|

EPI UPDATE
A weekly publication by the Bureau of Epidemiology
For May 3, 2000
"The reason for collecting, analyzing and disseminating information on a disease is to control that disease. Collection and analysis should not be allowed to consume resources if action does not follow."
--Foege WH et al. Int. J of Epidemiology 1976; 5:29-37.
Richard S. Hopkins, MD, MSPH, Bureau Chief, State Epidemiologist
Don Ward, Surveillance Section Administrator, Epi Update Managing Editor
Jill H. Parker, MSP, Epi Update Editor
Bureau of Epidemiology Frequent Contributors:
|
Steven Wiersma, MD, MPH,
Deputy State Epidemiologist |
William J. Bigler, PhD, MS,
Senior Epidemiologist |
Jodi Baldy, MPH,
Biological Scientist IV |
|
Ursula E. Bauer, PhD,
Chronic Disease Epidemiologist |
John Werth, MA,
Bureau Education Coordinator |
Lisa Conti, DVM, MPH,
State Public Health Veterinarian |
Regional Epidemiologists:
|
Dolly Katz, PhD, MPH,
SE Florida |
Roger Sanderson, RN, MA,
SW Florida |
Carina Blackmore, MS Vet. Med., PhD,
NE Florida Carina Blackmore, MS Vet. Med., PhD, |
Zuber Mulla, MSPH,
Central Florida Carina Blackmore, MS Vet. Med., PhD, |
Gérard Krause, MD, DTMH,
NW Florida |
Please print out this material and share with epidemiology staff, county health department directors, administrators, medical directors, nursing directors, environmental health directors and others with an interest in information of this type. Thank you.
The Bureau of Epidemiology is available 24 hours a day, 7 days
a week for consultation at our main number (850/245-4401) PLEASE NOTE:
Consultation after 5 p.m. & on weekends is intended for emergencies.
In this issue:
- Physicians Encouraged to Test for and Required to Report Mosquito-Borne Diseases
- Co-sleeping and the Risk of Infant Death: How Much Do We Know, What Should We Recommend?
- Highlights from the 10th International Symposium on Viral Hepatitis and Liver Disease
- New Mailing Address for the Bureau of Epidemiology
- Florida Past – Persistence Pays Off
- Weekly Disease Table: Week 17
1. Physicians are Encouraged to Test for and Required to Report Mosquito-Borne Diseases
Dr. Lisa Conti, State Public Health Veterinarian and Dr. Ming Chan, Chief, Bureau of Laboratories
Historically, Florida has suffered from repeated large epidemics of serious mosquito-borne diseases. In the 1870s and 1880s, outbreaks of yellow fever caused considerable mortality. In 1889, a physician and noted yellow fever expert was selected as the first head of the newly created State Board of Health in large part to control this disease. Large numbers of endemic dengue and malaria cases continued through the early part of the 1900s. Today, two diseases from endemic arboviruses remain: St. Louis encephalitis (SLE) with outbreaks occurring every seven to 10 years; and eastern equine encephalitis (EEE) with a range of 0 to five cases reported each year. In the nearby Caribbean and Central America, other mosquito-transmitted diseases are common (e.g., dengue and malaria). To date, West Nile virus (WNV) has not been identified in Florida.
Health care providers and laboratories are required to report all suspect or confirmed cases of arbovirus encephalitis and malaria to their county health departments. Identification of human cases of mosquito-borne disease may lead to the issuance of health alerts and/or mosquito abatement activities.
As a service to health care providers, the DOH Laboratory offers arbovirus (e.g., SLE, EEE, dengue and WNV) and malaria testing for patients with clinical manifestations. When possible, CSF and sera should be tested simultaneously. Acute sera will be tested for selective arboviral antibodies using HAI, and seropositive samples retested using ELISA IgM. An additional serum sample drawn 3-4 weeks later may be required for confirmation. A laboratory submission form must accompany specimens. For additional information, please contact the DOH Tampa Branch Laboratory or the DOH
Jacksonville Central Laboratory.
