Jonathan Sellman, MD, MPH

Vietnam War Dogs and an Unknown New Disease

Posted on June 17, 2015 | 1 comment

Most physicians are aware of the many medical advances developed by Army Medicine during wartime that are subsequently applied to patient care in the civilian realm. Contributions of Army Veterinary Medicine to civilian veterinary and human medicine is unfortunately often overlooked. This June marks the 99th year anniversary of the formal establishment of the U.S. Army Veterinary Corps by an Act of Congress on June 3, 1916. This watershed date brings to mind a piece of veterinary and medical history from the Vietnam War – a history that links an outbreak of canine disease in Southeast Asia to human disease in the United States. The story emphasizes the importance of collaboration between physicians and veterinarians.

USMC PFC Waldo Roame and his scout dog, Hobo, in action in 1968 during Operation Meade River, 13 miles southwest of Da Nang. More than 5,000 Marines participated in the cordon, the largest heli-based operation in Marine Corps history.
Photo Credit: USMC

Some History:
As in previous wars, US and Australian military forces used working dogs in a variety of capacities in the Vietnam conflict. These included scout, sentry, and tracker roles. At the end of 1968, 1,099 combat dogs were working for the US Army, Marines and Navy and the Australian armed forces in the Vietnam theater of operations. (Click here for a history of Vietnam War Dogs.)

Veterinarian, Capt. William T. Watson, on right, treating a scout dog, “Gunn,” wounded by shrapnel, at the 936th Vet Detachment War Dog Hospital, located at Tan Son Nhut Air Base. Nov 30, 1968
Photo Credit: Army Medicine.

US Army Veterinary units provided care to these animals, as well as performed other public health tasks in South Vietnam. In 1968, approximately 50 veterinarians were serving in South Vietnam across four tactical zones. (See map and table below. Click on the image for a larger version.)

An Outbreak Begins:
In September, 1968, veterinary units started treating dogs with epistaxis (bleeding from the nose). Epistaxis is profoundly unusual in dogs. And these dogs had severe outcomes. The first death was a sentry dog from the 212th Military Police Company stationed at Long Binh. As more cases occurred, it was recognized that nasal bleeding could be unilateral or bilateral. Affected dogs had vomiting with dehydration, weight loss, lethargy, lameness, and cutaneous bleeding (ecchymoses and petechiae). Clinical workup was notable for leukopenia (low white blood cell count) and progressive anemia. The disease inexorably led to death.

SP4 Francis Heyniger, lab technician, performing a WBC differential on a war dog at the 9th Med Lab, Long Binh, Vietnam.
Photo Credit: Army Medicine

The first cases of the disease were reported from units based at Long Binh, Chu Lai, Tan Son Nhut Air Base, and the area around Pleiku. By July 1, 1969, 160 fatal cases had been reported in 20 of the 22 US Army infantry scout dog platoons, all of the military police dog units, as well as some US Air Force and Marine dog units. Cases were reported from units throughout South Vietnam.

Epidemiologic observation led to the conclusion that the disease was being transmitted from dog to dog. All the sick animals had been kenneled together at two bases (Long Binh or Saigon) or had been exposed to sick dogs that had previously been at the two bases.

Tan Son Nhut Air Base was located Northwest of Saigon, South Vietnam. Inset, photograph of the air base in June, 1968.
Photo: Common Domain.

After September, 1968, all military dogs with epistaxis were referred to the 936th Medical Detachment at Tan Son Nhut Air Base located in southern Vietnam, Northwest of Saigon. (See Map and Photo Inset.) This was an attempt to avoid transmission of the disease from ill to healthy dogs. Because the etiology was unknown and the dogs died of hemorrhagic (bleeding) manifestations, the disease was initially named idiopathic hemorrhagic syndrome.

A thorough review of identified cases of the disease was conducted in January, 1969. Based on signs and symptoms, focus was on an unknown infectious cause. The “differential diagnosis,” the list of possible causes of the disease, included a diverse group of pathogens.

Routine blood cultures, which are used to identify bacterial pathogens, were negative, eliminating typical bacteria as a cause. The diagnostic focus turned to rickettsial, viral and hemoprotozoan pathogens.

Affected dogs were more likely to have been housed in kennels with heavy tick infestations. Researchers focused on a possible tick-borne pathogen. The Army veterinarians collaborated with researchers at Walter Reed Army Institute of Research. They drew blood from affected military dogs and inoculated test animals. These transmission studies showed disease could be transmitted by blood to beagles. On peripheral blood smears, Babesia was identified in the beagles.

Babesia: A tick-borne Protozoan Pathogen:
Babesia is a hemoprotozoan pathogen, similar to Plasmodium (which causes malaria) – both infect red blood cells causing anemia. However, Babesia is tick-borne and malaria is mosquito-borne. Multiple Babesia species infect a variety of mammal species. B microti, for example, is one species that infects humans and may cause disease, usually in immunocompromised or asplenic individuals, called babesiosis. Unfortunately, early experimental results suggesting Babesia infection were not consistently reproducible, nor was Babesia consistently found in affected dogs in Vietnam. This outbreak was not due to Babesia.

