating agents decitabine and 5-azacytidine.3,4 The only potentially curative treatment option is hematopoietic stem-cell transplantation, which is typically used to treat younger, high-risk patients.3,4 Supportive care alone remains a leading option for the treatment of lower-risk, older patients with MDS or those with comorbidities.3,4Data on the distribution of MDS in the general population are inconsistent, possibly because of misdiagnoses and/or underreporting of the disease.6,7 The most recent estimates of the annual incidence of MDS in the United States range from 3.3 to 5.0 per 100,000 persons.3,7,8 Some studies indicate that the median age of patients with MDS is approximately 65 years, whereas others note that more than 70% of cases occur in patients aged ≥70 years in the United States.3,6,9 The incidence of MDS in individuals aged ≥70 years is between 22 and 45 per 100,000 persons and increases with age.3,6,9–11Less than 10% of patients with MDS are aged <50 years; therefore, little is known about this disease in this younger age-group, particularly among patients who receive supportive care only.6,11,12 Some data suggest that younger patients with MDS have less aggressive disease.12,13 We compared hematologic complications, healthcare utilization, and costs in patients aged <50 years and in those aged ≥50 years who were newly diagnosed with MDS and received supportive care only.

KEY POINTS

• ▸ The more advanced and severe the myelodysplastic syndrome (MDS) is, the greater the risk of progression to acute myeloid leukemia. Therapy is currently based on risk category, age, and performance status.
• ▸ In the United States, the majority of newly diagnosed patients with MDS receive only supportive care, although for younger patients at high-risk, hematopoietic stem-cell transplantation is potentially the only curative option.
• ▸ This analysis compares the hematologic complications, healthcare utilization, and cost of care between patients with MDS aged <50 years and those aged ≥50 years who receive supportive care only.
• ▸ Although the younger patients had fewer office visits, they had longer mean length of hospital stay than the older group (21 vs 14 days, respectively).
• ▸ Mean total healthcare charges were $96,277 in younger patients compared with $84,102 in older patients.
• ▸ Based on this study, approximately 20% of patients with MDS are under age 50 years.
• ▸ The results of this study suggest that a small proportion of younger patients with MDS who receive supportive care only may have a higher healthcare utilization and cost-related burden of MDS than older patients with this condition.

     

Fixed-Dose Combination Gel of Adapalene and Benzoyl Peroxide plus Doxycycline 100 mg versus Oral Isotretinoin for the Treatment of Severe Acne: Efficacy and Cost Analysis

Background

Acne vulgaris is a chronic skin disease with a high prevalence. Left untreated or inadequately treated, acne vulgaris can lead to psychological and physical scarring, as well as to unnecessary medical expenses. Oral isotretinoin is an effective treatment for severe resistant nodular and conglobate acne vulgaris. A regimen consisting of a fixed-dose combination of adapalene and benzoyl peroxide gel, 0.1%/2.5% (A-BPO) with oral doxycycline 100 mg (A-BPO/D) has been demonstrated to be efficacious and well tolerated in patients with severe acne and may be an alternative to oral isotretinoin for some patients with severe acne.

Objective

The objective of this analysis was to compare the relative efficacy and associated costs of A-BPO/D versus oral isotretinoin.

Methods

In this analysis, comparisons of relative efficacy were made using previously published studies involving similar patient populations with severe acne that warrant the use of oral isotretinoin. The pricing for oral doxycycline and oral isotretinoin was estimated based on the maximum allowable cost from 9 states, and the pricing for A-BPO was calculated as the range between the average wholesale price and the wholesale acquisition cost. For this analysis, 2 treatment models were generated to compare costs: (1) a basic treatment model that examined the costs of an initial regimen of either A-BPO/D or oral isotretinoin without considering probable outcomes, and (2) a long-term model that factored in likely treatment outcomes and subsequent treatments into associated costs. The basic treatment model assumed that patients would be prescribed a single regimen of A-BPO/D for 12 weeks or oral isotretinoin for 20 weeks. The long-term model considered the probability of each treatment successfully managing patients'' acne, as well as likely additional regimens of A-BPO monotherapy or an additional regimen of oral isotretinoin. As a result of different treatment durations, the costs for each treatment were normalized to weekly cost of treatment.

Results

Based on evidence from the published literature, patients treated with A-BPO/D would be expected to have an initial 72% reduction in inflammatory lesions, and patients treated with oral isotretinoin would have an 80% to 90% reduction of these lesions. The median weekly cost for the basic treatment model was $44 for A-BPO/D and $62 for oral isotretinoin. The weekly median costs for the long-term model were $44 for patients initially receiving a regimen of A-BPO/D followed by a maintenance regimen of A-BPO monotherapy and $50 for patients receiving an initial regimen of A-BPO/D who required a subsequent regimen of oral isotretinoin. The weekly cost for oral isotretinoin in the long-term model was $62.

Conclusions

The comparison of these 2 treatments demonstrated that they are both effective in treating severe acne, and that A-BPO/D was less expensive weekly than oral isotretinoin. These models show that A-BPO/D is safer than and is a more cost-effective alternative to oral isotretinoin for treating patients with severe acne vulgaris.Acne vulgaris is a chronic skin disease predominantly affecting the face, trunk, and back.1 The prevalence of acne vulgaris is high in many countries: acne afflicts up to 87% of adolescents and up to 54% of adults.2,3 Skin diseases, including acne, are often dismissed as being trivial or not as important as diseases of other organ systems.4 However, acne can negatively affect the patient''s quality of life (QOL).4 Responses to the 36-Item Short Form Survey, a generic QOL questionnaire, demonstrate that patients with acne report social, psychological, and emotional problems at levels as great as patients with epilepsy, diabetes, back pain, disabling asthma, or arthritis.4 Patients with acne also have fewer feelings of pride, lower self-esteem, lower body image satisfaction, more depressive symptoms, and more feelings of uselessness than people without acne.5 Adolescents with severe acne have suicidal thoughts more frequently than those with less severe acne.6 If left untreated, acne can result in significant psychosocial morbidity.7 Treatment improves the QOL of patients with acne and can prevent scarring.8–10

KEY POINTS

• ▸ Acne vulgaris is a chronic, prevalent skin disease that can affect a patient''s quality of life and lead to unnecessary medical expenses.
• ▸ Oral isotretinoin is indicated for the treatment of severe resistant nodular and conglobate acne vulgaris and is the only therapy that targets all 4 causitive factors.
• ▸ However, oral isotretinoin is a teratogenic drug that is associated with significant side effects and carries a REMS program; and although it is indicated for severe recalcitrant acne, it is often prescribed for mild or moderate acne.
• ▸ A fixed-dose combination of adapalene and benzoyl peroxide gel, 0.1%/2.5% (A-BPO) is efficacious and well tolerated in patients with severe acne.
• ▸ This new analysis of previously published data shows that although oral isotretinoin and A-BPO plus oral doxycycline 100 mg (A-BPO/D) are both effective for treating severe acne, A-BPO/D is less expensive per patient per week.
• ▸ Because the 2 treatment regimens are different in nature, a weekly cost analysis was used for comparison, showing that the median weekly cost for A-BPO/D is $44 compared with $62 for oral isotretinoin.
• ▸ In addition to being safer than oral isotretinoin for the management of patients with severe acne vulgaris, A-BPO/D is a cost-effective alternative to oral isotretinoin, which is associated with potential serious side effects that may further increase the indirect costs of treatment.

The pathophysiology of acne is multifactorial, involving 4 causative factors, including inflammation, hyperkeratinization, Propionibacterium acnes proliferation, and excess sebum production.11 Several topical and oral treatment options target the various causative mechanisms. The Global Alliance to Improve Outcomes in Acne has published recommended guidelines for the treatment of acne.12 Topical treatment is recommended for milder forms of acne. Oral isotretinoin is indicated for the most severe forms of nodular and conglobate acne and is the only available therapy that targets all 4 causative factors.Although indicated for severe recalcitrant acne, oral isotretinoin is frequently prescribed for the treatment of mild or moderate acne.13 However, oral isotretinoin is a pregnancy category × teratogen and is associated with significant side effects.14 The reported side effects associated with the use of oral isotretinoin include depression, attempted suicide, cheilitis, dermatitis, myalgia, dry eyes, nonspecific gastrointestinal symptoms, and arthralgia, among others.14 Patients who are prescribed oral isotretinoin must enroll in the Risk Evaluation and Mitigation Strategy (REMS) program iPLEDGE.15 Patients also require laboratory tests to monitor liver function and serum lipid levels.14For patients with severe acne with less nodular involvement, an oral antibiotic with a topical retinoid and benzoyl peroxide is recommended.12 Doxycycline 100 mg once daily is efficacious against acne and is relatively well tolerated.16 Adapalene, a third-generation retinoid with an established safety profile, has anticomedogenic and anti-inflammatory properties that are effective against acne.17–21 Benzoyl peroxide is an antimicrobial agent with demonstrated efficacy in treating acne.22 Benzoyl peroxide is more advantageous than other topical antibiotics, because it does not induce bacterial resistance and because it is effective against resistant P acnes strains.23A fixed-dose combination of adapalene and benzoyl peroxide gel, 0.1%/2.5% (A-BPO; Epiduo Gel) was approved by the US Food and Drug Administration in 2008. This is the only fixed-dose drug combination that is formulated with a topical retinoid and benzoyl peroxide. The safety and efficacy of A-BPO for the treatment of acne have been established in clinical trials.24,25Two related clinical trials investigated the use of A-BPO with oral doxycycline 100 mg once daily (A-BPO/D) for 12 weeks,26 followed by a maintenance therapy of A-BPO in patients with severe acne for an additional 24 weeks.27 Severe acne vulgaris in these studies was defined as up to 3 nodules or cysts, 30 to 120 noninflammatory lesions, and at least 20 inflammatory lesions.26,27 In the study by Gold and colleagues, patients who were treated with A-BPO/D had significantly better improvement in acne symptoms and in the acne symptom portion of the Acne-QOL questionnaire than patients given vehicle gel and doxycycline 100 mg.9,26 Patients with at least a “good” improvement in the first study, whether they were in the A-BPO/D group or in the vehicle gel plus doxycycline group, were eligible for the second study and were randomized to a maintenance regimen of A-BPO or to vehicle gel. Symptoms of acne and the QOL of patients using A-BPO continued to improve, whereas in patients using vehicle gel, QOL and acne symptoms worsened during the 24-week period.9,27 The majority of adverse events were mild and included erythema, scaling, dryness, and stinging and burning.26,27In addition to treating severe acne, A-BPO is also recommended for the treatment of mild and moderate acne, making it a versatile topical medication that can treat a spectrum of disease severity.12A model was developed to compare the efficacy and related costs of A-BPO/D versus oral isotretinoin in treating severe acne vulgaris.     

West Nile virus encephalitis and myocarditis in wolf and dog

In the third season (2002) of the West Nile virus epidemic in the United States, two canids (wolf and dog) were diagnosed with West Nile virus encephalitis and myocarditis with similarities to known affected species (humans, horses, and birds). The West Nile virus infections were confirmed by immunohistochemistry and polymerase chain reaction.Since its 1999 introduction in New York, West Nile virus (WNV) has spread to >40 states, causing seasonal mosquito-borne disease in humans, horses, and birds (1–7). We recently identified two Illinois canids (a captive wolf and a domestic dog) with severe disease associated with WNV infection.Outside the Western Hemisphere, WNV has been endemic for decades (4,8–11). Canids have not been thought to be important in the epidemiology of this virus. However, a dog with neurologic disease that died in Africa in 1977 is now thought to have been infected with WNV (9,12). In a recent study in which four dogs were experimentally infected, no clinical disease was observed, and a low viremia developed in one dog (11). Natural infections occur in dogs, as indicated by serum antibodies; seropositivity in surveys was 37% in the 1980s in South Africa, 24% in the 1990s in India, and 5% in 1999 in New York City (10,11,13). In addition, a few individuals of some mammalian species have been listed as infected (not diseased): 14 bats, four rodents, three rabbits, two cats, two raccoons, and a skunk (6).     