|
Test |
Specimen Required
|
Special Preparation and Container |
Result Indicator |
|
Arbovirus Isolation |
Contact Tampa Branch Laboratory for Instructions |
Contact Tampa Branch Laboratory for Instructions |
See individual report |
|
EEE,SLE, dengue |
CSF |
CSF frozen, or with cold pack. Test available at Jacksonville & Tampa Branch Laboratories |
Positive or Negative |
|
EEE, SLE, dengue, WNV (total antibodies) |
Single or paired sera
(HAI and ELISA IgM for acute serum. Convalescent serum sample may be required.) |
Red top or serum separation tube. Test available at Jacksonville & Tampa Branch Laboratories (WNV at Tampa Lab only) |
Titer and Interpretation or no antibody detected |
|
Western equine encephalitis, Venezuelan equine encephalitis, Lacrosse, Yellow Fever (total antibodies) |
Single or paired sera. Travel and exposure history must be submitted with specimen. |
Red top or serum separation tube Jacksonville Laboratory only |
Titer and interpretation or no antibody detected |
|
Malaria (microscopy) |
Blood smears. Requires prior arrangement with Jacksonville Laboratory
|
Slides and/or EDTA preservative (lavender top) tube with whole blood. Jacksonville Laboratory Only |
Positive (includes species) or no parasites found |
Arboviral encephalitis: Arboviral infection from eastern equine encephalitis virus, St. Louis encephalitis virus, Western equine encephalitis virus or West Nile virus may result in febrile illness of variable severity associated with neurologic symptoms ranging from headache to aseptic meningitis or encephalitis. Symptoms include headache, confusion or other alteration in sonsorium, nausea and vomiting. Signs may include fever, meningismus, cranial nerve palsies, paresis or paralysis, sensory deficits, altered reflexes, convulsions, abnormal movements and coma of varying degree.
Dengue Fever: An acute febrile illness characterized by frontal headache, retro-ocular pain, muscle and joint pain, and rash. The principal vector is the Aedes aegypti mosquito and transmission usually occurs in tropical or subtropical areas. Severe manifestations (e.g., dengue hemorrhagic fever and dengue shock syndrome) are rare but may be fatal.
Malaria: Signs and symptoms are variable. Patients may experience fever, headache, back pain, chills, sweats, myalgia, nausea, vomiting, diarrhea, and cough. Untreated Plasmodium falciparum infection can lead to coma, renal failure, pulmonary edema, and death. The diagnosis of malaria should be considered for any person who has these symptoms and who has traveled to an area in which malaria is endemic. Asymptomatic parasitemia can occur among persons who have been long term residents of areas in which malaria is endemic.
2. Co-sleeping and the risk of infant death:
How much do we know, what should we recommend?
Gérard Krause, MD, DrMed, Epidemic Intelligence Service Officer, EPO, CDC
Bureau of Epidemiology, Florida Department of Health
In Northwest Florida, between March 1997 and January 2000, the Department of Children and Families investigated 7 cases of infant deaths due to suffocation associated with co-sleeping with older children or adults in adult beds or sofas. In January 2000 the Department of Children and Families and the directors of the county health departments in Escambia, Santa Rosa, Okaloosa and Walton counties had a meeting to address prevention of infant suffocation deaths due to co-sleeping. During this meeting the question was raised about whether available evidence justifies a general recommendation against bed sharing with infants. The following review intends to summarize recent publications on this subject and to discuss the current scientific evidence in order to make recommendations for the prevention of such deaths.
Terminology
It is important to distinguish between infant death due to overlay with subsequent mechanical suffocation and sudden infant death syndrome (SIDS). SIDS is the sudden death of an infant under 1 year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history [1]. SIDS occurs with or without co-sleeping. Death due to suffocation may be falsely classified as SIDS if the case investigation was not able to identify any specific cause of death.
In contrast, death due to suffocation of the infant because of overlay by another person sleeping in the same bed or sofa is an explained cause of death, and will be referred to as overlay death in the remainder of this document. Accidental mechanical suffocation can also occur through entrapment, hanging, entanglement etc. which could occur with and without co-sleeping, while unintentional overlay deaths occur only during co-sleeping.
Recent publications
Although co-sleeping has often been hypothesized as being a risk factor for SIDS, a recently published case control study by Blair and colleagues seems to be the only study that investigated the risk of co-sleeping with SIDS [2]. Overall, sharing a room with the parents was associated with lower SIDS risk. Co-sleeping with an infant on a sofa was associated with a higher risk of SIDS. Among parents who do not smoke, there was no association between co-sleeping in parental bed and SIDS, but there was an increased risk for SIDS when co-sleeping with parents who smoke. Among infants older than 14 weeks there was no association between co-sleeping in the parental bed and SIDS. Risk of SIDS in younger infants who share beds with parents seems associated with parental alcohol consumption, overcrowded housing conditions, extreme parental tiredness and infant being under a comforter (such as a quilt or duvet). This study, however, did not address the risk of other causes of death associated with co-sleeping such as mechanical suffocation.