With further review, it was noted that an identical disease had broken out among French military dogs in Tunisia and, more recently, in 1963 among British military dogs working in Singapore. Furthermore, the US military had purchased Labrador retrievers from the British Army and imported them from Singapore to Vietnam in late 1966 and early 1967. Perhaps these dogs were a source of disease? The British had termed the disease tropical canine pancytopenia, so given they had first naming rights, further work on the disease was pursued under this moniker.

DL Huxsoll speculated the disease was due to Ehrlichia in 1969. By mid-1970, he and his colleagues at Walter Reed confirmed tropical canine pancytopenia was due to canine Ehrlichiosis, related to infection by Ehrlichia canis. Ehrlichia are intracytoplasmic bacterial pathogens, in other words, they live inside the cytoplasm of host cells. In this case, the organism lives inside the very white blood cells that would normally fight off infection. Ehrlichia can not be identified by routine blood culture, though clusters of the infecting bacteria can be visualized microscopically on peripheral blood smears. You have to know to look for these inclusions, though, otherwise they are easy to overlook. In the case of tropical canine pancytopenia, researchers found intracytoplasmic inclusions (called morulae) on peripheral blood smears of affected dogs. In this particular case, clusters of bacterial cells were seen in monocytes, characteristic of Ehrlichia canis. Dogs that were experimentally inoculated were also universally found to have Ehrlichia inclusions.

Monocyte infected with Ehrlichia.
Photo Credit: CDC

Tropical Canine Pancytopenia, AKA Canine Ehrlichiosis:
Canine ehrlichiosis had been recognized in Africa starting in the 1930s. In 1957, the infection was described in the New World for the first time, in the Netherland Antilles. And it was first described in the United States in 1962 when it was reported from Oklahoma. Walker, et al 1970, noted in a prescient comment regarding the Vietnam outbreak, “with modern air travel and international movement of pets, tropical canine pancytopenia might be a diagnostic problem outside of tropical and semitropical areas.”

In actuality, the organism was already there. Dr. Sydney Ewing received his PhD from Oklahoma State University based on his work studying canine Ehrlichiosis in Oklahoma. So the disease the British named tropical canine pancytopenia was not only tropical, it was the previously known disease, canine ehrlichiosis. Based on Ewing’s work on ehrlichiosis, treatment with the antibiotic tetracycline was tried in Vietnam. Tetracycline was not only used both to treat ill dogs, but also to treat apparently well dogs in a prophylactic effort to prevent disease. The epizootic slowed after institution of these measures.

The brown dog tick (Rhipicephalus sanguineus) is the vector of canine Ehrlichiosis. This tick was found in the kennels in Vietnam, and it is the most common tick found on dogs in the US as well. A cosmopolitan species, it is found pan-globally. As an aside I should note, that this tick only rarely bites humans.

Rhipicephalus sanguineus (the brown dog tick)
Creative Commons License:
Dantas-Torres, F. 2010. Biology and ecology of the brown dog tick,Rhipicephalus sanguineus. Parasites & Vectors 3:26

Veterinary researchers were on the forefront of discovering Ehrlichia and the pathogen’s epizootiology, describing the clinical manifestations of disease, and determining most effective treatment regimens. Researchers developed cell culture systems and “clean” tick colonies that were crucial to study of the infection.

Ultimately, it is estimated that some 200- 250 military dogs in Vietnam died from tropical canine pancytopenia. Impact of the disease was greater than just the number of canine casualties, however. Operational efficiency of canine units was significantly impacted by ill dogs that recovered. At the end of the war when military units were withdrawn from South Vietnam, there was great concern that re-patriating military dogs would spread the disease to the United States. Partly because of this concern, the majority of war dogs were left behind in Vietnam.

The Canine-Human Connection:
This would be an interesting veterinary mystery if the story stopped there, but in 1987, infection with E canis was described for the first time in a human. The infection was zoonotic, i.e. the infection occurred in animals as well as humans. Ehrlichia were not known to infect humans, other than a rare illness caused by Neorickettsia sennetsu (formerly E sennetsu) in Japan and Malaysia.

But there’s more: in 1991, human infection with another Ehrlichia species was described by BE Anderson and colleagues in a US Army recruit stationed at Fort Chafee, Arkansas. Named Ehrlichia chaffeensis after the US Army installation, the species is related to E canis and, similar to that pathogen, infects monocytes. Infection with E chafeensis causes an illness in humans similar to Rocky Mountain spotted fever, with fever and rash. The organism also infects dogs and goats. In contrast to the tick vector of E canis, E chaffeensis is transmitted by the bite of the lone star tick, Amblyomma americanum. The disease was named human monocytic ehrlichiosis.

Female adult Amblyomma americanum tick.
Common name: Lone star tick.
Photo Credit: Public Health Image Library, CDC

In the early 1990s, Johan Bakken and colleagues described a similar illness in humans in Minnesota and Wisconsin, far from the epicenter of human monocytic Ehrlichiosis in the central United States. The morulae, those intracytoplasmic inclusions, were found in granulocytes rather than monocytes. Symptoms of this new illness are somewhat similar to human monocytic ehrlichiosis, though without a rash. And yet another tick – the deer tick (Ixodes scapularis) – is the vector.

