Malaria in the United States
Abstract & Commentary
By Stan Deresinski, MD, FACP, Clinical Professor of Medicine, Stanford; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, is Editor for Infectious Disease Alert
Synopsis: The CDC received reports of 1278 cases of malaria in the United States in 2003.
Source: Eliades MJ, et al. Malaria Surveillance—United States, 2003. CDC. MMWR. 2005;54(SS02):25-39.
Malaria was reported to the CDC to have occurred in 1278 individuals in the United States in 2003, a 4.4% decrease from 2002. Seven cases were fatal. Plasmodium falciparum accounted for 55.3% of the cases, P. vivax for 22.9%, P. malariae in 3.6%, and P. ovale in 2.6%, with an unknown species in the remainder. Twelve patients (0.9%) were infected with more than one species. Infection was acquired in the Americas in 11.5%, Asia in 13.8%, and in Africa in 65.7%. Of the infections acquired in Africa, 83.5% were due to P. falciparum, while the majority of those acquired in Asia and the Americas were due to P. vivax.
Among civilians with malaria for whom data was available, 62.8% took no chemoprophylaxis, 15.7% took inappropriate prophylaxis, and only 18.6% reported taking CDC-recommended chemoprophylaxis. Of the patients who reported taking the recommended prophylactic medication, only 34.7% reported having been compliant. Seven percent of the cases in women occurred during pregnancy; only 13% of pregnant women reported taking chemoprophylaxis, compared to 28.2% of nonpregnant women.
Ten infections were acquired in the United States—8 were introduced (ie, mosquito-borne transmission from an imported case), one was probably transfusion-related, and one was cryptic (ie, of unknown source). The latter occurred in a 14- year-old girl who shared a pediatric intensive care unit room for less than 24 hours with a boy being treated for P. falciparum infection acquired in Gambia. The girl’s infection was also due to P. falciparum and resulted from improper use of saline flush syringes.1 All the introduced cases occurred in Palm Beach County, Florida, and were due to P. vivax, with apparent strain identity demonstrated in the cases by PCR.
Commentary
Clinicians in the United States continue to be confronted with cases of malaria. Unfortunately, they do not always arise to the diagnostic challenge. I recently saw a young woman who had developed intermittent fever, chills, and headache shortly after returning from a 6 month visit to her home in India. She stated she had chosen to not take malaria prophylaxis because she was breastfeeding. I saw her on the 11th day of her illness when she was quite ill, necessitating hospitalization. Prior to seeing me she had twice been to an urgent care center and once to a hospital emergency room where she went in the middle of the night with a temperature of 103° F. She told me that she had had malaria growing up in India and believed that that might be the cause of her symptoms and that she told the examining physicians of this concern. Despite this, no malaria smear was ever performed. Fortunately, the infection proved to be due to P. vivax—if it had been P. falciparum, she probably would not have survived the incompetence of her previous caregivers.
The following is a summary of selected abstracts of papers presented at the 2005 International Conference Abstracts of the American Thoracic Society held in San Diego on May 20-25. They were published in Proceedings of the American Thoracic Society.
Community Acquired Pneumonia (CAP)
Diagnosis & Etiology
In further confirmation of the greater sensitivity of computed tomography in the detection of pulmonary lesions, a South African study of 49 HIV infected patients with CAP found that high resolution CT scan detected lesions not found on plain chest radiographs in 82% of patients (A455).
The sensitivity of the Binax NOW S. pneumoniae urinary antigen test was 84% in HIV infected individuals and 78% in those not HIV infected. The specificity and positive predictive values were only 81% and 78% in those who were HIV infected but were each 100% in those not so infected (A246).
Adherence to Guideline-based antibiotic therapy was associated with improved survival among patients with severe CAP (A44). However, current treatment guidelines do not take into account the possibility of MRSA as a cause of CAP. Examination of a large database with information from 138 US hospitals identified 13,544 cases of pneumonia, 31% of which were health care associated (HCAP). MRSA were detected in respiratory secretions in 16.6% of HCAP cases and in 6.9% of CAP (P < 0.0001). In an international study, initial blood cultures were positive in 12% of 1399 patients with CAP. Among the positive blood cultures, 39% yielded S. pneumoniae , 12% S. aureus, 9% H. influenzae, 5% P. aeruginosa, 4% E. coli, and 1% K. pneumoniae. Thus, S. aureus was the second most frequent cause of bacteremic CAP, having increased in frequency by approximately 150% since previous decades, a finding made all the more important since one-third of the isolates were MRSA (A173).
