| Two
New Cases of Hantavirus Pulmonary Syndrome in Utah
Two cases of Hantavirus Pulmonary
Syndrome (HPS) have recently occurred in Utah. The death of a 47-year-old female from
Carbon County and the hospitalization of a 23-year-old male, also from Carbon County, has
heightened the awareness of physicians and the general public about the seriousness and
lethality of HPS. Although three cases of hantavirus were reported in 1998, the recent
death is the first fatality since the fall of 1996.
Due to the rapid onset of shock and
respiratory failure, early recognition of the illness is critical in reducing the risk of
mortality. HPS begins four days to six weeks after exposure to infected rodents or their
excreta, although not all patients will give a history of rodent exposure. All patients
experience a prodromal phase with fever, chills and myalgias, persisting for 1 to 7 days
before progression to the cardiopulmonary phase. Pain in the legs and back can be very
severe during the hantavirus prodrome. Many patients also experience nausea, vomiting
and diarrhea. Cough and other upper respiratory symptoms are not present at the onset of
the prodromal phase but instead begin hours before the onset of the noncardiogenic
pulmonary edema and cardiogenic shock.
There is no way to clinically distinguish between the prodrome of HPS
and that of many other viral and bacterial infections, hence the liberal use of the
complete blood count (CBC) with differential and platelet count is recommended. A low
platelet count (<150,000 in 98% of cases; <130,000 in 92%) is the only CBC
abnormality consistently seen during the prodromal phase. All HPS cases eventually have
platelets <100,000. Other nonspecific lab results suggestive of prodromal HPS include
elevated LDH, elevated AST, and reduced serum bicarbonate. Patients with symptoms
consistent with early HPS but with platelets counts of >150,000 should be advised to
return to the clinic in 24 hours for re-evaluation. The transition from hantavirus
prodrome to respiratory failure occurs 4 to 12 hours after onset of cough and shortness of
breath. With the onset of pulmonary edema, the CBC now shows thrombocytopenia, elevated
hematocrit, leukocytosis with circulating myelocytes, promyelocytes, and immunblasts,
recognized as large atypical lymphocytes with deep blue cytoplasm. Patients with suspected
HPS (thrombocytopenia and compatible clinical picture) should be transported to a
critical-care unit as early as possible. All patients with suspected HPS should be under
respiratory isolation until the diagnosis of HPS is confirmed by serology.
HPS has emerged as a new disease since identified in the spring of
1993. Even though it is considered a new viral zoonosis, retrospective case-finding has
indicated that it is not new to the United States. The retrospective diagnosis of
case-patients from as early as the 1959 Utah case reveals that human hantavirus infections
resulting in HPS went unrecognized until May 1993. To date, Utah has identified 15 cases
of hantavirus of which 10 (66.6%) were male. The mean age is 37 with a range of 19 - 67.
Utah’s case fatality rate is 33.3% (Table).
The human-rodent interaction and the identification and
characterization of environmental and ecologic factors and their influence on the density
of rodent populations are critical to understanding the epidemiology of this zoonosis. The
epidemiology of HPS closely parallels the ecology of its rodent hosts. The majority of HPS
patients have had clearly identifiable peridomestic, recreational, or occupational
exposure to rodents of which the majority are the deer mouse (Peromyscus maniculatus),
the primary rodent host for hantavirus and the most abundant rodent in North America. The
most effective method to prevent infection with hantavirus is to avoid contact with any
rodent species. Activities that should be avoided are using rodent inhabited buildings,
cleaning barns or outbuildings infested with rodents, and disturbing rodent nests and
burrows while hiking or camping.
When eliminating rodent infestation in homes or buildings, the
following steps should be taken:
Keep mice and other rodents out of your house
Trap all mice within your home
Remember to wear gloves while handling
mice.
Use snap traps to trap and kill mice.
Spray mice and trap with disinfectant.
Place rodent in a double plastic bag for
disposal.
Leave several baited spring loaded traps
inside the house at all times.
Clean up after mice
Wear rubber gloves while cleaning.