Drago and Dannenberg reported on 2,178 infant mechanical suffocation deaths in the United States based on reports to the US Consumer Product Safety Commission (CPSC) in the time period from 1980-1997 [3]. Approximately one-third of those deaths occurred in infants who were sleeping in adult beds, while approximately 15% occurred in infants who were sleeping in a crib. The remaining 52% occurred by suffocation associated with other furniture, plastic bags, cords etc. The most frequent single causes of suffocation were being wedged between mattress and the wall and oronasal obstruction. They also observed an increase in cases due to overlay during the study period. This report, however, provides descriptive data only, and the design of the study does not allow the assessment of whether co-sleeping per se is a risk factor for infant death.
Nakamura and colleagues published a report on 515 deaths from 1990 through 1997 of children younger than 2 years who were sleeping in adult beds, daybeds or waterbeds [4]. One-hundred-and-twenty-one of those deaths were due to overlay of the child by an adult or sibling sleeping in the same bed. Three-hundred-and-ninety-four deaths were due to entrapment in the bed structure. This report provides no information on any comparison group and due to its descriptive nature a risk comparison is not possible.
The Task Force on Infant Sleep Position and Sudden Infant Death Syndrome of the American Academy of Pediatrics (AAP) has recently updated its recommendations on the prevention of SIDS. The AAP stated that "there are insufficient data to conclude that bed sharing under carefully controlled conditions is clearly hazardous or clearly safe [5].
The extent of the problem
Recent population-based studies on the incidence of overlay death or suffocation death among infants are not available. National mortality data can be used to estimate how frequently suffocation deaths occur compared to other causes of deaths such as SIDS [6]. ICD 9 code E913.0 represents accidental mechanical suffocation in bed or cradle, excluding suffocation by plastic bag. Nationally, from 1979 to 1997, the rate of deaths due to ICD 9 code 913.0 (mechanical suffocation in bed or crib) among infants was 3.4 per 100,000 live births without a significant trend over time. In contrast, national data for the same time period indicates that there were 127.5 deaths due to SIDS per 100,000 live births with a declining trend. The rate overall is similar to the rate in Florida and the four Northwestern counties (Escambia, Santa Rosa, Okaloosa and Walton): ICD9 code 913.0: Florida = 5.0, four counties = 4.6 ; ICD9 code 798.0 (SIDS): Florida = 115.7, four counties = 125.7. These data suggest that infant death due to mechanical suffocation in adult beds is a rare event and occurs approximately 20 times less frequently than SIDS.
Potential risks and benefits associated with co-sleeping
Two recent publications have shown that between 30 and 70 deaths may occur each year among infants and children under the age of 2 in the US while sleeping in adult beds [3-4]. However, both studies lack evidence that infant mortality for children co-sleeping in adult beds is higher than for children sleeping in cribs. Again, the only study that provides a comparative risk assessment with regard to co-sleeping is limited to SIDS and does not address mechanical suffocation due to overlay [2]. This study suggests that co–sleeping is a risk factor for SIDS only if associated with parental smoking or alcohol consumption, overcrowded housing conditions, extreme parental tiredness and infant being under a comforter (such as a quilt or duvet).
For known causes of death such as mechanical suffocation, we lack information on the prevalence of co-sleeping in the US population which is necessary to estimate the relative risk associated with co-sleeping, especially compared to the risks associated with infants sleeping in cribs. One of the few sources of information on co-sleeping prevalence is the Pregnancy Risk Assessment Monitoring System (PRAMS) in Alaska, which since 1991 has included a question about co-sleeping. The Alaska PRAMS data suggests that co-sleeping has increased considerably during the past 9 years and that approximately 75% of the mothers with infants report co-sleeping sometimes or always [8]. The data also show considerable differences across race-ethnicity groups, which suggests that the results may be different in and within Florida.
