Published Date: 1999-08-22 23:50:00
Subject: PRO> Staph. aureus, MRSA, community acquired - USA
Archive Number: 19990822.1467

STAPHYLOCOCCUS AUREUS, MRSA, COMMUNITY ACQUIRED - USA
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See Also

Staphylococcus, drug-resist., community acquired - USA 980225203144
Staphylococcus aureus, MRSA prevalence - Canada 980318221627
Staphylococcus aureus, MRSA prevalence - Canada (02) 980319232241
Infection Control: MRSA 960605
Infection control: MRSA (4) 960614
Infection control: MRSA/VRSA (2) 960617
Infection control: MRSA/VRSA: RFI 960614
Date: Thu, 19 Aug 1999 18:48:41 -0400
From: Marjorie P. Pollack <pollackmp@mindspring.com>
Source: MMWR, 20 Aug 1999
<http://www.cdc.gov/epo/mmwr/preview/mmwrhtml/mm4832a2.htm>

Four Pediatric Deaths from Community-Acquired Methicillin-Resistant
_Staphylococcus aureus_ -- Minnesota and North Dakota, 1997-1999
--------------------------------------------------
Methicillin-resistant Staphylococcus aureus (MRSA) is an emerging
community-acquired pathogen among patients without established risk factors
for MRSA infection (e.g., recent hospitalization, recent surgery, residence
in a long-term-care facility [LTCF, or injecting-drug use [IDU) (1).
Since 1996, the Minnesota Department of Health (MDH) and the Indian Health
Service (IHS) have investigated cases of community-acquired MRSA infection
in patients without established risk factors. This report describes four
fatal cases among children with community-acquired MRSA; the MRSA strains
isolated from these patients appear to be different from typical nosocomial
MRSA strains in antimicrobial susceptibility patterns and pulsed-field gel
electrophoresis (PFGE) characteristics.
Case Reports
Case 1. In July 1997, a 7-year-old black girl from urban Minnesota was
admitted to a tertiary-care hospital with a temperature of 103 F (39.5 C)
and right groin pain. An infected right hip joint was diagnosed; she
underwent surgical drainage and was treated with cefazolin. On the third
day of her hospital stay, antimicrobial therapy was changed to vancomycin
when cultures of blood and joint fluid grew MRSA. The same day, the patient
had another hip drainage procedure, but had respiratory failure and was
placed on mechanical ventilation. Her course was complicated by acute
respiratory distress syndrome, pneumonia, and an empyema that required
chest tube drainage. She died from a pulmonary hemorrhage after 5 weeks of
hospitalization.
MRSA isolated from her blood, hip joint, and sputum was susceptible to
multiple antibiotic classes (Table 1). An autopsy revealed bilateral
bronchopneumonia with abscesses. The patient was previously healthy with no
recent hospitalizations. No family members resided in LTCFs or worked in
health-care settings.
Case 2. In January 1998, a 16-month-old American Indian girl from rural
North Dakota was taken to a local hospital in shock and with a temperature
of 105.2 F (40.6 C), seizures, a diffuse petechial rash, and irritability.
She was treated with ceftriaxone but developed respiratory failure and
cardiac arrest and died within 2 hours of arriving at the hospital. Blood
and cerebrospinal fluid cultures drawn immediately postmortem grew MRSA
that was susceptible to multiple antibiotic classes (Table 1). An autopsy
revealed multiple small abscesses of the brain, heart, liver, and kidneys;
autopsy cultures of meninges, blood, and lung tissue grew MRSA. One month
earlier, the patient had been treated with amoxicillin for otitis media.
Neither the patient nor family members had been hospitalized during the
previous year; no family members resided in LTCFs or worked in health-care
settings.
Case 3. In January 1999, a 13-year-old white girl from rural Minnesota was
brought to a local hospital with fever, hemoptysis, and respiratory
distress. The day before admission she had a productive cough and a 2-cm
papule on her lower lip. A chest radiograph revealed a left lower lobe
infiltrate and a pleural effusion. She was treated with ceftriaxone and
nafcillin. Within 5 hours of arriving at the hospital, she became
hypotensive and was transferred to a pediatric hospital, intubated, and
treated with vancomycin and cefotaxime. Despite pulmonary and hemodynamic
support, the patient's respiratory status deteriorated, and she died on the
seventh hospital day from progressive cerebral edema and multiorgan failure.