Therapy
A randomized trial has demonstrated that levofloxacin treatment with a 750 mg daily dose for only 5 days resulted in similar outcomes the 500 mg given every day for 10 days.2 Questions have, however, been raised regarding the safety of the higher dose in elderly patients. A post hoc analysis of 343 outpatients 65 years of age and greater (mean, 73 years) enrolled in 3 randomized trials of levofloxacin treatment of Acute Bacterial Exacerbation of Chronic Bronchitis and one of CAP, found that the incidence of drug related adverse events was 6.2% in those who received 750 mg daily and 6.1% in those who received 500 mg daily (A45).
In a clinical trial whose primary end point was cardiac safety, 394 patients > 65 years of age with comorbidities who had CAP were randomized to receive, in double-blind fashion, either moxifloxacin 400 mg daily or levofloxacin 500 mg daily for 10 days. The mean age of the randomized patients was 77.8 years and two-thirds were >75 years; three-fourths had a history of cardiac disease. The change in QTc interval on day 3 was +6.4 ± 23.2 in moxifloxacin recipients and -2.5 ± 22.9 in levofloxacin recipients. Treatment emergent cardiac adverse events were observed in 8.2% and 11.1%, respectively. One patient from whom support had been withdrawn and who had received moxifloxacin suffered sustained ventricular tachycardia and cardiac arrest. Clinical cure of pneumonia was achieved in 92.9% of moxifloxacin recipients and 87.9% given levofloxacin (A44).
Healthcare Associated Pneumonia (HAP)
Diagnosis
It was reported last year that the detection of sTREM-1 (soluble triggering receptor expressed on myeloid cells) in bronchoalveolar lavage fluid was a sensitive and specific test for the diagnosis of ventilator-associated pneumonia.3 A group from Phoenix reported an approach that avoided the need for bronchoscopy by measuring sTREM in the exhaled breath condensate in the exhalation limb collection chamber of the ventilator circuit. The results of this very small study suggested that this approach may also provide accurate results (A246).
The detection of bacteria on Gram stain of non-bronchoscopic bronchoalveolar lavage (mini-BAL) fluid had a high positive predictive value (100%) and accuracy (88%) in predicting the recovery of >104 cfu/mL on culture of the fluid (A246). A comparison of performance of calibrated loop and serial dilution for quantitative culture of BAL fluid found good qualitative but poor quantitative agreement between the 2 methods. Colony counts were 10-fold lower with use of the calibrated loop compared to serial dilution (A246).
Tuberculosis
Diagnosis
Several studies demonstrated apparent superiority of whole blood interferon gamma release assays using RD1 antigens (ESAT-6 and CFP-10) over the use of PPD antigen, especially in individuals who had received BCG (A270, A271).
Bronchial wash specimens were superior to those obtained by bronchoalveolar lavage in the diagnosis of tuberculosis in patients unable to spontaneously produce sputum (A273). A comparison of AFB smear, nucleic acid amplification testing (NAAT) and culture of sputum in the diagnosis of active tuberculosis found that their sensitivities were 70%, 86%, 85%, while their specificities were 96%, 100%, and 100%, respectively (A272). Of 18 patients with suspected tuberculosis with consistently AFB smear negative but positive by Gen-Probe Amplified Mycobacterium Tuberculosis Direct (MTD) test, 13 (72.2%) were ultimately proven to have tuberculosis (A273).
Therapy
A retrospective analysis of 3377 patients started on INH for treatment of latent tuberculosis found that 19 (0.56%) developed AST > 5 times ULN, with 10 of these reaching > 10 times ULN. Almost all these significant transaminase elevations were detected in the absence of signs or symptoms of acute hepatitis (A271).
The activity of moxifloxacin was comparable to that of INH in a murine model of tuberculosis (A273).
The incidence of paradoxical reactions during treatment of tuberculosis was 9 of 29 (31%) in HIV infected patients and 9 of 47 (19%) in non-HIV infected patients, occurring at a median of 21 days (range, 7-83) in the former and 36 days (range, 14-119) in the latter. Reactions tended to be more severe in those with HIV infection (A273).
Non-Tuberculous Mycobacterial (NTM) Infections
Many clinicians have had the impression that they are encountering increasing numbers of patients with MAC (more precisely, Mycobacterium avium/intracellulare complex or MAIC, since many of these infections are due to M. intracellulare rather than M. avium) pulmonary infection. At least 2 reports supported this impression.
The frequency of NTM pulmonary infections was documented to have increased in Ontario, Canada (A870). In addition, the incidence of pulmonary MAC disease in Queensland, Australia doubled from 0.63 to 1.21 per 100,000 population between 1985 and 1994 (A870).