Minimal Diversity of Drug-Resistant Mycobacterium tuberculosis Strains,South Africa

Multidrug- (MDR) and extensively drug-resistant tuberculosis (XDR TB) are commonly associated with Beijing strains. However, in KwaZulu-Natal, South Africa, which has among the highest incidence and mortality for MDR and XDR TB, data suggest that non-Beijing strains are driving the epidemic. We conducted a retrospective study to characterize the strain prevalence among drug-susceptible, MDR, and XDR TB cases and determine associations between strain type and survival. Among 297 isolates from 2005–2006, 49 spoligotype patterns were found. Predominant strains were Beijing (ST1) among drug-susceptible isolates (27%), S/Quebec (ST34) in MDR TB (34%) and LAM4/KZN (ST60) in XDR TB (89%). More than 90% of patients were HIV co-infected. MDR TB and XDR TB were independently associated with mortality, but TB strain type was not. We conclude that, although Beijing strain was common among drug-susceptible TB, other strains predominated among MDR TB and XDR TB cases. Drug-resistance was a stronger predictor of survival than strain type. Key words: Mycobacterium tuberculosis, drug resistance, transmission, genotype, South Africa, HIV, bacteria, tuberculosis, tuberculosis and other mycobacteria, antimicrobial resistanceDrug-resistant tuberculosis (TB) has emerged as a substantial threat to advances in global TB control over the past several decades (1). Worldwide, an estimated 630,000 cases of multidrug-resistant (MDR) TB occurred in 2011, and extensively drug-resistant (XDR) TB has now been reported in 84 countries (2). MDR TB and XDR TB are each associated with very high mortality rates (3), and their transmission—both in community and health care settings—remains an ongoing challenge in resource-limited settings and in countries with high rates of HIV co-infection.In South Africa, the incidence of MDR TB has increased 5-fold since 2002 (2,4). MDR TB treatment is now estimated to consume more than half of the budget allocated for TB control in South Africa (5). The emergence of XDR TB, and its associated high mortality rates, have further underscored the need for clarifying the factors driving the drug-resistant TB epidemic to better focus control efforts (3,6,7).Drug-resistant TB is generally considered a human-made phenomenon that occurs when inadequate TB treatment creates selection pressure for the emergence of drug-resistant Mycobacterium tuberculosis subpopulations (acquired resistance) (1). Researchers initially believed that the mutations causing drug resistance would exert a “fitness cost,” rendering those strains too weak to be transmitted (8,9). Nonetheless, transmission of drug-resistant TB strains has now been well-documented (10–13), and laboratory studies have shown that clinical strains may have minimal fitness costs or even none (14). Emerging data suggest that most MDR TB and XDR TB cases in South Africa and worldwide are likely caused by primary transmission of drug-resistant strains (2,15–19).Although the M. tuberculosis W/Beijing strain family has been described among cases of drug-susceptible, MDR TB, and XDR TB in South Africa, numerous other strain types have also been identified (20,21). Little is known about the transmissibility and virulence of M. tuberculosis strains aside from the W/Beijing strain family (22,23). In the Eastern Cape and Western Cape Provinces of South Africa, strains from the W/Beijing family have most often been associated with transmission of drug-resistant TB (24–27). At our study site in KwaZulu-Natal Province, however, the LAM4/KZN strain type has predominated among MDR TB and XDR TB cases and has been linked to nosocomial transmission and high mortality rates (3,16,17,28,29). This strain is a member of the Euro-American strain family and was first described in this region in 1994, evolving into an increasingly resistant phenotype over time (29).The reasons for why the LAM4/KZN strain is prominent in KwaZulu-Natal Province, rather than the Beijing strain, which is seen globally and in other parts of South Africa, is unclear. Moreover, it is unknown whether the higher mortality among patients with MDR TB and XDR TB in KwaZulu-Natal can be explained, in part, by a difference in genotypic prevalence and associated differences in strain virulence (3,6,7,28). In this study, we sought to characterize the genotypic diversity of M. tuberculosis strains among isolates causing drug-susceptible TB, MDR TB, and XDR TB in KwaZulu-Natal Province, South Africa. We also examined the relationship between M. tuberculosis strain, drug resistance, and patient survival.     

Trends in Biologic Therapies for Rheumatoid Arthritis: Results from a Survey of Payers and Providers

Background

Advances in therapies for rheumatoid arthritis (RA), particularly biologics, have transformed the treatment paradigm for RA. However, the associated costs of these therapies result in a significant economic burden on the healthcare system. As a chronic disease requiring lifelong treatment, most health plans now position RA drugs as a high-priority therapeutic category.

Objective

To identify provider and payer practices and perceptions regarding coverage of RA biologics in the current marketplace, as well as emerging trends in reimbursement practices.

Method

In November 2011, Reimbursement Intelligence, a healthcare research company, collected and analyzed quantitative and qualitative data via parallel-structure online surveys of 100 rheumatologists and 50 health plan payers (medical and pharmacy directors) who represent more than 80 million covered lives. The surveys included approximately 150 questions, and the surveys were designed to force a response for each question.

Results

Payers reported using tier placement, prior authorization, and contracting in determining coverage strategies for RA biologics. Among providers, experience with older RA agents remains the key driver for the choice of a biologic agent. A majority of payers and providers (68% and 54%, respectively) reported that they did not anticipate a change in the way their plans would manage biologics over the next 2 to 4 years. Payers’ responses indicated uncertainty about how therapeutic positioning of newer, small-molecule drugs at price parity to biologics would affect the current reimbursement landscape. Survey responses show that approval of an indication for early treatment of RA is not likely to change the prescribing and reimbursement landscape for RA biologics. This survey further shows that payers and providers are generally aligned in terms of perceptions of current and future treatments for RA.

