Arthropod-borne viruses (arboviruses) are transmitted to humans primarily through the bites of infected mosquitoes and ticks. West Nile virus (WNV) is the leading cause of domestically acquired arboviral disease in the United States (1). Other arboviruses, including La Crosse, Jamestown Canyon, Powassan, eastern equine encephalitis, and St. Louis encephalitis viruses, cause sporadic disease and occasional outbreaks. This report summarizes surveillance data for nationally notifiable domestic arboviruses reported to CDC for 2019. For 2019, 47 states and the District of Columbia (DC) reported 1,173 cases of domestic arboviral disease, including 971 (83%) WNV disease cases. Among the WNV disease cases, 633 (65%) were classified as neuroinvasive disease, for a national incidence of 0.19 cases per 100,000 population, 53% lower than the median annual incidence during 2009-2018. More Powassan and eastern equine encephalitis virus disease cases were reported in 2019 than in any previous year. Health care providers should consider arboviral infections in patients with aseptic meningitis or encephalitis, perform recommended diagnostic testing, and promptly report cases to public health authorities. Because arboviral diseases continue to cause serious illness, and annual incidence of individual viruses continues to vary with sporadic outbreaks, maintaining surveillance is important in directing prevention activities. Prevention depends on community and household efforts to reduce vector populations and personal protective measures to prevent mosquito and tick bites such as use of Environmental Protection Agency-registered insect repellent and wearing protective clothing.*,†.
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Objective. To investigate an outbreak of New Delhi metallo- β -lactamase (NDM)–producing carbapenem-resistant Enterobacteriaceae (CRE) and determine interventions to interrupt transmission. Design, Setting, and Patients. Epidemiologic investigation of an outbreak of NDM-producing CRE among patients at a Colorado acute care hospital. Methods. Case patients had NDM-producing CRE isolated from clinical or rectal surveillance cultures (SCs) collected during the period January 1, 2012, through October 20, 2012. Case patients were identified through microbiology records and 6 rounds of SCs in hospital units where they had resided. CRE isolates were tested by real-time polymerase chain reaction for bla NDM . Medical records were reviewed for epidemiologic links; relatedness of isolates was evaluated by pulsed-field gel electrophoresis (PFGE) and whole genome sequencing (WGS). Infection control (IC) was assessed through staff interviews and direct observations. Results. Two patients were initially identified with NDM-producing CRE during July–August 2012. A third case patient, admitted in May, was identified through microbiology records review. SC identified 5 additional case patients. Patients had resided in 11 different units before identification. All isolates were highly related by PFGE. WGS suggested 3 clusters of CRE. Combining WGS with epidemiology identified 4 units as likely transmission sites. NDM-producing CRE positivity in certain patients was not explained by direct epidemiologic overlap, which suggests that undetected colonized patients were involved in transmission. Conclusions. A 4-month outbreak of NDM-producing CRE occurred at a single hospital, highlighting the risk for spread of these organisms. Combined WGS and epidemiologic data suggested transmission primarily occurred on 4 units. Timely SC, combined with targeted IC measures, were likely responsible for controlling transmission.
Nucleic acid amplification testing (NAAT) is increasingly being adopted for diagnosis of Clostridium difficile infection (CDI). Data from 3 states conducting population-based CDI surveillance showed increases ranging from 43% to 67% in CDI incidence attributable to changing from toxin enzyme immunoassays to NAAT. CDI surveillance requires adjustment for testing methods.