The patient's blood, sputum, and pleural fluid grew MRSA that was multidrug
susceptible (Table 1). An autopsy revealed consolidated hemorrhagic
necrosis of the left lung. The patient had no chronic medical conditions
and no recent hospitalizations; no family members were health-care workers
or employees of an LTCF or had a history of IDU.
Case 4. In February 1999, a 12-month-old white boy from rural North Dakota
was admitted to a tertiary-care hospital with bronchiolitis, vomiting, and
dehydration. He had a temperature of 105.2 F (40.6 C) and a petechial rash.
Chest radiograph revealed an infiltrate in the right lung consistent with
pneumonitis. On the second hospital day, the patient was diagnosed with a
large right pleural effusion. He was transferred to the intensive-care
unit, a chest tube was inserted, and treatment with vancomycin and
cefuroxime was initiated. The patient developed severe respiratory distress
and hypotension the following day and died.
The patient's admission blood culture was negative, but his pleural fluid
and a postmortem blood culture grew multidrug-susceptible MRSA. An autopsy
revealed acute necrotizing pneumonia with extensive hemorrhage and numerous
gram-positive cocci in the right lung. The patient had not been
hospitalized since birth and had no known medical problems; no family
members were health-care workers or employees of an LTCF or known to be
IDUs. His 2-year-old sister had been treated for a culture-confirmed MRSA
buttock infection 3 weeks earlier. MRSA isolates from the sister and the
patient had identical antibiotic susceptibility profiles.
Laboratory Summary
MRSA isolates from these four cases were susceptible to all antimicrobial
agents tested except beta-lactams. All vancomycin minimum inhibitory
concentrations were less than or equal to 2 micrograms/L. Isolates from all
four cases had the mecA gene by PCR assay at MDH. Isolates from cases 1 and
4 shared an indistinguishable PFGE pattern; isolates from cases 2 and 3
differed by two and three bands, respectively, suggesting clonal
relatedness among these cases (2). In comparison, these PFGE patterns
differed by an average of greater than 10 bands compared with PFGE patterns
among nosocomial MRSA isolates from several Minnesota hospitals. Sma I was
the restriction enzyme used for PFGE. No isolate produced toxic shock
syndrome toxin-1.
Reported by: C Hunt, M Dionne, M Delorme, D Murdock, A Erdrich, MD, Indian
Health Svc; D Wolsey, MPH, A Groom, MPH, J Cheek, MD, Indian Health Svc
Epidemiology Program; J Jacobson, B Cunningham, MS, L Shireley, MPH, State
Epidemiologist, North Dakota Dept of Health. K Belani, MD, S Kurachek, MD,
P Ackerman, Children's Hospital and Clinics--Minneapolis; S Cameron, P
Schlievert, PhD, Fairview Univ Medical Center; J Pfeiffer, MPH, Hennepin
County Medical Center, Minneapolis; S Johnson, D Boxrud, J Bartkus, PhD, J
Besser, MS, Minnesota Dept of Health Laboratory; K Smith, DVM, K LeDell,
MPH, C O'Boyle, PhD, R Lynfield, MD, K White, MPH, M Osterholm, PhD, K
Moore, MD, Acute Disease Epidemiology Section; R Danila, PhD, Acting State
Epidemiologist, Minnesota Dept of Health. Div of Applied Public Health
Training, Epidemiology Program Office; and EIS officers, CDC.
Editorial Note:
Since the first case reports of MRSA infections in the United States in
1968 (3), MRSA has become an increasing problem. The percentage of
nosocomial _S. aureus_ isolates that were methicillin resistant increased
from 2% in 1974 to approximately 50% in 1997 (4,5). Methicillin resistance
is usually conferred by the chromosomal mecA gene, which encodes an altered
penicillin-binding protein (PBP-2A) that causes resistance to all
beta-lactam antibiotics, including cephalosporins. However, many nosocomial
MRSA strains have acquired resistance to numerous other antibiotic classes
through a variety of mechanisms. Approximately 50% of MRSA isolates
identified at National Nosocomial Infection Surveillance (NNIS) system
hospitals are susceptible only to vancomycin (5).