We lack data that enable us to compare the risk associated with co-sleeping as compared with that of sleeping in cribs. In addition, in the US, babies who co-sleep are more likely to be breast-fed, which, in turn is known to reduce the risk of infant morbidity. Other factors that are not taken into account are the possible effects that co-sleeping or lack thereof might have on the psychosocial development of the child or parents, or on the bonding between child and parents.
Which recommendations are warranted?
It appears that currently there is not sufficient scientific evidence to advise against or for co-sleeping. However, there is good evidence that certain sleeping conditions are hazardous for the infant’s health and should be recommended against. Most of those recommendations address the prevention of SIDS, which has been better studied and is also twenty times more frequent than mechanical suffocation deaths.
Such recommendations might include:
- The sleeping position of the infant should be on the back (unless recommended otherwise by a pediatrician due to special health conditions of the child)
- Household members should not smoke
- Co-sleeping with an infant on a sofa should be avoided
- Infants should sleep in the same room as the parents (if parents do not smoke)
- Co-sleeping in the parents’ bed should be avoided under the following conditions:
- After recent parental alcohol and drug consumption, including medications which cause tiredness
- During extreme parental tiredness
- In overcrowded living conditions
- If parents smoke
- Infants should not sleep under a comforter (such as a quilt or duvet)
- Sleeping conditions in the bed as well as in the crib should be such that entanglement, wedging and entrapment between parts of the bed are avoided. The sleeping surface should be firm. Soft pillows and toys should be avoided in the sleeping area. Infants should not sleep in waterbeds.
The single most important intervention that appears to have significantly contributed to the reduction of SIDS in several countries is the recommendation to place infants on their back when sleeping [5]. Public health intervention efforts should therefore focus on this recommendation rather than advising against co-sleeping generally, until further data clarify the relationship between co-sleeping and infant death [5].
References
- Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol 1991;11:677-84.
- Blair PS, Fleming PJ, Smith IJ, Platt MW, Young J, Nadin P, Berry PJ, Golding J. Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome. CESDI SUDI research group. BMJ. 1999 Dec 4;319(7223):1457-61.
- Drago DA, Dannenberg AL. Infant mechanical suffocation deaths in the United States, 1980-1997 Pediatrics 1999 May;103(5):e59
- Nakamura S, Wind M, Danello MA Review of hazards associated with children placed in adult beds. Arch Pediatr Adolesc Med 1999 Oct;153(10):1019-23
- Task Force in Infant Positioning and SIDS. Changing concepts of sudden infant death syndrome: Implications for infant sleeping environment and sleep position. Pediatrics 2000; 105 (3): 650-6.
- Centers for Disease Control and Prevention, compressed
mortality file summary, March 22, 2000
- US Consumer Product Safety Commission, News release,
September 29, 1999, Release # 99-175
Perham-Hester K. Co-sleeping in Alaska: Data from the Pregnancy Risk Assessment Monitoring System (PRAMS), Executive Session of the Alaska Maternal-Infant Mortality Review in December 1999
3. Highlights from the 10th International Symposium on Viral Hepatitis and Liver Disease
Bonnie W. Kwan, M.P.H., Hepatitis Program Coordinator
The 10th International Symposium on Viral Hepatitis and Liver Disease was held in Atlanta, Georgia, between April 9-13, 2000. Approximately 2,000 delegates from over 70 countries attended the symposium. The meeting consisted of plenary sessions, workshops, and satellite symposiums on the molecular virology, epidemiology, diagnosis, treatment, and prevention of viral hepatitis. Brief highlights from the meeting are reported below.
Hepatitis A is the most common vaccine-preventable disease. It also accounts for the greatest morbidity and mortality for vaccine-preventable diseases in travelers; almost a thousand times that of cholera. Incidence of this disease varies widely geographically. Clinical manifestations of this disease include asymptomatic, symptomatic, cholestatic, relapsing, and fulminant hepatitis. The hepatitis A vaccine is highly immunogenic with almost 100% seroconversion after two doses. Studies have been conducted in both Alaska and New York on the usage of the hepatitis A vaccine in outbreaks. In order to halt an outbreak in a timely manner, over 70-80% of the susceptible population needs to be immunized.
Lamivudine has shown effectiveness in North American trials for the treatment of hepatitis B infection among treatment-naïve patients and selected subgroups of previous interferon non-responders. In addition, patients treated with this nucleoside analog have demonstrated, in both the North American and Asian trials, either improvement in histology, loss of hepatitis B e antigen, and/or normalized alanine aminotransferase (ALT) levels. However, global control of hepatitis B requires routine immunization. Although the biology of this virus favors eradication, potential inhibitors include genetic mutants escape, in-utero transmission, disruption of public health infrastructure, and the lack of political will.
The risk of developing hepatocellular carcinoma is highest among hepatitis C patients with cirrhosis. Unfortunately, treatment for chronic hepatitis C with interferon has been sub-optimal. Currently, the use of a water-soluble polymer, polyethylene glycol (PEG) with interferon alpha, or pegylation, appears to reduce renal clearance and increase sustained response. Furthermore, there is also limited success in hepatitis C vaccine development. This can be due in part to the following: lack of a good in-vitro cell culture system, lack of a reliable animal model, a highly mutable genome, genetic diversity of the hypervariable region 1, and a poor immune response following infection. Therefore, risk reduction education and identification of high-risk persons for counseling, testing, and medical management remain the most effective prevention and control strategies for hepatitis C.
Hepatitis D is endemic in many parts of the world. It is a defective virus because it requires coinfection with hepatitis B for its replication cycle. Although lamivudine has shown great success with hepatitis B infection, it is of limited therapeutic advantage for individuals infected with hepatitis D. Therefore the current treatment options are mainly limited to alpha interferon or liver transplantation. The clinical presentation of hepatitis D includes asymptomatic, cirrhosis, and fulminant hepatitis. Acute hepatitis occurs in over 50% of the individuals who are infected. Progression to cirrhosis is rapid (around 9 years) compared with other forms of chronic hepatitis. In addition, survival rates are short among those with histological and clinical cirrhosis.
Hepatitis E is distributed broadly worldwide outside of the United States with high rates of fulminant hepatitis and case fatality. Especially among pregnant women, case fatality rates can be as high as 25%. Hepatitis E is transmitted primarily fecal-orally with minimal person to person transmission. This form of viral hepatitis is most common in developing countries, so improved sanitation is the key to prevention. At present, protein vaccines appear to be of most practical use since DNA vaccines have been disappointing.
Oral and poster presentations (abstracts) from this symposium will be referenced in Antiviral Therapy 2000; Volume 5, supplement 1.
4. New Mailing Address for the Bureau of Epidemiology
Please note that as of April 1, 2000, the Bureau of Epidemiology’s mailing address has changed. All correspondence should be sent to the following address:
Florida Department of Health
Bureau of Epidemiology
BIN #A-12
4052 Bald Cypress Way
Tallahassee, FL 32399-1720
Overnight packages should be addressed to our physical address, which has changed to:
Florida Department of Health
Bureau of Epidemiology
2585 Merchant’s Row Boulevard
Tallahassee, FL 32399
5. Florida Past – Persistence Pays Off
William J. Bigler, PhD
It is pretty much common knowledge that the Florida State Board of Health, the originating agency for the present day Department of Health, was established in 1889. That was the culmination of a long hard struggle on the part of many dedicated individuals, as well as the Florida Medical Association. A summary of the critical events leading up to the creation of this agency was published in a 1959 issue of Health Notes entitled "Our Early Days." Some excerpts follow:
We know now that for 16 years (before its actual establishment) there had been repeated attempts by Governors, legislators and interested individuals to establish a State board of Health to assure uniform health and sanitary regulations in Florida. In 1873, a legislative bill had been introduced to provide an appropriation of $200 for a health program, but it was defeated mainly because the amount was considered exorbitant! Two years later, Dr. John Wall, of Tampa, advocated legislation along the same lines and was named to a committee by the Florida Medical Association to study health boards of other states. In 1877, Dr. T. M. Palmer of Monticello, through his connection with the Association, recommended a health plan, but to no avail. In 1879, an appropriation of $1500 was sought in the legislature, but was not allowed. Afterward, a succession of unsuccessful attempts were made by Governors William D. Bloxham and Edward A Perry, Dr. R. B. Burroughs of Jacksonville and Tampa, Dr. N.D. Phillips of Gainesville and Dr. J. W. Hicks of Orlando. Twice, a plan was introduced in the state legislature of 1887, but both failed. It was not until a yellow fever epidemic occurred, (in 1888) crippling the economy of all of Florida, that a concerted effort was made to unify public health regulations.