Conclusion

Advances in RA therapies allow patients increasing options for effective disease management. However, the high cost of biologic therapies and the need for lifelong treatment raise economic concerns. Payer satisfaction with current therapies and uncertainty about added value of new therapies will create challenges for new medications coming to market.Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder and the most common form of inflammatory arthritis.1 RA affects 1% of the population, most often adults aged 40 to 70 years.2 Recent epidemiologic data indicate that the incidence of RA in women has risen in the past 10 years.3Because RA affects many individuals who are of working age and remains a major cause of disability, the economic burden of RA adds a significant cost not only to patients and their families, but also to society as a whole.1,4 In addition, reduced quality of life, loss of work productivity, and substantial healthcare utilization are factors that must be considered in RA management.4,5Because complications of RA may begin to develop within months of disease onset, early and aggressive treatment is considered clinically necessary to manage immediate symptoms of pain associated with inflammation, but also to slow disease progression to prevent long-term disability.1,6,7 Historically, estimates of work disability rates for RA have been high, with higher rates associated with longer disease duration; work disability estimates have been shown to reach 30% within 2 to 3 years of diagnosis.4,5 Recent estimates suggest that RA-related work disability rates remain high, although potentially lower than in earlier estimates.8 This 2008 longitudinal analysis showed estimates of 23% work disability at 1 to 3 years of disease onset and of 35% within 10 years.8

KEY POINTS

• ▸ Advances in RA medications, particularly biologics, have transformed the treatment paradigm for RA; however, the associated costs of these therapies result in a significant economic burden on the healthcare system.
• ▸ With a chronic disease requiring lifelong treatment, most health plans are positioning RA drugs as a high-priority therapeutic category.
• ▸ This survey of 100 rheumatologists and 50 payers representing >80 million lives revealed that provider experience and satisfaction with older RA agents remains the underlying driver for choice of biologics.
• ▸ Payers and providers alike reported that they did not anticipate a change in the way their plans would manage biologics over the next 2 to 4 years.
• ▸ Payers were uncertain about the therapeutic positioning for newer, small-molecule drugs at price parity to biologics.
• ▸ Survey responses also suggest that an indication for a biologic to treat early RA will likely not change current prescribing and reimbursement patterns.

Clinical studies have shown better clinical outcomes when aggressive treatment is initiated early, including treatment with a wide range of disease-modifying antirheumatic drugs (DMARDs) and non-DMARD combination therapies.7–9 A recent joint collaboration of the American College of Rheumatology (ACR) and the European League Against Rheumatism has led to the development of an updated classification system of RA, to shift the focus from late-stage disease features—such as structural changes and joint damage that can be determined from various imaging techniques—to early-stage disease features that are associated with persistent disease.6 Given the advances in treatment for RA, including nonbiologic and biologic options, along with the associated improved outcomes, this classification system update to include early-disease features marked a major shift in the RA disease construct.6The ACR guidelines outline clinical treatment pathways by first defining disease duration and activity.7 Disease duration is divided into 3 major categories: <6 months (equivalent to early disease), 6 to 24 months (equivalent to intermediate disease duration), and >24 months (equivalent to longer disease duration).7 Disease activity measurements are often qualitative in early-stage disease, and measures are subject to clinical judgment.7Pharmacotherapy for RA often includes a non-steroidal antiinflammatory drug, selected use of glucocorticoids, and initiation of a DMARD early in the disease course.1,7 Biologic therapies may be added when adequate disease control has not been met by previously initiated drug therapies, which may occur within the first year of diagnosis.1,7 With regard to biologic therapies, the ACR further subdivides “early disease” by disease duration of <3 months or 3 to 6 months, to accommodate the needs for early advancement of the patient to biologic therapies when disease activity is high.7Despite positive clinical outcomes from treatment advances, healthcare costs associated with the treatment of a prevalent and lifelong disease such as RA are a considerable issue for health plans. The ACR estimates that per-patient treatment with biologic therapies is typically in excess of $12,000 annually.10 The Agency for Healthcare Research and Quality estimates the annual costs for RA medications from as low as a few hundred dollars for oral, nonbiologic DMARDs to a high of more than $16,000 for injectable biologic DMARDs.11 As new therapeutic options for RA become available, provider practices and payer strategies to support evidence-based care within the confines of cost management demand close examination.This study was conducted to identify provider and payer practices and perceptions regarding therapeutic options and reimbursement for RA. To this end, Reimbursement Intelligence, a healthcare research company, conducted parallel online surveys with health plan payers and rheumatologists. Payers were asked to also consider market trends and potential for formulary coverage of RA therapies currently in development.     

Small colony variants of Staphylococcus aureus and pacemaker-related infection

We describe the first known case of a device-related bloodstream infection caused by Staphylococcus aureus small colony variants. Recurrent pacemaker-related bloodstream infection within a 7-month period illustrates the poor clinical and microbiologic response to prolonged antimicrobial therapy in a patient infected with this S. aureus subpopulation.Infections caused by Staphylococcus aureus range from mild skin infections to acute life-threatening diseases such as pneumonia, osteomyelitis, and endocarditis. However, S. aureus may also cause a chronic disease with persistent and recurrent infections. Skin and soft tissue infections, chronic osteomyelitis, and persistent infections in patients with cystic fibrosis have been associated with small colony variants, a naturally occurring subpopulation of the species S. aureus (1–6). S. aureus small colony variants are characterized as electron transport deficient bacteria because of their auxotrophism to hemin or menadione or are recognized as thymidine-dependent. These variants produce very small, mostly nonpigmented and nonhemolytic colonies. In addition, they also demonstrate various other features that are atypical for S. aureus, including reduced coagulase production, failure to use mannitol, and increased resistance to aminoglycosides and cell-wall active antibiotics (3–10). Furthermore, the ability of these variants to persist intracellularly within nonprofessional phagocytes has been described (3,5,11). Because of their fastidious growth characteristics and unusual morphologic appearance, small colony variants present a challenge both to the microbiologist and the clinician, often resulting in misidentification and misinterpretation (1,2,7,8). Prerequisite for recovering and identifying these variants is the application of extended conventional culture and identification techniques (3,5,8). We report the first case of a pacemaker-related bloodstream infection caused by S. aureus small colony variants. This case illustrates the poor clinical and microbiologic response to prolonged antimicrobial therapy in patients infected with these variants.     