Most documented MRSA infections are acquired nosocomially; previously,
community-acquired cases were restricted to patients residing in LTCFs and
among IDUs (6). However, both of these groups have extensive exposure to
hospitals, and their infections are generally caused by nosocomial MRSA
strains. More recently, however, community-acquired MRSA infections have
been identified at a Chicago pediatric hospital, in day care centers, and
among minority communities in other countries (1,7-9). Unlike nosocomial
MRSA isolates, community-acquired isolates from patients without known MRSA
risk factors are generally multidrug susceptible (except to beta-lactams)
and have distinctive molecular characteristics, as did the four isolates
from the fatal cases presented in this report.
These four cases demonstrate the potential severity of community-acquired
MRSA infections. Beta-lactam antibiotics (including cephalosporins) are
used as empiric therapy for various adult and pediatric infections, but
these agents are uniformly ineffective in treating MRSA infections. All
patients in this report were initially treated with a cephalosporin
antibiotic; the delayed use of antibiotics to which MRSA were susceptible
may have contributed to the fatal outcomes. As a result, where such
infections exist, obtaining appropriate cultures of infected sites is
important. Clinicians should consider MRSA as a potential pathogen in
severe pediatric pneumonia or sepsis syndromes in areas where community
MRSA infections have been reported. In critically ill patients with
invasive infections, empiric treatment with vancomycin (in addition to a
third-generation cephalosporin) pending culture results may be necessary to
treat cephalosporin-resistant _S. pneumoniae_ (10) or MRSA.
The rural/urban and racial diversity among these cases suggest that MRSA
colonization may be widespread, especially in this region of the United
States. The extent of community-acquired MRSA infection in the United
States is unknown. Few data are available to define the molecular
characteristics of these strains. It is also unclear how to limit the
spread of MRSA within the community and whether it is feasible to
decolonize selected high-risk persons. The role that increased antibiotic
use in children--particularly beta-lactams and cephalosporins--has played
in selecting for MRSA strains in the community also is unknown. Local or
state-based surveillance is needed to characterize and monitor
community-acquired MRSA infections and to develop strategies that will
improve MRSA treatment and control.
References
Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired
methicillin-resistant _Staphylococcus aureus_ in children with no
identified predisposing risk. JAMA 1998;279:593-8.
Tenover FC, Arbeit RD, Goering RV, et al. Interpreting chromosomal DNA
restriction patterns produced by pulsed-field gel electrophoresis: criteria
for bacterial strain typing. J Clin Micro 1995;33:2233-9.
Barrett FF, McGehee RF, Finland M. Methicillin-resistant _Staphylococcus
aureus_ at Boston city hospital. N Engl J Med 1968;279:441-8.
Panlilio AL, Culver DH, Gaynes RP, et al. Methicillin-resistant
_Staphylococcus aureus_ in U.S. hospitals, 1975-1991. Infect Cont and Hosp
Epid 1992;13:582-6.
Lowy F. _Staphylococcus aureus_ infections. N Engl J Med 1998;339:520-32.
CDC. Community-acquired methicillin-resistant _Staphylococcus aureus_
infections--Michigan. MMWR 1981;30:185-7.
Embil J, Ramotar K, Romance L, et al. Methicillin-resistant _Staphylococcus
aureus_ in tertiary care institutions on the Canadian prairies, 1990-1992.
Inf Control and Hosp Epid 1994;15:646-51.
Maguire GP, Arthur AD, Boustead PJ, Dwyer B, Currie BJ. Clinical experience
and outcomes of community-acquired and nosocomial methicillin-resistant
_Staphylococcus aureus_ in a northern Australian hospital. J Hosp Infect
1998;38:273-81.
Adcock PM, Pastor P, Medley F, et al. Methicillin-resistant _Staphylococcus
aureus_ in two child-care centers. J Infect Dis 1998;78:577-80.
American Academy of Pediatrics. 1997 red book: report of the committee on
infectious diseases. 24th ed. Elk Grove Village, Illinois: American Academy
of Pediatrics, 1997:415.
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