Air out area for 30 minutes.
Do not create dust by sweeping or
vacuuming.
Spray rodent droppings and nests with
disinfectant.
Place rodent droppings, nests, and other
contaminated items in double bag for disposal.
Wash gloved hands in a general household
disinfectant and then in soap and water.
Wash bare hands after removing gloves.
Utah Hantavirus
Cases By County |
County |
#
of Cases (Deaths) |
| Carbon |
5
(3) |
| Emery |
2 |
| Juab |
2 |
| Millard |
2
(2) |
| Salt Lake |
1 |
| Sevier |
1 |
| Tooele |
1 |
| Uintah |
1 |
| TOTAL |
15
(5) |
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Septicemic
Plague Case in Southern Utah
The
Bureau of Epidemiology received notification of a positive Yersinia pestis from a
blood culture in early June, 2000. The patient, a 57-year-old male from Washington County,
has a ranch in a rural area and reported burying a dead squirrel a few days before being
hospitalized with fever, chills, myalgia and bloody stools. Staff from the Communicable
Disease Control Program, Southwest Health District, and the Centers for Disease Control
and Prevention (CDC), Zoonotic Diseases Branch, did conduct a field investigation.
On the patient’s property there was a barn, several dilapidated
structures, woodpiles , and numerous burrows providing evidence of heavy rodent activity.
Neighbors of the case consented to trapping on their property and several allowed blood
samples to be collected on their dogs. One of the 69 rodents collected and one of the dogs
were positive for Y. pestis. Results on the numerous fleas collected are still
pending.
Plague is maintained in nature through transmission between certain
rodent species and their fleas. The introduction of plague to the U.S. is thought to have
occurred at the beginning of the last century (1899-1900) from rat-infested ships where
the disease caused outbreaks among humans in port areas along the Pacific and Gulf Coasts.
The plague bacterium quickly spread from the San Francisco Bay area to wild rodents and
their fleas in surrounding areas. It then spread to other rodent populations in the
remaining western states until, by the 1930s, it had reached its present easternmost
extent at the western edge of the Great Plains.
Humans can become infected with Y. pestis as a result of a flea
bite (most common), direct contact with infectious body fluids from an infected animal or
human, or by inhaling infectious respiratory droplets, usually following close contact
(within 6 ft) with an infected human or animal (primarily cats). Under natural conditions
plague causes widespread, irregularly occurring outbreaks (epizootics) among susceptible
rodent populations. Human risks are highest during such outbreaks because of the increased
likelihood of exposure to infectious fleas.
Plague occurs in three clinical forms: bubonic, pneumonic, and
septicemic. Most often, cases acquired from a flea bite or a break in the skin will
develop the classical sign of the bubonic form, which is a very painful, swollen lymph
node called a bubo. Buboes most commonly occur in the groin, axillary or cervical regions.
Finding a bubo, accompanied by fever, extreme exhaustion, and a history of possible
exposure to rodents or their fleas in the western United States should lead to suspicion
of plague. In addition, plague should be suspected in persons who have the above findings
and have handled sick or dead cats, rabbits, or wild carnivores from this same region.
Plague can be transmitted through inhalation of infectious respiratory droplets expelled
from persons or animals (particularly cats) with pneumonic plague and cough. Persons
exposed in this manner develop primary pneumonic plague. Primary septicemic plague most
likely occurs among persons handling infected animals, especially among those with cuts or
abrasions on their hands.
The onset of illness for most cases of bubonic or primary septicemic
plague is usually 2 to 6 days after exposure, but can be as short at 1 to 2 days for
primary pneumonic plague. Initial symptoms typically include fever, headache, myalgias,
arthralgias, prostration, and, in bubonic cases, development of painful, swollen regional
lymph nodes or buboes. Nausea and vomiting also are commonly observed. Occasionally,
buboes appear a day or so after onset of other symptoms. Plague progresses rapidly without
treatment, leading to invasion of the bloodstream and septicemic plague (secondary
septicemic plague in bubonic cases). Continued progression of the disease leads to
infection of the lungs (secondary pneumonic plague). In septicemic plague, Y. pestis
is disseminated throughout the body via the blood. Symptoms such as abdominal pain,
nausea, vomiting, and diarrhea, are commonly seen, in addition to fever, headache, chills,
and myalgias. Pneumonic plague symptoms may be similar to other forms of severe pneumonia
and include high fever, cough, lung congestion, difficulty breathing, chest pain, and,
sometimes, the presence of bloody sputum that contains large numbers of Y. pestis.
Diagnostic specimens, such as whole blood, serum, and bubo aspirates,
should be obtained from all suspected cases and submitted without delay to the Utah Public
Health Laboratory. Actual confirmation of plague infection requires either culturing the
bacteria and performing bacteriophage typing, or demonstrating 4-fold changes in antibody
titers to the F1 antigen of Y. pestis in passive hemagglutination assays or
enzyme-linked immunosorbent assays. Fluorescent antibody analyses of blood, tissue, lymph
node aspirate, and sputum samples can be extremely useful in providing rapid, although
presumptive, evidence of Y. pestis infection.
Prompt diagnosis and treatment with appropriate antibiotics are
essential. Streptomycin given intramuscularly is the drug of choice for treatment of
plague. The availability of streptomycin is often restricted so gentamicin is increasingly
used as an effective substitute. Tetracycline and chloramphenicol are acceptable
alternatives in many circumstances. Penicillins, cephalosporins, and macrolide
antimicrobials should not be used for treatment, as they have a less than optimal effect.
Plague is endemic in Utah and people living in rural or semirural areas
in plague-enzootic regions are at greatest risk for exposure. Most plague exposures occur
near where the patient lives. Often, members of the case household have unintentionally
provided rodents with sources of food and shelter. These animals can be infested with
fleas that are proven vectors of plague. Cats and dogs can also act as carriers for fleas
which are brought into homes. In addition to transporting potentially infectious fleas,
cats are very susceptible to Y. pestis infection and can place persons handling
these animals at risk of infection. A cat-associated human case of pneumonic plague
occurred in northern Utah in 1994. The patient had a pet cat which had disappeared for
about a week and returned with a draining lesion and wheezing. The recommendations in
Table 1 should be followed to reduce the risk of human plague.
| Table 1. Ways to Minimize Exposure to
Plague |
- Avoid sick or dead animals, especially rodents.
- Do not feed or attract rodents to your home, and eliminate
clutter and trash around the home that can harbor rodents.
- Stay away from rodent burrows and nests.
- Report rodent die-offs to local or state health departments.
- Prevent flea bites by using insect repellents, and tuck
pants into boots or socks to minimize openings into clothing.
- Do not allow pets to roam freely, and treat pets with
appropriate insecticidal flea powders or sprays.
- If you own a cat and live in a plague-enzootic area,
promptly take the cat, when sick, to a veterinarian.
- If you hunt or trap, wear rubber gloves when skinning game.
- If you develop fever and/or lymphadenopathy within 7 days of
a possible plague exposure, consult a physician immediately.
|
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Quarterly Report
of Diseases of Low Frequency
Year-to-Date January 1 - June 30, 2000
(including a comparison for same time period 1996 –1999)
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Monthly Morbidity Summary
June 2000 - Provisional Data
The Epidemiology
Newsletter is published monthly by the Utah Department of Health, Division of Epidemiology
and Laboratory Services, Bureau of Epidemiology, to disseminate epidemiologic information
to the health care professional and the general public.
Send comments to: The Bureau of Epidemiology, Box 142104, Salt Lake
City, UT 84114-2104, or call (801) 538-6191
Approval 8000008: Appropriation 3705
Rod Betit, Executive Director, Utah Department of Health
Charles Brokopp, Dr.P.H., Division of Epidemiology and Laboratory Services
Craig R Nichols, MPA, Editor, State Epidemiologist, Director Bureau of Epidemiology
Gerrie Dowdle, MSPH, Managing Editor
Connie Dean, Production Assistant
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