Mycobacterium marinum is an “atypical” mycobacterium also known as a mycobacterium other than tuberculosis belonging to the Runyon group I, the photochromogens. 1 Colonies form a yellow pigment upon exposure to light, and optimal growth of the organism occurs at 30 to 32°C. First described in 1926 when Aronson isolated it from saltwater fish that had died in the Philadelphia aquarium, 2M. marinum is now a well-known cause of cutaneous infection in humans, usually occurring because of minor trauma in association with fresh, salt, or brackish water. 3 Most commonly, the infection produces localized cutaneous lesions, but sporotrichoid spread along lymphatics may occur 4,5 and infection can extend to deeper structures. 6–12 Cutaneous dissemination has been reported rarely, 6,8,12–19 and systemic dissemination with involvement of deep-seated tissues and organs is extremely rare, most cases being associated with immunocompromising conditions. 20–23 Unfortunately, the correct diagnosis of cutaneous M. marinum infection is frequently delayed. Diagnosis requires knowledge of the disease, an adequate exposure history, physical findings consistent with M. marinum, and confirmation of the clinical findings by culture of the organism. 24 Diagnostic delay coupled with immunosuppression may result in an uncomplicated local infection becoming a serious systemic illness. We report a case of fatal disseminated M. marinum infection with bacteremia in a patient who received an escalating regimen of immunosuppressive agents for an erroneous diagnosis of pyoderma gangrenosum. CASE REPORT In October 2001, a 73-year-old man with a history of steroid-dependent chronic obstructive lung disease, coronary artery disease, and congestive heart failure developed an open draining ulceration of his left elbow during an admission for a myocardial infarction. He was treated with local wound care after discharge with no improvement. He saw his dermatologist 2 months later, at which time he had a persistent ulceration on the left elbow and new ulcerations on his left 4th finger and right 2nd finger. Pathology from a shave biopsy of the left finger showed epidermal hyperplasia with markedly inflamed granulation tissue throughout the dermis with abscess formation, thought to be most consistent with pyoderma gangrenosum. The patient’s prednisone was increased from his chronic dose of 10 to 60 mg/d for treatment of presumptive pyoderma gangrenosum. One week later, the patient reported no improvement and had developed new lesions on his left forearm. Azathioprine, 25 mg/d, was added to his high-dose prednisone. Two weeks after starting azathioprine, his dose was increased to 50 mg/d. Three days later, he was seen again and was noted to have bilateral papulopustular lesions on his hands, arms, and legs. He was started empirically on clindamycin for 1 week and his azathioprine was increased to 75 mg/d. His lesions continued to progress, and he was subsequently referred to our institution. In January 2002, punch biopsies were performed on the lesions of his left hand and left thigh. Because of the working diagnosis of pyoderma gangrenosum, cyclosporine was briefly added to his immunosuppressive regimen while awaiting the results of the biopsies. The biopsies revealed a dense nodular to diffuse dermal inflammatory infiltrate composed predominantly of neutrophils with scattered lymphocytes and fibrohistiocytic cells, with leukocytoclasis and basophilic debris (Fig. 1). Extension of the process into the subcutaneous fat was noted. There was no granulomatous component. The differential diagnosis of these findings included a neutrophilic dermatosis, including rheumatoid dermatosis, Sweet syndrome, pyoderma gangrenosum, and infectious processes. Kinyoun stains of the biopsies were found to be positive for 3+ acid-fast bacilli from both sites.FIGURE 1: Nodular to diffuse predominantly neutrophilic inflammatory infiltrate in the dermis without granulomas (hematoxylin-eosin, magnification × 50).Upon this finding, the patient returned to the dermatology clinic and was found to have painful oral ulcers causing poor oral intake, weakness, and hypotension. He was admitted to the intensive care unit. He had deep ulcerations over his right distal ulna and 4th and 5th metacarpophylangeal joints (Fig. 2) and multiple nodules and ulcerations on his left arm, left hand and right leg. X-rays of his forearms and wrists showed soft tissue ulcerations with no evidence of osteomyelitis. Hand films revealed bilateral osteoarthritis.FIGURE 2: Deep, suppurating ulcerations of the right hand and wrist caused by M. marinum.A history obtained from the patient on admission revealed that he frequently went boating in a lagoon behind his house in New Jersey. In addition, in August 1998, he underwent an incision and drainage of a left finger abscess after being pinched by a crab. In November 1999, he developed arthritis of the left hand with nodules and was diagnosed with rheumatoid arthritis. Review of outpatient medical records revealed that in July 2000, he presented to his dermatologist with multiple erythematous scaly papules of both arms. He was diagnosed with psoriasis and treated topically. Over a year later, multiple scaly plaques persisted, and he subsequently developed a nonhealing ulceration over his left elbow. Shortly after admission to our institution, acid-fast bacilli growing from the skin biopsies were identified as M. marinum. He was started on clarithromycin and rifampin. Within 24 hours after admission, the patient became progressively hypotensive, requiring aggressive volume resuscitation, and developed respiratory distress leading to intubation. He was placed on pressors and stress-dose steroids and broad-spectrum antibiotics were added to his regimen. The patient developed non-sustained ventricular tachycardia, and an echocardiogram revealed a severely dilated left ventricle with marked global dysfunction. The patient subsequently arrested and could not be resuscitated. Blood cultures for mycobacteria obtained prior to his death grew M. marinum after 32 days. DISCUSSION We report an unusual case of disseminated M. marinum infection with bacteremia in an immunocompromised patient. Because M. marinum grows optimally at 30°C to 32°C and poorly if at all at 37°C, infection is usually limited to the skin of the extremities and typically occurs on areas that are predisposed to minor trauma, such as the finger, hand, or knee. 3 Exposure to virtually any type of aquatic environment, including fresh, salt, and brackish water, can lead to infection, often with a history of preceding minor trauma or skin abrasion. 3 The 3 most common types of exposure are aquariums, fish-associated or shell-fish-associated injuries, and injuries associated with saltwater or brackish water. 