Minnesota Department of Health (MDH) Bug Bytes

April 15, 2010
Vol. 11: No. 3

Topics in This Issue:
1.  Cat-to-Human Tularemia Transmission
2.  West Nile Virus Summary
3.  Anaplasmosis Diagnostics
4.  E. coli O157:H7 Clusters – How Good Are We Doing?


1.  Cat-to-Human Tularemia Transmission

We just published a case report (Feb. 16 Zoonoses and Public Health) of a 2008 cat-to-human transmission of tularemia. Tularemia is a zoonotic disease caused by Francisella tularensis. It is transmitted from animals to humans through arthropod and horsefly bites, direct contact with infected animals, ingestion of contaminated food and water, and inhalation. It is not transmitted person-to-person. The incubation period in humans is 3 to 5 days (range, 2 to 14 days). Acute symptoms include sudden onset of high fever, chills, joint and muscle pain, headache, and nausea. Patients often present with an indolent ulcer at the site of inoculation and regional lymphadenopathy. There may be no apparent primary ulcer, but one or more enlarged lymph nodes that may suppurate. Pneumonia or septicemia may occur after inhalation of the organism or as a complication of the more common glandular or ulceroglandular forms.

Tularemia is generally considered to be a rural disease. Infection following contact with cats has been documented. Cats are infected through predation of infected rabbits and rodents.  In Minnesota, we see 0-3 human cases of tularemia annually, with just 6 cases (not including this case report) reported from 1994-2008.  All 6 cases occurred in Greater Minnesota. Vectorborne transmission was suspected for 3 cases (2 from fly bites and 1 from a tick bite), 2 cases reported wood sliver punctures, and for 1 the route of transmission was unknown.

In this report, a 5-year-old cat from the Twin Cities area was presented to a veterinarian with fever, ulcerations on the tongue and palate, lymphadenopathy, dehydration, and lethargy. It died 2 days later and lymph node and spleen specimens taken from necropsy tested positive for F. tularensis subsp. tularensis Type A (1 of 2 U.S. subspecies; associated with lagomorph/tick enzootic cycles). Upon interview of the cat’s owner, we found that he had been bitten and scratched while caring for and feeding the ill cat, and that he had malaise and fever, with onset 1 week after being scratched. He was advised to seek immediate treatment. An acute and convalescent serology was indicative of tularemia. We conducted an environmental search of a wooded area near the owner’s house where the cat was known to hunt but found no evidence of dead rabbits or rodents.

In the last month we have been investigating a case of tularemia in a dog from Greater Minnesota. There appears to be no human illness associated with the case. A culture taken from a pustule from the inner thigh of the dog was positive for the other Francisella subspecies, horlarctica (Type B). 

Learn more about: Tularemia>>
Learn more about: Disease Transmitted from Animals to Humans (Zoonosis)>>

2. West Nile Virus Summary

A recent MMWR Surveillance Summary (http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5902a1.htm) documented the first 10 years of West Nile virus (WNV) in the United States. Since WNV was first detected in 1999, it has become the leading cause of arboviral encephalitis in the United States. Approximately 80% of WNV infections are asymptomatic. Most symptomatic persons experience an acute systemic febrile illness that often includes headache, myalgia, or arthralgia. Less than 1% of infected persons develop neuroinvasive disease, which typically manifests as encephalitis, meningoencephalitis, meningitis, or poliomyelitis-like acute flaccid paralysis. Risk factors for developing neuroinvasive disease include older age and solid organ transplantation and might include other immunocompromising conditions, diabetes, and hypertension.

During 1999-2008, 28,961 confirmed and probable cases of WNV disease, including 11,822 (41%) WNV neuroinvasive disease, were reported from 47 states and the District of Columbia. No cases were reported from Alaska, Hawaii, Maine, or any U.S. territories. A total of 93% of all WNV cases had illness onset during July-September. Neuroinvasive disease incidence increased with increasing age, with the highest incidence (1.35 cases per 100,000 population) occurring among persons aged ≥70 years. The hospitalization rate and case-fatality ratio increased with increasing age among persons with neuroinvasive disease.

Non-mosquito WNV transmission through transfusions, transplanted organs, transplacentally from mother to fetus, and via exposure in a lab setting has been reported. Blood donation screening began in 2003 and has decreased but not eliminated WNV transfusion transmission. Through 2008, 10 breakthrough WNV transmissions occurred nationally from blood donations that had virus levels below the limit of detection. Since 2003, 61 WNV-viremic blood donors have been identified in Minnesota. Fortunately, no transfusion-associated cases of WNV disease have been reported here.