Spontaneous Rupture: An Uncommon Complication of Ventral Hernia

BACKGROUND: Literature is scarce about spontaneous rupture of hernia because spontaneous rupture of here is uncommon (1). Reported cases are complications of incisional hernias, recurrent inguinal hernia, and umbilical hernias. It is potentially life threatening (1) because the ensuing entrapment and tension on bowel mesentery may lead to vasovagal shock or strangulation.In addition to systemic problems and increased intra-abdominal pressure that lead to the herniation, the spontaneous rupture and evisceration is usually preceded by other factors such as inflammation that weaken the hernia covering (1, 2).We a report a case of spontaneous rupture of an incisional ventral hernia referred to the University of Ilorin teaching hospital.     

The Impact of 5-HT3RA Use on Cost and Utilization in Patients with Chemotherapy-Induced Nausea and Vomiting: Systematic Review of the Literature

Background

Individual studies have assessed the impact of standard prophylactic therapy with 5-hydroxytryptamine receptor antagonists (5-HT₃RAs) for chemotherapy-induced nausea and vomiting (CINV) on cost and utilization, but no synthesis of the findings exists.

Objective

To systematically review published literature on costs and utilization associated with CINV prophylaxis with palonosetron and other 5-HT₃RAs.

Methods

PubMed and the National Institute for Health Research Centre for Reviews and Dissemination databases, conferences of 4 organizations (ie, Academy of Managed Care Pharmacy, American Society of Clinical Oncology, International Society for Pharmacoeconomics and Outcomes Research, and Multinational Association of Supportive Care in Cancer), and the bibliographies of relevant articles were queried for the medical subject headings and key terms of “ondansetron,” “granisetron,” “palonosetron,” “dolasetron mesylate,” “costs,” “cost analysis,” and “economics.” We included records published (full-length articles after 1997 and conference presentations after 2010) in English and with human patients, reporting data on cost and utilization (rescue medication, outpatient and inpatient services) associated with the use of 5-HT₃RAs for the treatment or prevention of CINV.

Results

Of the 434 identified studies, 32 are included in the current analysis: 7 studies report costs, 18 report utilization, and 7 studies report both. The costs are reported in US dollars (7 studies), in Euros (5 studies), and in Canadian dollars (2 studies). The studies vary in designs, patients, 5-HT₃RA regimens, and the definition of outcomes. The US studies report higher drug costs for CINV prophylaxis with palonosetron compared with ondansetron, lower medical outpatient and inpatient costs for palonosetron versus other 5-HT₃RAs, and higher acquisition costs for palonosetron versus ondansetron or other 5-HT₃RAs. Fewer patients receiving palonosetron versus with ondansetron or other 5-HT₃RAs required rescue medication or used outpatient or inpatient care. In Europe and in Canada, the total pharmacy costs and use of rescue medications reported are lower for patients receiving prophylaxis with palonosetron.

Conclusions

This analysis shows that prophylaxis with palonosetron for the treatment of CINV is associated with higher acquisition treatment costs, but also with lower use of rescue medications and outpatient and inpatient services compared with ondansetron or other 5-HT₃RAs in the United States. Therefore, the use of palonosetron as a standard treatment may lead to reduced service utilization for CINV.Chemotherapy-induced nausea and vomiting (CINV) is an adverse effect of cancer treatment. It may occur within a few minutes of or up to 24 hours after the administration of chemotherapy (ie, acute CINV), or it may occur more than 24 hours after treatment (ie, delayed CINV). CINV may last up to 7 days.1–7Although there are several patient-specific factors that place patients at an increased risk for developing CINV (eg, female sex, low consumption of alcohol, history of motion or morning sickness, age under 50 years, previous CINV), the most contributory risk factor is the emetogenic potential of the chemotherapy regimen itself.8

KEY POINTS

• ▸ Poorly controlled CINV may lead to nutrient depletion, reduced functional ability, diminished quality of life, or the premature discontinuation of chemotherapy.
• ▸ Previous studies have examined the impact of CINV prophylaxis with palonosetron and other 5-HT₃RAs on cost and utilization, but this is the first systematic review of the published literature on this topic.
• ▸ A total of 32 studies were included in this systematic literature review, of which 14 studies report costs and 25 reported utilization.
• ▸ This review indicates that palonosetron is associated with higher treatment costs but also with lower rescue medication use and outpatient and inpatient services use compared with other 5-HT₃RAs.
• ▸ Based on this analysis, the use of palonosetron as a standard treatment may lead to reduced service utilization for CINV.