25 Infections related to swimming pool exposure are now relatively uncommon, most likely because of improved chlorination practices. 25 Infection usually begins as a single papulonodular lesion at the site of inoculation which may enlarge and progress into nodular plaques, pustules, ulcers, and abscesses. 5 In the sporotrichoid form, which occurs in about 20% of cases, nodular or ulcerating lesions ascend from the point of primary inoculation to the regional lymph nodes. 3–5 Cases of spread to deeper structures, resulting in tenosynovitis 6–9 as well as septic arthritis and osteomyelitis 9–12 have been reported less commonly. Although the infection usually remains localized to 1 extremity, cases of disseminated cutaneous disease have been reported in both immunocompromised 6,8,12–14 and immunocompetent 15–19 patients. Systemic infection with organ involvement is extremely rare, presumably because of the organism’s poor growth at 37°C and has been reported most often in immunocompromised patients. 20–23 We are aware of only 2 cases of M. marinum bacteremia documented in the English literature. The first case was a patient with acquired immunodeficiency syndrome (AIDS) who developed fatal disseminated infection with M. marinum cultured from skin, blood, bone marrow, and bronchial secretions. 21 Eighteen months prior, he had undergone surgical excision of skin nodules on his hand caused by M. marinum. He did not receive antimicrobials at the time of excision due to concomitant cerebral toxoplasmosis and herpes zoster. On initial presentation, the patient revealed that he kept fishes as pets and that 2 of them had recently died. The second case was a child with severe combined immunodeficiency who presented with disseminated cutaneous lesions, osteomyelitis, and bacteremia. 23 A history revealed that the infant was bathed in a bathtub where a tropical fishtank was frequently cleaned. As is illustrated in our case, delay in diagnosis of M. marinum infections is extremely common, often being considered only after the patient has failed multiple courses of antibiotics. 24 The lag time between appearance of skin lesions and the correct diagnosis may range from a few weeks to as long as several years, with a mean of ∼3 to 4 months. 25 In patients with atypical skin infections, a pertinent history needs to be obtained to elicit possible exposures to aquatic environments, aquariums, swimming pools, fish, or shellfish, especially in association with a skin injury. It should be noted that the incubation period of M. marinum, generally reported to be around 2 to 4 weeks, 3,25 may be as long as 9 months, 25 and questions should be directed this far back if no recent exposure can be recalled. Our patient had a several year history of what was thought to be rheumatoid arthritis in the left hand and multiple skin lesions, diagnosed as psoriasis, following a left hand injury by a crab. His complex of symptoms is highly suggestive of long-standing M. marinum infection. Chronic arthritis caused by M. marinum may be clinically mistaken for rheumatoid arthritis as well as gout, pyogenic infections, and carpal tunnel syndrome. 26 Also, histology of synovial lesions may resemble rheumatoid arthritis, although small epithelioid granulomas may be present with M. marinum infection, pointing toward an infectious etiology. 26 The histopathologic findings in cutaneous M. marinum infection are variable and often nonspecific, and this may lead to difficulty in recognizing the infectious nature of the lesions on biopsy prior to culture results. 26 Histologic changes tend to evolve over time, especially in immunocompromised patients, with well-formed granulomas being more common later in the disease. 27 Most cases show varying degrees of acute or subacute inflammation, with or without poorly formed granulomas. 26 The finding of acid-fast bacilli on smear, while common in cases of disseminated infection, is rare in the localized form of the disease. 8 Nonspecific findings on histology and negative acid-fast smears should therefore not discourage the culturing of specimens for mycobacteria. The laboratory should be notified of the suspicion for M. marinum so that cultures are incubated at 30°C to 32°C in addition to 37°C. The patient in this case was erroneously diagnosed with pyoderma gangrenosum which led to an escalating regimen of immunosuppressive agents. Mycobacterial infections are among many conditions that may mimic pyoderma gangrenosum. 28 In general, the misdiagnosis of pyoderma gangrenosum may be as high as 10%, exposing patients to the risks of treatment, including exacerbation of disease and resulting in delay in diagnosis. 29 It is therefore essential that appropriate cultures are done before a diagnosis is established and repeated biopsy performed if necessary. While there have been no controlled studies evaluating treatments for M. marinum, various effective agents exist. Limited cutaneous infection may resolve spontaneously, although complete resolution can take several years. 3M. marinum, which is uniformly resistant to isoniazid, is most commonly treated with regimens that include clarithromycin, tetracycline (usually minocycline or doxycycline), rifampin plus ethambutol, and trimethoprim-sulfamethoxazole. 3,5 Monotherapy is usually reserved for patients with infection limited to the skin and soft tissue, whereas drug combinations are commonly used for more serious infections. 5 Although quinolones have shown good in vitro activity against M. marinum, their in vivo efficacy is less encouraging. 5 The role of surgery with regard to severity of infection has not been well-established. Surgical intervention is often necessary for infections involving deep structures, although antibiotics alone may be used in selected cases. 7 Response to antibiotic treatment is usually slow and requires an extended course of therapy. A treatment duration of 3 to 6 months is generally recommended for localized disease, 3,30 while up to 9 to 12 months may be required for disseminated disease. 8 Failure of treatment is generally due to deep structure involvement rather than antimicrobial choice. 5 Unfortunately, the rapidity of our patient’s death precluded response to treatment of his M. marinum infection. In a case of atypical cutaneous infection, an adequate exposure history must be elicited to assess for risk factors for unusual infections such as M. marinum. To make the diagnosis of M. marinum, tissue cultures need to be performed and incubated under the appropriate conditions for isolation of the organism. This case demonstrates the potential consequences of delay in diagnosis of M. marinum infection in conjunction with immunosuppression.