Editorial Note: Dr. John P. Wall successfully inserted into the Florida Constitution of 1885, Article XV entitled Public Health, which stated that " The legislature shall establish a State Board of Health and also county boards of health in all counties where it may be necessary; the State Board of Health shall have supervision of all matters relating to public health, with such duties, powers and responsibilities as may be prescribed by law; and the county boards of health shall have such powers and be under the supervision of the State Board of Health to such extent as the Legislature may prescribe."
6. Weekly Disease Table: Week 17
County-Confirmed Cases, Sorted Alphabetically by Disease
(NR represents years that the disease lacked status as a reportable condition)
|
DISEASE |
1997 TO DATE |
1998 TO DATE |
1999 TO DATE |
3 YEAR AVERAGE
TO DATE |
1999 TOTAL CASES |
2000 TO DATE |
|
Amebiasis |
14 |
14 |
12 |
13.3 |
66 |
1 |
|
Anthrax |
0 |
0 |
0 |
0 |
0 |
0 |
|
Botulism |
0 |
0 |
0 |
0 |
4 |
0 |
|
Brucellosis |
0 |
1 |
0 |
0.3 |
3 |
1 |
|
Campylobacteriosis |
232 |
182 |
220 |
211.3 |
987 |
224 |
|
Ciguatera |
2 |
0 |
0 |
0.7 |
2 |
0 |
|
Cryptosporidiosis |
25 |
27 |
23 |
25 |
178 |
13 |
|
Cyclosporiasis |
10 |
2 |
0 |
4 |
5 |
1 |
|
Dengue |
0 |
1 |
1 |
0.7 |
3 |
1 |
|
Diphtheria |
0 |
0 |
0 |
0 |
0 |
0 |
|
E. coli O157:H7 |
14 |
4 |
11 |
9.7 |
54 |
9 |
|
E. coli , other (known serotype) |
2 |
2 |
7 |
3.7 |
16 |
4 |
|
Ehrlichiosis, Human |
0 |
0 |
0 |
0 |
2 |
1 |
|
Encephalitis, Eastern Equine |
0 |
0 |
0 |
0 |
2 |
0 |
|
Encephalitis, St. Louis |
0 |
0 |
0 |
0 |
4 |
0 |
|
Encephalitis, other (known organism) |
5 |
3 |
2 |
3.3 |
5 |
3 |
|
Encephalitis, post-infectious1 |
3 |
0 |
2 |
1.7 |
14 |
1 |
|
Giardiasis (acute) |
389 |
301 |
235 |
308.3 |
1318 |
258 |
|
Haemophilus influenzae , invasive1 |
6 |
16 |
15 |
12.3 |
50 |
17 |
|
Hansen’s Disease (Leprosy) |
0 |
3 |
0 |
1 |
3 |
0 |
|
Hantavirus Infection |
0 |
0 |
0 |
0 |
0 |
0 |
|
Hemolytic Uremic Syndrome |
2 |
0 |
1 |
1 |
7 |
2 |
|
Hemorrhagic Fever |
0 |
0 |
0 |
0 |
0 |
0 |
|
Hepatitis A |
132 |
177 |
181 |
163.3 |
799 |
168 |
|
Hepatitis B |
109 |
96 |
96 |
100.3 |
536 |
107 |
|
Hepatitis C2 |
NR |
NR |
11 |
NR |
58 |
12 |
|
Hepatitis Non-A, Non-B |
21 |
20 |
0 |
13.7 |
11 |
6 |
|
Hepatitis, perinatal B2 |
NR |
NR |
0 |
NR |
|
1 |
|
Hepatitis, unspecified |
1 |
1 |
4 |
0 |
16 |
4 |
|
Hepatitis, +HBsAg, pregnant woman2 |
NR |
NR |
1 |
NR |
237 |
83 |
|
Lead Poisoning |
392 |
465 |
169 |
342 |
916 |
242 |
|
Legionellosis |
6 |
14 |
7 |
9 |
27 |
14 |
|
Leptospirosis |
0 |
0 |
0 |
0 |
1 |
0 |
|
Listeriosis2 |
NR |
NR |
5 |
NR |
33 |
8 |
|
Lyme Disease |
4 |
7 |
3 |
4.7 |
50 |
7 |
|
Malaria |
23 |
16 |