More than 90% of patients undergoing highly emetogenic chemotherapy (HEC) will experience emesis without antiemetic prophylaxis, and 30% to 90% of those undergoing moderately emetogenic chemotherapy (MEC) will vomit without the prophylactic administration of antiemetics.8 From 10% to 30% of the patients receiving low emetogenic risk chemotherapy (LEC), and <10% of patients receiving minimal emetogenic risk chemotherapy (MinEC), will experience emesis without the administration of antiemetics.3,6,7,9 The dose, frequency, and length of administration, as well as the combination of agents may impact the emetogenicity of the chemotherapy.7Poorly controlled CINV may lead to nutrient depletion, reduced functional ability, diminished quality of life, or the premature discontinuation of chemotherapy.1-4,6,7,9 The use of prophylactic antiemetic medications in patients undergoing HEC may reduce the incidence of CINV to as low as 30%.7 A multidrug regimen containing a 5-hydroxytryptamine receptor antagonist (5-HT₃RA) is the standard approach for CINV prophylaxis.7 Drugs in this category include dolasetron mesylate, granisetron, ondansetron, palonosetron, and tropisetron, with palonosetron recommended as the preferred 5-HT₃RA for CINV prophylaxis with MEC by the guidelines of the National Comprehensive Cancer Network (NCCN), the Multinational Association of Supportive Care in Cancer/Economic Society for Medical Oncology (MASCC/ESMO), and the American Society of Clinical Oncology (ASCO).5,7,10Secondary rescue medications are used to treat breakthrough CINV among patients who have received prophylaxis.7 These medications may include metoclopramide, lorazepam, diphenhydramine, olanzapine, prochlorperazine, or dexamethasone.CINV increases direct costs (eg, medication, office visits, or hospitalizations) and indirect costs (eg, missed work).3,4,9 The effective prevention of CINV may reduce these costs. The clinical and economic impact of CINV underscore the importance of achieving CINV prophylaxis.3,4,9 Palonosetron—which has greater binding affinity and a longer half-life than the other 5-HT₃RAs, binds allosterically, stimulates receptor internalization, demonstrates positive cooperativity, and cross talks with the neurokinin (NK)-1 signaling pathway—prevents both acute and delayed CINV more effectively than the other 5-HT₃RAs.7,11-14The extent to which the clinical benefit of 5-HT₃RAs translates into reduced costs or utilization of healthcare services among patients with CINV has been shown in individual studies for subsets of outcomes,3,15 but no summary of the literature exists. We conducted a systematic literature review of published research on the healthcare costs and utilization associated with the use of 5-HT₃RAs for the prevention of CINV in patients receiving chemotherapy, with the goal of comparing palonosetron with the other 5-HT₃RAs.     

Escherichia coli O157 exposure in Wyoming and Seattle: serologic evidence of rural risk

We tested the hypothesis that rural populations have increased exposure to Escherichia coli O157:H7. We measured circulating antibodies against the O157 lipopolysaccharide in rural Wyoming residents and in blood donors from Casper, Wyoming, and Seattle, Washington, by enzyme immunoassay (EIA). EIA readings were compared by analysis of variance and the least squares difference multiple comparison procedure. Rural Wyoming residents had higher antibody levels to O157 LPS than did Casper donors, who, in turn, had higher levels than did Seattle donors (respective least squares means: 0.356, 0.328, and 0.310; p<0.05, Seattle vs. Casper, p<0.001, rural Wyoming vs. either city). Lower age was significantly correlated with EIA scores; gender; and, in rural Wyoming, history of bloody diarrhea, town, duration of residence, and use of nontreated water at home were not significantly correlated. These data suggest that rural populations are more exposed to E. coli O157:H7 than urban populations.Escherichia coli O157:H7 is an important human pathogen. This organism can affect humans in a variety of ways, ranging from asymptomatic carriage (1) to diarrhea, bloody diarrhea (the most common manifestation of illness in culture-proven cases), and the postdiarrheal thrombotic microangiopathy, hemolytic uremic syndrome (HUS) (2). Infections with E. coli O157:H7 in the Pacific Northwest of the United States have been endemic (3) and epidemic (4). Vehicles transmitting this pathogen include unpasteurized milk and juice (5,6), undercooked beef (7), drinking water (8), and contact with infected persons (9).Data from the Centers for Disease Control and Prevention (CDC) demonstrate higher incidences of E. coli O157:H7 infections in rural counties in the United States than urban (Paul Mead, unpub. data). Worldwide, rural populations have been postulated to be at greater risk for exposure to E. coli O157:H7 by virtue of increased exposure to animals or their excreta in Scotland (10,11); dairy farm visits have been implicated as a source for infection in Finland (12) and the United States (13); and animal contacts are a risk factor for the development of HUS in Switzerland (14). Serologic studies from Canada demonstrated higher frequencies of antibodies to the O157 lipopolysaccharide (LPS) side chain among residents of rural areas compared to residents of urban areas (15), and in Wisconsin children, manure and sheep contact were recently demonstrated to be risk factors for O157 seropositivity (16). Taken together, these data suggest more intense or more frequent human exposure to E. coli O157:H7 in nonurban areas.Populations in the Pacific Northwest and Rocky Mountain states provide an opportunity to assess the frequency of exposure to E. coli O157:H7 through serologic studies. Antibodies to the O157 LPS follow natural infection with E. coli O157:H7 (17) and are believed to be quite specific (18) because they are rarely found in healthy people. Thus, circulating antibodies to the O157 LPS are potential markers of population exposure to E. coli O157:H7. We therefore attempted to assess the distribution of antibodies to this antigen in three different populations, encompassing a gradient of population density.     

Hypertension Management: An Update

Hypertension is a significant and costly public health problem. It is a major, but modifiable contributor for the development of cardiovascular disease. Randomized controlled trials have shown that controlling hypertension reduces the risk of stroke, coronary artery disease, congestive heart failure, end-stage renal disease, peripheral vascular disease, as well as overall mortality. The risk of developing these hypertension-related complications is continuous, starting at a blood pressure level as low as 115/75 mm Hg. Despite the inherent health risks associated with uncontrolled hypertension, elevated blood pressure remains inadequately treated in the majority of patients. This article reviews guidelines for optimal evaluation of hypertension and current therapeutic options available to combat this common yet pervasive disease.Hypertension affects approximately 1 of 3 adults in the United States, and about 2 million new cases are diagnosed each year.1,2 An additional 28% of the US population is afflicted with prehypertension, and approximately 7% of Americans are not aware that they even have hypertension.3 Globally, hypertension affects more than 1 billion people and is projected to reach 1.56 billion by 2025.4 It is the leading cause of death and the second leading cause of lost disability-adjusted life-years worldwide.4 Randomized controlled clinical trials have shown that control of hypertension reduces the risk of stroke, coronary artery disease, congestive heart failure, end-stage renal disease, peripheral vascular disease, and mortality.1,5 The risk of developing these complications is continuous, starting at a blood pressure (BP) level as low as 115/75 mm Hg.6The total direct and indirect cost for hypertension in the United States in 2009 is estimated at $73.4 billion.3 Approximately 10% ($15 billion) of the US total annual drug expenditure is on antihypertensive medications.7 Despite these staggering costs, only 34% of Americans with hypertension are at their BP goal (<140/90 mm Hg).1 The reason for this failure is multi-factorial and only speculative, and not because of the lack of awareness or lack of effective pharmacologic agents or lack of understanding of the role of lifestyle modification. Since hypertension will develop in most Americans in their lifetime,8 early preventive measures and prompt management, including lifestyle and pharmacologic options, are essential to minimize complications associated with this condition.     

Superantigens and streptococcal toxic shock syndrome

Superantigens produced by Streptococcus pyogenes have been implicated with streptococcal toxic shock syndrome (STSS). We analyzed 19 acute-phase serum samples for mitogenic activity from patients with severe streptococcal disease. The serum samples from two patients in the acute phase of STSS showed strong proliferative activity. Streptococcal mitogenic exotoxin (SME) Z-1 and streptococcal pyrogenic exotoxin (SPE)-J were identified in one patient with peritonitis who recovered after 2 weeks in intensive care. SMEZ-16 was found in a second patient who died on the day of admission. Sequential serum samples taken on day 3 after admission from patient 1 showed clearance of mitogenic activity but absence of neutralizing anti-SMEZ antibodies. Serum samples taken on day 9 from this patient showed evidence of seroconversion with high levels of anti-SMEZ antibodies that neutralized SMEZ-1 and 12 other SMEZ-variants. These results imply that a high level of SMEZ production by group A streptococcus is a causative event in the onset and subsequent severity of STSS.Since the 1980s, a marked increase has occurred in highly invasive group A streptococcal (GAS) infections, in particular streptococcal toxic shock syndrome (STSS) associated with necrotizing fasciitis or myositis (1–4). The classical case definition for STSS is similar to staphylococcal toxic shock, caused by Staphylococcus aureus, but the outcome is more serious in STSS, with a reported death rate of 30% to 70% (2,5,6).The multiorgan involvement in STSS suggests that a toxin produced by GAS might be involved in pathogenesis. Prime candidates are the streptococcal superantigens (SAgs), a family of highly mitogenic proteins secreted individually or in certain combinations by many Streptococcus pyogenes strains (7–10), although other virulence factors, such as Streptolysin O and various cell wall antigens can also cause toxic shock (11). Superantigens simultaneously bind to major histocompatibility complex class II molecules and T-cell receptor molecules bearing a particular V-β region. This binding results in the activation of a large proportion of antigen-presenting cells and T cells, with subsequent release of high systemic levels of cytokines (12–15).Several lines of evidence support the hypothesis of SAg involvement in STSS. Toxic shock syndrome (TSS) toxin, produced by S. aureus, has been associated with most menstrual TSS cases (7). TSS toxin is a typical SAg that is functionally and structurally related to the staphylococcal and streptococcal SAgs (16). Moreover, animal models have shown that TSS toxin and other SAgs induce TSS-like symptoms in rabbits and rodents (17,18). The lack of neutralizing anti-SAg antibodies appears to be a key risk factor for the development of staphylococcal and streptococcal toxic shock (19,20).The major cytokines released from antigen-presenting cells and T cells after activation by SAgs are tumor necrosis factor alpha (TNF-α), tumor necrosis factor beta (TNF-β), interleukin (IL)-1, and IL-2 (11–14). TNF-α is the prime mediator of shock; anti–TNF-α has been shown to inhibit the progression of SAg-driven shock in mice and baboons (17,18,21).In contrast to TSS toxin and staphylococcal TSS, the association of individual streptococcal SAgs to STSS is much less understood. Several studies described the potential involvement of streptococcal pyrogenic exotoxin (SPE) A in invasive streptococcal disease (2,19,22,23), while others reported an association with SPE-C (24,25). In addition, some cases of STSS are not associated with SPE-A or SPE-C (26). Notably, these studies were performed without knowledge of other streptococcal SAgs that are now known to exist.Superantigen activity found in acute-phase serum samples from streptococcal disease patients has been reported. (In this article, the term “acute-phase serum” refers to serum taken on the day of admission). Sriskandan et al. published a study of seven patients with severe streptococcal infections: SPE-A was detected in serum samples from four patients (27). Recently, Norby-Teglund and Berdal reported a strong proliferative response in an acute-phase serum sample collected from a patient with STSS, indicating that the sample contained an unknown SAg (28). Mitogenic activity was also detected in serum samples from mice infected with a SAg-producing S. pyogenes strain (29).Since these reports, several novel streptococcal SAgs have been identified, including streptococcal mitogenic exotoxin Z (SMEZ; 30), SMEZ-2, SPE-G, SPE-H (31), SPE-J, and SPE-I (32), all possessing typical SAg features and highly mitogenic on human T cells. In addition, several variants of SMEZ showed significant antigenic variation (33). These findings suggest that, in addition to SPE-A and SPE-C, one or more of these novel toxins might be involved in STSS.All known streptococcal SAgs (with the exception of SMEZ, SPE-G, and SPE-J) are localized on mobile DNA elements (34). As a consequence, each GAS isolate usually carries the genes for SMEZ, SPE-G, and SPE-J, plus a certain combination of other sag genes. Not much is known about the control of sag gene expression, but a recent study indicates that an unknown host factor is involved in the control of SPE-C expression (35)We analyzed serum samples from 19 patients with severe streptococcal infections for mitogenic activity to identify bioactive SAgs and find a correlation between SAg activity and disease severity. In addition, we genotyped the matching streptococcal isolates from these patients for all known streptococcal sag genes and tested them for their ability to produce SAg protein in vitro.     