Female adult Ixodes scapularis tick.
Common name: Deer tick or black-legged tick.
Photo Credit: Public Health Image Library, CDC

Originally named Ehrlichia phagocytophila, this bacterial species has been moved based on molecular studies into another, closely related genus, and is now named Anaplasma phagocytophilum. Aside from identifying Ehrlichia canis in Oklahoma, Sydney Ewing also described another species, Ehrlichia ewingii, that infects dogs. In 1999, Buller et al described E ewingii infection in humans, so it too is zoonotic. A flurry of new diseases in humans and animals have been recognized in the wake of the outbreak of tropical canine pancytopenia in military dogs in Vietnam.
In Conclusion:
For decades, from the time Ehrlichia was first identified in Tunisia, the species existed in relative obscurity in the veterinary literature. As a result of a major outbreak of canine ehrlichiosis in Vietnam, US military and research veterinarians focused their attention on Ehrlichia. Directly because of the outbreak in Vietnam, the groundwork was laid for human medicine to recognize this fascinating group of vector-borne infections in people beginning in the 1980s. As tick-borne pathogens, Ehrlichia and Anaplasma infections are second only to Lyme disease in the number of people sickened annually. Earlier work of veterinarians paved the way to our understanding of these infections in humans. This is another parable of One Health, the integrative concept that the health of humans, animals, and the environment are connected.

(Click on table for a larger version.)

Acknowledgements:
I want to specifically acknowledge Dr. Sydney Ewing who first told me the remarkable story of canine pancytopenia in the late 1990s. His research has been crucial to our understanding of these diseases and I suspect I would not have ever heard the story of military war dogs and ehrlichiosis if it were not for meeting him.

The military history of tropical canine pancytopenia in Vietnam can be found in Dr. William Kelch’s master’s thesis cited below. His paper provided the military history of the epizootic, which is otherwise not found in the medical-veterinary literature.
References:

Anderson, BE, et al. 1991. Ehrlichia chaffeensis, a new species associated with human ehrlichiosis. J Clin Microbiol 29: 2838- 42.

Bakken, JS. 1998. The discovery of human granulocytic ehrlichiosis. J Lab Clin Med 132(3): 175- 80.

Buller, RS, et al. 1999. Ehrlichia ewingii, a newly recognized agent of human ehrlichiosis. N Engl J Med 341: 148- 55.

Chen, S, et al. 1994. Identification of a granulocytotropic Ehrlichia species as the etiologic agent of human disease. J Clin Microbiol 32(3): 589- 95.

Donatien, A & F Lestoquard. 1935. Existence en Algerie d’une Rickettsia du chien. Bull Soc Pathol Exot 28: 418- 19.

Dumler, JS, et al. 2005. Human granulocytic anaplasmosis and Anaplasma phagocytophilum. Emerg Infect Dis 11(12): 1828- 34

Ewing, SA, et al. 1971. A new strain of Ehrlichia canis. J Am Vet Med Assoc 159: 1771- 4.

Huxsoll, DL, et al. 1969. Ehrlichia canis- The cause of a haemorrhagic disease of dogs? Veterinary Record 85: 587.

Kelch, WJ. 1977. Military working dogs and canine Ehrlichiosis (tropical canine pancytopenia) in the Vietnam War. Fort Leavenworth, KS. (Available here.)

Maeda, KE, et al. 1987. Human infection with Ehrlichia canis, a leukocytic Ehrlichia. N Engl J Med 316: 853- 6.

Nims, RM, et al. 1971. Epizootiology of tropical canine pancytopenia in Southeast Asia. J Am Vet Med Assoc 158: 53- 63.

Smith, RD, et al. 1976. Development of Ehrlichia canis, causative agent of canine ehrlichiosis, in the tick Rhipicephalus sanguineus and its differentiation from a symbiotic richettsia. American Journal of Veterinary Research. 37: 119-126.

Walker, JS, et al. 1970. Clinical and clinicopathologic findings in tropical canine pancytopenia. J Am Vet Med Assoc 157: 43- 55.

1 Comment

Posted in Uncategorized

Tagged Anaplasmosis, Army Medicine, Canine disease, Dogs, Ehrlichiosis, Tick-borne disease, Vector-borne disease

Dogbites: Management of Infections, A Practical Blogpost

Posted on May 27, 2015 | Leave a comment

This past week was National Dogbite Prevention Week. Every year, more than 4.5 million people in the US are bitten by dogs. As an infectious diseases doc, I get involved only after prevention has failed: the patient is now in the ER after being mauled and I am called regarding post-bite infection prophylaxis, rabies prophylaxis, or (if the patient presents late and with infection) about appropriate antibiotic treatment for an infected bite. This post will detail my general approach to any bitewound and specifically focus on management of dogbites.

So, first let’s establish the legal rules of engagement: Don’t take anything stated here as medical advice and please consult a doctor if you have been bitten by any animal (including human). The internet is an inadequate source of medical information to treat yourself, family or friends.