No evidence could be found that Toll-Like Receptor (TLR2) gene polymorphisms are associated with susceptibility to NTM disease in humans (A871). GERD was frequently present in patients with NTM pulmonary disease (A871). Chronic sinusitis was found in 38 of 80 (47%) patients with pulmonary MAC disease in Japan (A872).
Solitary pulmonary nodules in 16 patients in Japan were resected for fear of malignancy. Eleven of the 16 proved to be due to MAIC (A872). In a small study of patients with pulmonary NTM infection, neither clinical nor radiographic progression was detected in the absence of pulmonary nodules, irrespective of treatment (A870).
In the Queensland experience (see above), of 60 HIV negative patients with pulmonary MAIC prospectively evaluated beginning in 1999, the mean age was 64.6 years; 53% were female, 35% were non-smokers, and 43% had COPD. Chest radiography demonstrated cavitary disease in 55%, nodules in 55%, and bronchiectasis in 47%. After 5 years of follow-up, 27 (45%), 3 of whom were not treated, were in remission, 8 (13%) improved but remained culture positive, and 8 without sputum were also improved. Five patients who had been successfully treated later had recurrence of disease. Twelve (20%) remained stable without treatment and 18 (30%) had progressive disease (A870).
The mean age of 18 patients with pulmonary MAC treated at a Tan Tock Seng Hospital in Singapore was 62 years and half were male; 10 (56%) had previously been treated for tuberculosis. The patients were treated with rifampin, ethambutol, and clarithromycin for a mean of 13.7 months; two-thirds converted their sputum cultures to negative. The mean time to culture conversion was 3.5 months and only one patient took longer than 6 months to convert (A872).
Pneumocystosis
Two studies suggest that smoking and smoking related pulmonary disease may predispose to colonization of the respiratory tract with Pneumocystis irovecii. P. jirovecii mitochondrial rRNA was detected by nested PCR in the sputum of 8 of 50 (16%) patients with COPD and in none of 30 immunocompetent health volunteers (P = 0.018) (A456). Two of 7 (28.6%) non-HIV infected patients undergoing bronchoscopy for clinical reasons had Pneumocystis detected in BAL by PCR. Neither of the 2 had evidence of immunocompromise, but both were active smokers with chronic cough and complained of fever (A456).
Aspergillosis
Tracheal and/or bronchial lesions, consisting of areas of mucosal erythema with either patchy necrosis or non-removable false membranes, were detected in 9 of 37 (24%) patients with suspected invasive aspergillosis during bronchoscopy. Mucosal biopsy revealed hyphae in each of the 9. An additional 10 patients had invasive aspergillosis in the absence of mucosal lesions; thus, 47% of patients with this infection had this finding. While mucosal lesions were observed in some of the 18 patients who did not prove to have invasive aspergillosis, none had patchy necrosis or non-removable pseudomembranes (A456).
Paragonimiasis
Of 30 patients with pleuropulmonary paragonimiasis in Kwangju, South Korea, 28 (93%) presented with respiratory symptoms, with cough in 82%, hemoptysis in 33%, chest pain in 27%, and dyspnea in 23%. Peripheral blood eosinophilia was present in all but one patient. Pleural lesions (effusion, pneumothorax, etc.) were present in 21 (70%), and pulmonary parenchymal lesions in 18 (60%). Pleural fluid was characterized by eosinophilia, low pH and glucose, and high LDH (A173).
Of 36 patients with pleuropulmonary paragonimiasis in Seoul, South Korea, 34 (98%) presented with respiratory symptoms, including hemoptysis in 56%, cough in 47%, dyspnea in 22%, and chest pain and fever each in 14%. Pulmonary parenchymal lesions were present in 72%, including 39% with nodules, 17% with linear opacities, and 11% with air-space consolidation; 28% had pleural lesions (A174).
References
- Komar N, et al. Detection of West Nile Virus in Oral and Cloacal Swabs Collected From Bird Carcasses. Emerg Infect Dis. Available at www.cdc.gov/ncidod/EID/vol8no7/02-0157.htm.
- Dunbar LM, et al. High-Dose, Short-Course Levofloxacin for Community-Acquired Pneumonia: A New Treatment Paradigm. Clin Infect Dis. 2003;37: 752-760.
- Gibot S, et al. Soluble Triggering Receptor Expressed on Myeloid Cells and the Diagnosis of Pneumonia. N Engl J Med 2004;350:451-458.
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