Abstract Background In early 2020, an outbreak of coronavirus disease 2019 occurred among passengers and crew of the Diamond Princess cruise ship. During February 16–17, some US citizens, residents, and their partners voluntarily repatriated to the US from Japan. Methods We conducted a retrospective, longitudinal evaluation of repatriated travelers where the outcome of interest was a positive test for SARS-CoV-2. Travelers who tested positive for SARS-CoV-2 were isolated in hospitals or at home under county isolation orders and underwent serial testing by real-time reverse transcription polymerase chain reaction (RT-PCR) approximately every other day, as contemporaneous US guidance required two consecutive negative tests collected ≥24 hours apart and symptom improvement before release from isolation. Results Among quarantined repatriated travelers, 14% tested positive for SARS-CoV-2. One-fifth of infected travelers initially tested negative but were identified on subsequent testing. All infected travelers remained asymptomatic or developed mild symptoms during isolation. Many travelers remained in prolonged isolation because of persistent viral detection based on contemporaneous policies. Conclusion Our findings support testing within 3-5 days after possible SARS-CoV-2 exposure to comprehensively identify infections and mitigate transmission and lend support to symptom- and time-based isolation recommendations, rather than test-based criteria.
Abstract Background Cache Valley virus (CVV) is a mosquito-borne virus that is a rare cause of disease in humans. In the fall of 2020, a patient developed encephalitis 6 weeks following kidney transplantation and receipt of multiple blood transfusions. Methods After ruling out more common etiologies, metagenomic next-generation sequencing (mNGS) of cerebrospinal fluid (CSF) was performed. We reviewed the medical histories of the index kidney recipient, organ donor, and recipients of other organs from the same donor and conducted a blood traceback investigation to evaluate blood transfusion as a possible source of infection in the kidney recipient. We tested patient specimens using reverse-transcription polymerase chain reaction (RT-PCR), the plaque reduction neutralization test, cell culture, and whole-genome sequencing. Results CVV was detected in CSF from the index patient by mNGS, and this result was confirmed by RT-PCR, viral culture, and additional whole-genome sequencing. The organ donor and other organ recipients had no evidence of infection with CVV by molecular or serologic testing. Neutralizing antibodies against CVV were detected in serum from a donor of red blood cells received by the index patient immediately prior to transplant. CVV neutralizing antibodies were also detected in serum from a patient who received the co-component plasma from the same blood donation. Conclusions Our investigation demonstrates probable CVV transmission through blood transfusion. Clinicians should consider arboviral infections in unexplained meningoencephalitis after blood transfusion or organ transplantation. The use of mNGS might facilitate detection of rare, unexpected infections, particularly in immunocompromised patients.
Investigation of an outbreak of Clostridium difficile infection (CDI) at a hemodialysis facility revealed evidence that limited intrafacility transmission occurred despite adherence to published infection control standards for dialysis clinics. Outpatient dialysis facilities should consider CDI prevention, including environmental disinfection for C. difficile , when formulating their infection control plans. Infect. Control Hosp. Epidemiol . 2015;36(8):972–974
In recent years, the incidence and severity of Clostridium difficile-associated disease (CDAD) have increased dramatically. Beginning in 2000, widespread regional outbreaks associated with a previously uncommon hypervirulent strain of C. difficile have occurred in North America and Europe. Most likely because of increased toxin production as well as other virulence factors, this epidemic strain has caused more severe and refractory disease leading to complications, including intensive care unit admission, colectomies, and death. Worldwide increasing use of fluoroquinolones and cephalosporins has likely contributed to the proliferation of this epidemic strain, which is highly resistant to both. The elderly have been disproportionately affected by CDAD, but C. difficile has also recently emerged in populations previously considered to be at low risk, including healthy outpatients and peripartum women, although it is unknown if these cases are related to the epidemic strain. Nevertheless, transmission within hospitals is the major source of C. difficile acquisition, and previous or concurrent antimicrobial use is almost universal among cases. Applying current evidence-based strategies for management and prevention is critically important, and clinicians should maintain an awareness of the changing epidemiology of CDAD and take measures to reduce the risk of disease in patients.
