Seizures in an Immunocompetent Adult From Treatment of Latent Tuberculosis Infection: Is Isoniazid to Blame?

Isoniazid-induced seizures are a rare adverse reaction especially in immunocompetent adults. We report a case of a healthy man with seizures shortly after ingestion of his first therapeutic dose of isoniazid with rifapentine therapy for treatment of latent tuberculosis infection. Only 6 other similar cases are reported in the literature.

Tuberculosis Mortality in the United States: Epidemiology and Prevention Opportunities.

Rationale: More information on risk factors for death from tuberculosis in the United States could help reduce the tuberculosis mortality rate, which has remained steady for more than a decade.Objective: To identify risk factors for tuberculosis-related death in adults.Methods: We performed a retrospective study of 1,304 adults with tuberculosis who died before treatment completion and 1,039 frequency-matched control subjects who completed tuberculosis treatment in 2005 to 2006 in 13 states reporting 65% of U.S. tuberculosis cases. We used in-depth record abstractions and a standard algorithm to classify deaths in persons with tuberculosis as tuberculosis-related or not. We then compared these classifications to causes of death as coded in death certificates. We used multivariable logistic regression to calculate adjusted odds ratios for predictors of tuberculosis-related death among adults compared with those who completed tuberculosis treatment.Results: Of 1,304 adult deaths, 942 (72%) were tuberculosis related, 272 (21%) were not, and 90 (7%) could not be classified. Of 847 tuberculosis-related deaths with death certificates available, 378 (45%) did not list tuberculosis as a cause of death. Adjusting for known risks, we identified new risks for tuberculosis-related death during treatment: absence of pyrazinamide in the initial regimen (adjusted odds ratio, 3.4; 95% confidence interval, 1.9-6.0); immunosuppressive medications (adjusted odds ratio, 2.5; 95% confidence interval, 1.1-5.6); incomplete tuberculosis diagnostic evaluation (adjusted odds ratio, 2.2; 95% confidence interval, 1.5-3.3), and an alternative nontuberculosis diagnosis before tuberculosis diagnosis (adjusted odds ratio, 1.6; 95% confidence interval, 1.2-2.2).Conclusions: Most persons who died with tuberculosis had a tuberculosis-related death. Intensive record review revealed tuberculosis as a cause of death more often than did death certificate diagnoses. New tools, such as a tuberculosis mortality risk score based on our study findings, may identify patients with tuberculosis for in-hospital interventions to prevent death.

Chemotherapy of Tuberculosis.

The management of tuberculosis (TB) can be a challenging process that has implications both for the affected patient and public health. Effective anti-TB chemotherapy both cures and renders the patient noncontagious. Biological factors specific to M. tuberculosis necessitate the use of multiple drugs for prolonged durations to adequately eradicate infection. Recommended regimens address the complexities of eliminating organisms from diverse reservoirs while preventing the emergence of drug resistance. First-line anti-TB therapy for drug susceptible disease effectively cures almost all patients within 6-9 months. The loss of first-line agents, due to resistance or intolerance, necessitates lengthy treatment courses, frequently 12-18 months or longer. Due to the long treatment times and the implications of missed doses, directly-observed therapy (DOT) is considered the standard of care. Drugs used for the treatment of TB have serious potential toxicities that require close monitoring and prompt response. A strong public health infrastructure and robust social supports are important elements to assure successful treatment. These numerous factors compel public health entities to take a lead role in the management of TB, either through the direct management of TB treatment or by assuring the activities of partner organizations.

Multiclonal methicillin-resistant Staphylococcus aureus (MRSA) outbreak and its control after use of the Veterans Affairs (VA) MRSA bundle in a VA long-term care facility, 2004-2014.

A multiclonal methicillin-resistant Staphylococcus aureus (MRSA) outbreak with 91 infections occurred in our Veterans Affairs (VA) community living center over 46 months. Both similar and unique strains were shown by repetitive polymerase chain reaction to contribute to the outbreak, including 1 strain causing infections over a 33-month period. Most infections were soft tissue infections (67%). For 21 months after the initiation of the VA MRSA bundle, no infections were identified, and low rates of infection have been sustained an additional 4 years. The average annual rate of MRSA infection decreased by 62% (P < .001) from 0.6 per 1,000 resident days for 4 years prior to the bundle implementation to 0.09 per 1,000 resident days for 4 years after the bundle implementation.

Three indigenous cases of leprosy in the Mississippi delta.

Three native-born patients from the Mississippi Delta presented with leprosy over a 13-month period. None had a history of foreign travel, contact with each other, or known leprosy patients. Two patients' lesions lacked anesthesia, and all had a history of armadillo exposure. These cases add to the association of armadillo exposure and the subsequent development of leprosy.

Epidemiologic and molecular characterization of an outbreak of Candida parapsilosis bloodstream infections in a community hospital.

Candida parapsilosis is an important cause of bloodstream infections in the health care setting. We investigated a large C. parapsilosis outbreak occurring in a community hospital and conducted a case-control study to determine the risk factors for infection. We identified 22 cases of bloodstream infection with C. parapsilosis: 15 confirmed and 7 possible. The factors associated with an increased risk of infection included hospitalization in the intensive care unit (adjusted odds ratio, 16.4; 95% confidence interval, 1.8 to 148.1) and receipt of total parenteral nutrition (adjusted odds ratio, 9.2; 95% confidence interval, 0.9 to 98.1). Samples for surveillance cultures were obtained from health care worker hands, central venous catheter insertion sites, and medical devices. Twenty-six percent of the health care workers surveyed demonstrated hand colonization with C. parapsilosis, and one hand isolate was highly related to all case-patient isolates by tests with the DNA probe Cp3-13. Outbreak strain isolates also demonstrated reduced susceptibilities to fluconazole and voriconazole. This largest known reported outbreak of C. parapsilosis bloodstream infections in adults resulted from an interplay of host, environment, and pathogen factors. Recommendations for control measures focused on improving hand hygiene compliance.

Clinical spectrum of muscle weakness in human West Nile virus infection.

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV-associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV-associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment.