Bureau of Epidemiology
Bureau of Epidemiology June 2000 Utah Department of Health
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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

  • Seal all openings into your home that are greater than 1/4 inch.

  • Keep all weeds, woodpiles, and garbage at least 100 feet from your home.

  • Keep all food, including pet food, in rodent proof containers.

  • Keep kitchens and food preparation areas clean.

 

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

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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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