WNV has become endemic in Minnesota with disease risk greatest in western and central agricultural regions of the state. In the absence of an effective human vaccine, prevention will continue to be based on preventing exposures to mosquitoes through use of repellents, protective clothing, and avoidance of outdoor exposure at dusk and dawn when mosquitoes are most active. 

Learn more about: West Nile Virus (WNV)>>

3. Anaplasmosis Diagnostics

Human anaplasmosis (HA) is an acute febrile illness often accompanied by leukopenia, thrombocytopenia, or elevated liver enzymes. Its etiologic agent, Anaplasma phagocytophilum, is a rickettsia that forms distinctive morulae (aggregates) within granulocytes and is transmitted by Ixodes scapularis (blacklegged) ticks in Minnesota. Illness onsets in Minnesota peak from May to July, corresponding to peak nymphal I. scapularis feeding activity. Its incidence has increased greatly in Minnesota with 278 cases reported in 2008, a 54% increase over the median number of cases reported in 2004 through 2007.  Many clinical laboratories rely primarily on the identification of morulae in peripheral blood smears (PBS) to diagnose HA. We recently evaluated the potential for under-ascertainment and under-reporting of HA resulting from this practice.

From May-July 2007, a clinical laboratory in a highly HA-endemic Minnesota area identified a random sample of whole blood specimens that were tested by PBS at their laboratory. We tested the banked samples for A. phagocytophilum by PCR and reviewed associated medical records. Of 191 specimens received, 24 PBS-positive specimens also were positive for A. phagocytophilum by PCR (PBS+/PCR+), 28 smear-negative specimens were PCR-positive (PBS-/PCR+), and 139 specimens were both smear- and PCR-negative (PBS-/PCR-). PBS+/PCR+ patients had lower median platelet counts (83,700/µL vs. 148,000/µL, p < 0.001) and higher median AST values (108 U/L vs. 47 U/L, p=0.014) compared to PBS-/PCR+ patients. Compared to PBS-/PCR- patients, both PBS+/PCR+ and PBS-/PCR+ patients were older, were more likely to have fever, and had lower white blood cell counts, lower platelet counts, and higher AST levels. 

PCR testing was more sensitive than PBS for detection of HA cases, more than doubling the number of identified infections. A. phagocytophilum is markedly under-detected by PBS examination as a sole laboratory diagnostic method; therefore, HA is under-ascertained even when a physician suspects the disease. Among patients who tested positive by PCR, those with negative PBS findings had less severe disease based on clinical laboratory values.

Learn more about: Human Anaplasmosis (HA)>>

4. E. coli O157:H7 Clusters – How Good Are We Doing?

There is no question, and we have repeatedly demonstrated the benefit of molecular subtyping by pulsed-field gel electrophoresis (PFGE) of Escherichia coli O157:H7 (O157) in outbreak detection and investigations. We routinely subtype all O157 isolates, interview all cases in real time, and investigate all clusters of 2 or more cases. However, there is no consensus about when an O157 PFGE cluster warrants further investigation, and almost no data exists on characteristics of PFGE clusters that predict a common source will be identified.  We reviewed all O157 cases in Minnesota residents that were reported during 2000-2008.

As is our usual protocol all cases had been interviewed with a detailed standard exposure form. We defined a cluster as ≥2 O157 cases in different households with isolates of the same Xba1 PFGE subtype and specimen collection dates within 2 weeks. A cluster was considered solved if it led to the identification of a confirmed outbreak. Subtyping was performed on 1,163 O157 isolates, yielding 100 PFGE clusters. Forty outbreaks were confirmed, including 18 foodborne, 15 person-to-person, 5 animal contact, and 2 waterborne outbreaks. Twenty outbreaks were identified solely through PFGE subtype surveillance. Clusters of ≥3 cases were more likely to be solved than clusters of 2 cases. Clusters in which the first 2 isolates were received by us within 7 days of each other were more likely to be solved than clusters in which the first 2 isolates were received by us >7 days of each other. Twenty outbreaks were identified through means other than PFGE subtyping; 11 outbreaks among vulnerable populations (e.g. daycare attendees and long-term care facility residents) were identified through the routine follow-up of 1 case, and 9 outbreaks were identified through a call to us from a physician or the public.

Learn more about: Escherichia coli O157:H7 Infection (E. coli O157:H7)>>

Bug Bytes is a combined effort of the Infectious Disease Epidemiology, Prevention and Control Division and the Public Health Laboratory Division of MDH. We provide Bug Bytes as a way to say THANK YOU to the infection control professionals, laboratorians, local public health professionals, and health care providers who assist us.

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Updated Friday, November 19, 2010 at 02:16PM