General Approach for any Bitewounds, History:

When evaluating patients who have been bitten by an animal, it is vital to obtain detailed history of the attack. Such information is not only important to guide evaluation and treatment of the patient, but also is of legal importance. An animal bite case may proceed to a lawsuit for personal injury. And animal control may weigh whether the involved animal is a nuisance to be seized and destroyed.

Key aspects of the history of attack to be obtained:

Type of animal
Ownership of animal
Rabies vaccination history (of the animal and the bite victim)
Attack provoked or unprovoked
Health of animal: Is it in custody?

I’m not sure this mnemonic, TORAH, will make sense for others, but it has worked for me.

The provider also needs to obtain typical medical history of the patient-victim. I would note the special importance of the following items in the history, however:

Allergies
Medications with potential drug-drug interactions:

Coumadin
Digoxin
Carbamazepine
Calcium supplements
Ca or Mg containing antacids

Medical problems increasing risk of infectious complications:

Diabetes
Liver disease
Aplenia/ hyposplenia
Immunosuppression
Steroid use

Examination:

A focused examination of a patient who has been bitten by an animal should not overlook the possibility of occult injury. A thorough search should be conducted to assure no other wounds are present that escaped the patient’s attention.

Wounds should be accurately described or diagramed in the medical record. Special attention should be given to determine if there is neuromuscular compromise. Joint range of motion and tendon function should be assessed. Wounds should be probed. Even wounds that appear superficial may penetrate deep to bone.

Assessing for Bitewound Infection:
In the setting of a patient presenting late after the bite, careful assessment for infection should be performed including noting presence of purulent discharge, surrounding cellulitis, lymphangitis, and proximal lymphadenopathy. Wound cultures should be obtained from wounds that are clearly infected and from significant bite wounds due to animals other than cats and dogs. Do NOT culture dog or cat bite wounds that clinically do not appear infected. (Culture results will not inform decision making regarding choice of antibiotics in this setting.)
Imaging:
Imaging should be obtained on bitewounds in the following scenarios:

– Fracture is suspected
– Concern for foreign body (eg, embedded tooth)
– Potential for bone or joint involvement
Wound Management:
Wounds should be cleaned with normal saline. A variety of wound irrigation systems are commercially available, though at its simplest, an 18 or 19 gauge needle on a 35 cc syringe will do the trick. A splashguard protects from bloody spray. Use 100- 200 cc of saline for every 5 cm of wound length. Devitalized tissue should be debrided.

Avoid suturing bite wounds in the following settings:

Punctures
Bites to distal extremities (especially hands)
Bites of older age
> 6 – 12 hours on extremities
> 12 – 24 hours on the face
Human bite wounds

Monofilament suture is preferred over braided suture due to less infectious risk with the former. Subcutaneous sutures should be used sparingly.

Infectious prophylaxis:
Tetanus
Bitewounds, by definition, are tetanus prone wounds and tetanus prophylaxis needs to be considered. If the patient has received the three doses of the primary tetanus series and has received tetanus toxoid (Td) in the preceding 5 years, no tetanus prophylaxis is indicated. If it has been greater than 5 years since the most recent Td immunization, then Td should be administered. If the patient has not completed the three doses of the primary series (or if unknown), then the patient should receive Td (as well as complete the 3 dose series) and receive tetanus immune globulin.

Rabies
Rabies prophylaxis also needs to be assessed following a dog bite (as well as any mammalian bite). If in doubt, contact your state or local public health authorities for up to date guidance. If the attacking dog is suspected to be rabid based on behavior or if the attack was particularly ferocious with significant trauma and/or involvement of the head or neck, then Human Rabies Immune Globulin (HRIG) and rabies vaccine should be administered per standard protocol.
If there is low suspicion the dog is rabid and the animal is in custody, then it can be observed for ten days, watching for signs or symptoms of rabies. If no rabies in the 10 day time frame then the dogbite victim does not need rabies prophylaxis. If the animal develops symptoms, then Human Rabies Immune Globulin (HRIG) and rabies vaccine should be administered. If an attacking dog escaped and rabies determination cannot be made, then a phone call to public health authorities for guidance is reasonable. In most jurisdictions with ongoing epizootic rabies, rabies prophylaxis would be indicated given the fatal nature of human rabies infection.

Bacterial Infection
It is estimated that 5% of dogbites become infected. This is in contrast to catbites, where ~80% are estimated to become infected. Antibiotic prophylaxis for dogbites, should be considered based on the host and the severity of the mauling. If the patient has diabetes, immunosuppression, hyposplenism, or chronic immunosuppressive medications, antibiotic prophylaxis would be prudent. Additionally, even in the normal host, it is reasonable to prophylaxis a patient with extensive injuries.

Dogbite infections (like other bitewound infections) are polymicrobial. In the case of dogbites, the more important pathogens include:

Capnocytophaga canimorsus
Pasteurella canis
Staphylococcus aureus
Oral Streptococci
Neisseria spp.
Corynebacterium spp.
Moraxella spp.
Enterococcus spp.
Bacillus spp.
Fusobacterium spp.
Porphyromonas spp.
Prevotella spp.
Propionibacterium spp.
Bacteroides spp.
Peptostreptococci

Capnocytophaga canimorsus is of special importance in the asplenic or hyposplenic patient where it can cause overwhelming sepsis. Classically an eschar is present at the site of inoculation or bite. Disseminated intravascular coagulation is typical. Several years ago, I was involved in a case of a hospitalized patient with Capnocytophaga infection. He was a middle aged cirrhotic patient. His clinical course was impressive with overwhelming septic shock, renal and hepatic failure, purpura fulminans, peripheral dry gangrene with auto-amputation of the nose, ears, feet, and hands. He had an inexorable progression despite appropriate antibiotics administered in a timely manner from the point of his initial presentation for medical care. It was a humbling experience, demonstrating how futile our medical interventions can be.

Pasteurella species are an important cause of animal bite infections. P. canis occurs in dogs. P. multocida is typical in cats (including interestingly, not only housecats, but also big cats). It is relevant to consider these pathogens, because of their spectrum of antibiotic resistance. The species are resistant to cephalexin, dicloxacillin, clindamycin, and variably resistant to erythromycin.

Staphylococcus intermedius is an important canine zoonotic pathogen that can be acquired via bite. Medical microbiology labs may incorrectly identify the pathogen as Staph aureus, because S. intermedius is also coagulase positive. In contrast to S. aureus, however, S. intermedius has beta-galactosidase activity and fails to produce acetoin. Automated microbiology systems may incorrectly identify S. intermedius as methicillin resistant Staph aureus (MRSA). An astute clinician may need to speak to the microbiologist ’working up’ the specimen in order to pursue molecular techniques of identification in the setting of an appropriate canine exposure.

For empiric coverage of dog bite infections, oral amoxicillin-clavulanate or intravenous ampicillin-sulbactam are first line antibiotic options. In the penicillin allergic patient, clindamycin plus a flouroquinolone can be considered. In children, where a quinolone would be contraindicated, clindamycin plus trimethoprim-sulfamethoxazole is an option. Decisions regarding choice of antibiotics should always be informed by local resistance patterns, patient factors, and the patient’s specific culture results.

And for future prevention, the patient should be educated regarding dog bite prevention.

REFERENCES:

Abrahamian, FM & EJC Goldstein. 2011. Microbiology of animal bite wound infections. Clin Microbiol Rev 24(2): 231- 46.

Cummings, P. 1994. Antibiotics to prevent infection in patients with dog bite wounds: A meta analysis of randomized trials. Ann Emerg Med 23: 535- 40.

Gaastra, W & LJ Lipman. 2010. Capnocytophaga canimorsus. Vet Microbiol 140(3-4): 339-46.

Goldstein, EJC, DM Citron, and GA Richwald. 1988. Lack of in vitro efficacy of oral forms of certain cephalosporins, erythromycin, and oxacillin against Pasteurella multocida. Antimicrob Agents Chemother 32: 213-5.

Goldstein, EJC. 1992. Bite wounds and infection. Clin Infect Dis 14: 633- 40.

Holm, M and A Tärnvik. 2000. Hospitalization due to Pasteurella multocida-infected animal bite wounds: Correlation with inadequate primary antibiotic medication. Scand J Infect Dis 32: 181- 3.

Quinn, PJ, ME Carter, B Markey, And GR Carter. 1999. Clinical Veterinary Microbiology Mosby, New York.

Sacks, JJ, M Kresnow, and B Houston. 1996. Dog bites: How big a problem? Inj Prev 2: 52- 4.

Stevens, DL, et al. 2014. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis doi: 10.1093/cid/ciu296

Talan, DA, DM Citron, FM Abrahamian, et al. 1999. Bacteriologic analysis of infected dog and cat bites. NEJM 340: 85-92.

Talan, DA, et al. 1989. Staphylococcus intermedius: clinical presentation of a new human dog bite pathogen. Ann Emerg Med 18: 410- 3.

Talan, DA, et al. 1989. Staphylococcus intermedius in canine gingiva and canine-inflicted human wound infections: Laboratory characterization of a newly recognized zoonotic pathogen. J Clin Microbiol 27: 78- 81.

Another Month, Another Zoonosis: Plague in Colorado

Posted on May 8, 2015 | 5 comments

This month, the Morbidity Mortality Weekly Report and the New England Journal of Medicine reported a cluster of pneumonic plague that occurred in Colorado during the summer of 2014.

Yersinia pestis on blood agar plate (left) and chocolate agar plate (right).
Source: CDC Public Health Image Library.
Common Domain.

For a review of plague and its forms (bubonic, septicemic, and pneumonic), please refer to the CDC webpage.

There are several points to be made about this outbreak.

(1) This outbreak is the largest pneumonic plague epidemic in the United States in 90 years. The index case was a dog. The dog’s owner, two veterinary employees, and a companion of the dog’s owner became ill. Pneumonic plague is rare. Of reported cases of plague in the United states, over 80% have been bubonic. It’s a lucky thing that pneumonic plague is rare because it is the most dangerous form of the disease from an epidemiologic perspective. Patients with pneumonic plague can spread the bacterial infection person-to-person via droplets (produced with coughing for example). This can lead to rapid amplification of case numbers.