Characterization of waterborne outbreak-associated Campylobacter jejuni, Walkerton, Ontario

The Walkerton, Canada, waterborne outbreak of 2000 resulted from entry of Escherichia coli O157:H7 and Campylobacter spp. from neighboring farms into the town water supply. Isolates of Campylobacter jejuni and Campylobacter coli obtained from outbreak investigations were characterized by phenotypic and genotypic methods, including heat-stable and heat-labile serotyping, phage typing, biotyping, fla–restriction fragment length polymorphism (RFLP) typing, and pulsed-field gel electrophoresis. Two main outbreak strains were identified on the basis of heat-stable serotyping and fla-RFLP typing. These strains produced a limited number of types when tested by other methods. Isolates with types indistinguishable from, or similar to, the outbreak types were found only on one farm near the town of Walkerton, whereas cattle from other farms carried a variety of Campylobacter strains with different type characteristics. Results of these analyses confirmed results from epidemiologic studies and the utility of using several different typing and subtyping methods for completely characterizing bacterial populations.An outbreak of Campylobacter jejuni in a farming community in southern Ontario, Canada, in 1985 resulted from contamination of well water caused by spring run-off and heavy rains (1). In May 2000, a second waterborne outbreak of Escherichia coli O157:H7 and Campylobacter occurred in Bruce County, Ontario. Well water serving the town of Walkerton was contaminated by surface water carrying livestock waste immediately after heavy rains (2,3). A detailed microbiologic and epidemiologic analysis of the most recent outbreak may provide insights that could help make this type of outbreak less frequent.Most sporadic cases of campylobacteriosis are associated with preparation or consumption of poultry products (4). Outbreaks have been associated with consumption of unpasteurized milk or unchlorinated water (5). An estimated 20% of cases of illness caused by C. jejuni are due to vehicles of infection other than food, including water (6). Waterborne outbreaks of Campylobacter tend to occur in spring or early fall, an association attributed to seasonality of surface water contamination and infection in cattle herds (5). Contaminated water sources have been implicated in outbreaks involving E. coli O157:H7 and Campylobacter together in Scotland (7) and in New York State (8,9). The former outbreak resulted from sewage contamination of the water supply of a small village in Fife, Scotland. The latter outbreak was associated with contamination of wells at a state fair (10). Excrement from birds and animals, including cattle, has been shown to contaminate surface water supplies used by humans infected with Campylobacter (9).Campylobacter spp. have been found to cause water-borne outbreaks worldwide; such outbreaks are a particular problem in Scandinavian countries where many people drink untreated water from streams and other sources (11). Untreated surface water has also been implicated in Campylobacter outbreaks in New Zealand (12,13), Finland (14), England, Wales (15,16), Australia (17), and the United States (18). In Canada, outbreaks have been rarely detected and have been associated with contamination of surface water (19,20) and consumption of unpasteurized milk (21).In the United States, disease caused by C. jejuni or C. coli has been estimated to affect 7 million people annually, causing 110–511 deaths and costing $1.2–$6 billion (22). These organisms are responsible for 17% of all hospitalizations related to foodborne illness in the United States, and although associated with a much lower case-fatality rate than Salmonella spp. and E. coli O157:H7, they account for 5% of food-related deaths (6). Although the incidence of Campylobacter infections generally appears to be higher in industrialized than in developing nations, some evidence exists that campylobacteriosis may be important from a social and economic point of view (23).Epidemiologic and microbiologic analyses were undertaken to better understand the circumstances leading to the Walkerton outbreak. C. jejuni was isolated from patients associated with the outbreak, and C. jejuni and C. coli were isolated from animals and animal manure on farms located near the town wells. This work summarizes the phenotypic and genotypic typing results for isolates associated with the outbreak.     

Multidrug-Resistant Salmonella enterica Serotype Typhi,Gulf of Guinea Region,Africa

We identified 3 lineages among multidrug-resistant (MDR) Salmonella enterica serotype Typhi isolates in the Gulf of Guinea region in Africa during the 2000s. However, the MDR H58 haplotype, which predominates in southern Asia and Kenya, was not identified. MDR quinolone-susceptible isolates contained a 190-kb incHI1 pST2 plasmid or a 50-kb incN pST3 plasmid.Typhoid fever, which is caused by Salmonella enterica serotype Typhi, is endemic to the developing world; there were an estimated 26.7 million cases in 2010 (1). The incidence of typhoid fever in sub-Saharan Africa was an estimated 725 cases/100,000 persons in 2010, despite a lack of incidence studies conducted in West and central Africa (1). Antimicrobial susceptibility data are also scarce for this part of Africa. This issue is problematic because treatment with appropriate antimicrobial drugs is essential for recovery in the context of the global emergence of multidrug resistance.In the Indian subcontinent and Southeast Asia, the multidrug-resistant (MDR) Salmonella Typhi H58 clone, which was named after its haplotype (a combination of defined chromosomal single-nucleotide polymorphisms [SNPs]) (2,3), has spread rapidly and become endemic and predominant. During the 1990s, this clone acquired a large conjugative incHI1 pST6 plasmid encoding resistance to ampicillin, chloramphenicol, and co-trimoxazole (4,5); also in the 1990s, this MDR clone became resistant to quinolones and showed decreased susceptibility to ciprofloxacin because of point mutations in the chromosomal gyrA gene (2). The H58 clone has also spread to eastern Africa, where it has been the most prevalent haplotype (87%) in Kenya since the early 2000s (6).During 1997–2011, high incidence of MDR Salmonella Typhi was reported in some countries near the Gulf of Guinea in Africa, including Nigeria (7), Ghana (8,9), Togo (10), and the Democratic Republic of the Congo (11). During 1999–2003, a British surveillance system reported a prevalence of 19% (49/421) for MDR Salmonella Typhi isolates among imported cases of typhoid fever acquired in Africa, particularly in Ghana (12). However, nothing is known about the genotypes of these isolates, including whether they belong to the spreading MDR H58 clone.We report data for the occurrence, genotypes, and characterization of the resistance mechanisms of MDR Salmonella Typhi isolates. These isolates were obtained from the French National Reference Center for Salmonella (FNRC-Salm), Institut Pasteur (Paris, France), and Centre Pasteur du Cameroun (Yaoundé, Cameroon).