23 |
20.7 |
97 |
16 |
|
Measles |
1 |
1 |
1 |
1 |
2 |
0 |
|
Meningococcal Disease (N. meningitidis) |
64 |
46 |
37 |
49 |
122 |
35 |
|
Meningitis, Group B Streptococci |
4 |
6 |
5 |
5 |
14 |
5 |
|
Meningitis, Haemophilus influenzae1 |
4 |
5 |
7 |
5.3 |
14 |
1 |
|
Meningitis, Streptococcus pneumoniae |
34 |
40 |
49 |
41 |
98 |
41 |
|
Meningitis, Listeria monocytogenes |
0 |
3 |
2 |
1.7 |
13 |
1 |
|
Meningitis, other bacterial (including unspecified) |
15 |
16 |
16 |
15.7 |
60 |
28 |
|
Mercury Poisoning |
0 |
0 |
1 |
0.3 |
7 |
3 |
|
Mumps |
7 |
8 |
1 |
5.3 |
6 |
1 |
|
Neurotoxic Shellfish Poisoning2 |
0 |
0 |
0 |
0 |
0 |
0 |
|
Pertussis |
28 |
11 |
7 |
15.3 |
85 |
10 |
|
Pesticide Poisoning |
0 |
1 |
1 |
0.7 |
32 |
3 |
|
Plague |
0 |
0 |
0 |
0 |
0 |
0 |
|
Poliomyelitis |
0 |
0 |
0 |
0 |
0 |
0 |
|
Psittacosis |
0 |
0 |
0 |
0 |
0 |
0 |
|
Rabies, Animal |
97 |
72 |
55 |
74.7 |
176 |
43 |
|
Rocky Mountain Spotted Fever |
1 |
1 |
1 |
1 |
2 |
0 |
|
Rubella, including congenital |
0 |
1 |
0 |
0.3 |
1 |
1 |
|
Salmonellosis |
418 |
409 |
449 |
425.3 |
3062 |
392 |
|
Shigellosis |
302 |
404 |
389 |
365 |
1489 |
366 |
|
Smallpox2 |
NR |
NR |
0 |
NR |
0 |
0 |
|
Staphylococcus aureus, (GISA/VISA)2 |
NR |
NR |
0 |
NR |
0 |
0 |
|
Staphylococcus aureus, (GRSA/VRSA)2 |
NR |
NR |
0 |
NR |
0 |
0 |
|
Streptococcal Disease, invasive Group A |
13 |
19 |
16 |
16 |
93 |
52 |
|
Streptococcus pneumoniae , invasive disease |
71 |
178 |
186 |
145 |
690 |
342 |
|
Tetanus |
0 |
1 |
1 |
0.7 |
3 |
0 |
|
Toxic Shock Syndrome |
0 |
3 |
2 |
1.7 |
6 |
0 |
|
Toxoplasmosis |
2 |
4 |
4 |
3.3 |
17 |
2 |
|
Typhoid Fever |
3 |
7 |
19 |
9.7 |
23 |
1 |
|
Vibrio cholerae (serogrp O1) |
0 |
0 |
0 |
0 |
1 |
0 |
|
Vibrio cholerae (serogrp Non-O1) |
3 |
1 |
3 |
2.3 |
9 |
3 |
|
Vibrio vulnificus |
1 |
1 |
2 |
1.3 |
23 |
0 |
|
Vibrio other (including unspecified) |
9 |
4 |
10 |
7.7 |
48 |
7 |
|
Yellow Fever |
0 |
0 |
0 |
0 |
0 |
0 |
1 Haemophilus influenzae can be the agent responsible for disease under three of the reportable conditions listed-: "Haemophilus influenzae, invasive" and under "Encephalitis, post infectious." Cases of Haemophilus influenzae meningitis are reported under "Meningitis, H. influenzae."
2 The reportable disease rule was revised in July, 1999. Kawasaki Disease, Histoplasmosis, Reye Syndrome, and Typhus were deleted from the weekly disease table since cases are no longer reportable as of July 4, 1999. Hepatitis C; perinatal hepatitis B; hepatitis B +HbsAg, pregnant woman; listeriosis; smallpox, S. aureus (GISA/VISA) and S. aureus (GRSA/VRSA) were added to the reporting requirements as of July 4, 1999. Paralytic shellfish poisoning is now referred to as neurotoxic shellfish poisoning.
|