(2) The automated blood culture system misidentified the bacteria cultured from the index human patient. Rather than correctly identifying it as Yersinia pestis, the machine misidentified it as Pseudomonas luteola. This resulted in a delay of diagnosis. Errors in the identification of Y. pestis by automated blood culture systems have previously been described. This highlights the risk of relying solely on sophisticated equipment to identify pathogens without the ability to perform traditional microbiological and biochemical methods of bacterial identification.

(3) Plague is enzootic to the American Southwest and West. (See map.)

Source: CDC
http://www.cdc.gov/plague/maps/

The diagnosis of plague needs to be considered in the differential of patients who present with lymphadenitis, undifferentiated septicemia, and community acquired pneumonia in the context of exposure to ill animals. The risk of transmission from pets is greatest with cats. Dogs are a rare source of plague in humans.

(4) Y. pestis is a potential agent of bioterrorism, listed as a category A agent by the CDC. As such, plague may need to be considered in the differential anytime there is an unusual cluster of severe illness or progressive pneumonia.

(5) This case again highlights the importance of communication across health specialties including veterinary medicine, human medicine, public health, and ecology / wildlife biology.

REFERENCES:

Foster, CL, et al. 2015. Sick as a dog. NEJM 372(19): 1845- 50.

Gage, KL, et al. 2000. Cases of cat-associated human plague in the Western US, 1977- 1998. Clin Infect Dis 30:893- 900.

Gould, LH, et al. 2008. Dog-associated risk factors for human plague. Zoonoses Public Health 55:448- 54.

Kool, JL. 2005. Risk of person-to-person transmission of pneumonic plague. Clin Infect Dis 40:1166- 72.

Kugeler, KJ, et al. 2015. Epidemiology of human plague in the United States, 1900-2012. Emerg Infect Dis 21:16- 22.

Nichols, MC, et al. 2014. Yersinia pestis infection in dogs: 62 cases (2003–2011). J Am Vet Med Assoc 244:1176- 80.

Runfola, JK, et al. 2015. Outbreak of Human Pneumonic Plague with Dog-to-Human and Possible Human-to-Human Transmission- Colorado, June–July 2014. MMWR 64(16): 429- 34.

Wang, H, et al. 2011. A dog-associated primary pneumonic plague in Qinghai Province, China. Clin Infect Dis 52:185- 90.

5 Comments

Posted in Uncategorized

Tagged Plague, Yersinia, Zoonosis

Glanders

Posted on April 16, 2015 | Leave a comment

Glanders is in the news. Recently, the Texas Animal Health Commission confirmed the disease in a Mexican donkey which strayed across the southern US border.

Glanders is a nearly forgotten bacterial disease of equids (horses, donkeys, mules) that can also cause infections of other animals as well as humans. Identification of glanders in a donkey in the US is significant because this is the first naturally occurring case of equine glanders in the US since 1942.

Burkholderia mallei on blood & chocolate agar plates.
CDC Public Health Image Library.
Public Domain.

Glanders is a disease of antiquity described by Hippocrates and the Romans. It is caused by a Gram negative rod, Burkholderia mallei, and is an obligate pathogen of mammals (ie, there is no environmental reservoir). I am always amazed to think of a disease that has survived millennia hopping from host to host in an unbroken chain. To think the bacteria infecting this Mexican donkey may be descended from bacteria that felled horses in the time of the Caesars – incredible!

The genus Burkholderia includes 3 significant pathogens: B. mallei, B. pseudomallei, and B. cepacia. (See separate text box.)

Table 1: Other Burkholderia species

Because of the organism’s proclivity towards infection of draft animals, B. mallei became a potential weapon of war. At a time when horses were crucial to military campaigns, both for cartage and cavalry, an outbreak of glanders among horses could devastate military readiness and alter the course of battle. Glanders was widespread among the horses of both sides during the American Civil War (Sharrer, 1995).

US Army Veterinary Hospital No. 11, Gievres, France, WW 1.
Testing horse for glanders.
Source: National Library of Medicine.
Common Domain.

The disease was suspected to have been used as a biological agent in both World Wars One and Two. The United States actively researched glanders as a biological warfare agent beginning in the 1940s. (Sidell, FR, ET Takafuji, and DR Franz, eds. 1997). Despite accusations, and some evidence of use, the ultimate outcomes of the these wars were not affected by attempts at biological warfare.

Though the disease was eradicated from the United States in 1942, infections have occurred among laboratory workers since then. An illustrative (and relatively recent) case occurred in May, 2000, when a microbiologist working at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) initially presented with a left axillary mass and fevers. He was treated with an intra-muscular injection of ceftriaxone and a 10 day course of cephalexin, but he continued to be ill with fevers, fatigue, night sweats, malaise, and weight loss. He was prescribed a 10 day day course of clarithromycin, but his symptoms continued and he developed abdominal pain. A subsequent CT scan documented multiple hepatic and splenic abscesses and culture of a liver aspirate yielded B. mallei. (Anon. MMWR 49(24): 532- 5.)

Despite eradication of the disease in the United States, the disease continues to be enzootic in Central and South America, Asia, Africa, and the Middle East. Thus there is the risk in the US of imported animal and human cases. Infectious diseases thought to have been successfully eradicated may re-emerge from areas of endemnicity. In this case, a wayward infected donkey crossed from Mexico into Texas.

Diseases of low incidence (and even thought eradicated) should not be forgotten despite the low likelihood any particular clinician will see one of these diseases in clinic. Yes, if you hear hoofbeats, think of horses – but that does not mean you should forget that zebras are out there. As an example, in my clinical practice I have managed three cases of Hanson’s disease (leprosy) in the past five years. Yes, the disease is rare – especially in Minnesota – but leprosy continues to affect people worldwide. Healthcare workers (of the veterinary and human sort) should consider diseases in the differential that are rare – one may quickly eliminate them based on probabilities – but they need to be considered.

And finally, a number of rare to relatively rare zoonotic diseases are potential agents of bioterrorism. (See table below.) Public health, veterinary, and human health care workers need to maintain vigilance for these infections because of this potential nefarious use. A human or animal case of glanders would be notifiable to public health authorities, including the OIE (World Organization for Animal Health).

REFERENCES AND FURTHER READING:

Anonymous. Laboratory acquired human glanders – Maryland, May 2000. MMWR 49(24): 532- 5. June 23, 2000.

CIDRAP: Glanders and melioidosis.

Khan, I, et al. 2013. Glanders in animals: A review on epidemiology, clinical presentation, diagnosis and countermeasures. Transboundary and Emerging Diseases 60: 204- 21.

Larsen, JC and NH Johnson. 2009. Pathogenesis of Burkholderia pseudomallei and Burkholderia mallei. Military Med 174: 647- 51.

OIE Technical Disease Card: Glanders.

Sharrer, GT. 1995. The great glanders epizootic, 1861-1866: A Civil War legacy. Agricultural History 69(1): 79-97.

Van Zandt, KE, MT Greer, and HC Gelhaus. 2013. Glanders: An overview of infection in humans. Orphanet J Rare Diseases 8: 131- 7.

Sidell, FR, ET Takafuji, and DR Franz, eds. 1997. Medical aspects of chemical and biological warfare. Office of the Surgeon General, Dept of the Army.
OTHER WEBLINKS:

New York Dept of Health Glanders Page.

CDC Glanders page.

Merck Manual link on glanders

Equuus Magazine news article on glanders.

Calvin Schwabe

Posted on March 13, 2015 | 1 comment

Today’s post is in honor of Calvin Schwabe who was born on March 15, 1927. He died June 24, 2006.

Calvin Schwabe, DVM
Source: UC Davis Vet School, http://www.vetmed.ucdavis.edu/onehealth/about.cfm
?Original photo from CDC?

Schwabe, as a veterinarian, is sadly unknown to most physicians. This should be rectified. He is considered the “father of modern epidemiology.” In a career that spanned 52 years, he made crucial and astute linkages between animal health, human health, and the environment. Current healthcare providers would benefit greatly from his perspective of these interrelationships.

For ten years (1956- 1966) he was on the faculty at the American University of Beirut. His research focused on parasitic zoonoses, including hydatid disease which was (and remains) endemic in the mideast. In 1966, Schwabe returned to the United States and was one of the founding members of the University of California Davis veterinary school. He established the Department of Epidemiology and Preventive Medicine – the first such department in a veterinary school in the world. The program offered the first graduate degree in preventive veterinary medicine and is a model replicated at numerous other veterinary schools.

Veterinary Medicine and Human Health, 3rd edition
Calvin Schwabe, DVM

He first published his seminal work, Veterinary Medicine and Human Health, in 1969. Though animal and human medicine was historically seen as united until modern times, it was Schwabe and his textbook that revived the view that veterinarians, physicians (and public health workers) are all toiling at the same task.

I was introduced to Schwabe and Veterinary Medicine and Human Health, by Dr. Marguerite Pappaioanou when she was faculty at the University of Minnesota’s School of Public Health. Marguerite is one of many pupils of Schwabe who are now leaders in public health, epidemiology, and veterinary medicine. Some ~12 years ago, I met Marguerite to discuss my interest in conservation medicine. In a conversation that remains a pivotal point in my educational career, she told me about Schwabe and the history of One Health. She showed me her copy of Vet Med & Human Health. I was thrilled. I was subsequently able to buy a used copy of the 3rd and final edition of the book (published in 1984). It remains one of my most valued science/ medicine texts.

Schwabe’s influences can be seen in burgeoning global One Health efforts. It is not a coincidence that the 3rd International One Health Congress starts on the anniversary of his birth. One Health teaching programs are flourishing at veterinary schools and the One Health approach is pursued by governmental and non-governmental agencies working to improve quality of life globally. Unfortunately, physicians and medical schools have been slow to understand the value of the One Health model. I would hope that this oversight will be rectified.

REFERENCES/ LINKS:

Calvin Schwabe One Health Project

Calvin W. Schwabe

In Memorium, University of California.

1 Comment

Posted in Uncategorized

Tagged One Health

Bald Eagles and Aquaria

Posted on February 24, 2015 | Leave a comment

I am currently on a 3 week stint on the inpatient consultation service, necessitating a brief blog post this week.

If you haven’t read my previous post, How vultures, cattle, and a minority religious sect are interconnected, I ask you read that post before this one.

Bald Eagle
Creative Commons Attribution Share Alike: Eric Frommer. Wikipedia.

I wanted to follow-up my Vultures… post, with a story from the United States about a similar mystery: an emerging, occult disease affecting another raptor, the bald eagle.

In 1994, unexpected mortality was noted among bald eagles (Haliaeetus leucocephalus) in Arkansas’ lakes, including De Gray Lake.

Necropsies were conducted on dead birds at the USGS National Wildlife Health Center in Madison, WI. Pathologist Dr. Nancy Thomas described the characteristic pathologic finding: intramyelinic edema. Swelling (or edema) was noted within myelin sheaths of the nerve tracts. Myelin sheaths are the insulation encompassing the nerves, somewhat like the brightly colored plastic insulating copper wire in your electronic devices. You mess with myelin and, in essence, the brain short-circuits. In the case of these birds, lesions were found primarily in the cerebellum (a part of the brain that coordinates movements) and in the optic tectum (an area of the midbrain that coordinates movement to visual inputs.) As would be expected from deficits in these areas of the brain, afflicted birds had trouble flying, including an inability to land on a perch. Birds behaved as though drunk. They eventually appeared blind and would collide with objects. Most birds died, though some were able to recover. The syndrome was termed Avian Vacuolar Myelinopathy and abbreviated AVM. (Link)

No existing infectious agent or toxin was known to create this unique pathologic lesion. The search was on to identify a new culprit killing the eagles.

American coot.
Creative Commons Attribution Share alike License: Connormah. Wikipedia.

Over the next three years, American coots (Fulica americana) were also noted to be affected. Necropsies on these birds showed similar pathology. The coots became easy prey for eagles, so one explanatory hypothesis was a toxin or infection transmitted up the food chain from coots to eagles. And, indeed, Fischer and colleagues, in a small feeding study, were able to demonstrate this using 6 red tailed hawks (Buteo jamaicensis). Five red tailed hawks were fed coots affected by AVM (ie, tainted meat). One red tail was fed coots not apparently affected by AVM (ie, USDA Grade A). All five hawks fed the tainted coots were found to have AVM lesions on necropsy, whereas the one red tailed hawk fed the Grade A coots did not develop the pathologic findings of AVM. Though a small study, this did suggest transmission of the syndrome via the food chain.

Dodder et al (2003) examined potential environmental toxins as a cause of AVM. They compared sediments from affected sites and non-affected sites for specific chemical compounds including polychlorinated biphenyls, octachlorodibenzo-p-dioxin, polycyclic aromatic hydrocarbons such as retene, penta- and hexa-chlorobenzene, oxychlordane, p,p’-DDE, and dieldrin. There was no significant difference in the concentrations of these chemicals between sites, arguing against these chemicals being the cause.

Afflicted birds caged in proximity to unaffected birds did not acquire the syndrome, arguing against an infectious pathogen.

Where AVM was found in birds, the waterways were choked with invasive, exotic aquatic plant species. The lakes, rivers, and reservoirs were dominated by several species:

Eurasian watermillfoil (Myriophyllum spicatum) is a species native to Europe, Asia, and North Africa that was introduced into US waterways sometime between the 1880s and 1940s. It is uncertain whether it arrived as a hitchhiker in ship’s ballast water or if it escaped from the aquarium trade.

Brazilian elodea (Egeria densa) was imported from South America and was introduced in US waterways in 1893. All of the plants found in the US are male, but they spread when by fragments of the plant hitch a ride on boats.

And, finally, Hydrilla (Hydrilla verticellata). Yes, what sounds like a 1960s Japanese monster of the likes of Godzilla and Mothra, is an invasive aquatic plant from Asia. The plant was imported to the US as part of the aquarium trade but was subsequently introduced into US waterways in the 1950s.
All three of these invasive species are transported from one waterway to another primarily as hitchhikers on boats and boat motors. They outcompete native aquatic plants, overgrow the water table and choke the water column of oxygen.

Hydrilla verticillata collection on Lake Seminole, FL.
Common domain. Stephen Ausmus, USDA

Cyanobacteria (also known as blue-green algae) often live in dense mats of submerged vegetation, affiliated with plants such as these aquatic species. And cyanobacteria are known to produce neurologic toxins. But studies did not reveal any blooms of known toxic cyanobacterial species.

Ultimately, attention focused on a novel cyanobacterial species growing on the underside of Hydrilla leaves. This previously undescribed species was found in all 19 sites where AVM has been described in birds across six southern states (Arkansas, Texas, Florida, Georgia, South Carolina, and North Carolina).

Hydrilla verticillata.
Common domain. USDA.

Toxicologic testing was performed on chickens and farm raised mallards fed field-collected Hydrilla containing the identified cyanobacterial species and AVM was reproducibly produced. This has clinched the cause of AVM.

This cyanobacterium is completely new, representing not only a new genus and species, but a new family as well. (Wilde, et al, 2014)

The organism has been named Aeokthonas hydrillicola; Aetokthonos is Greek and translates to ‘eagle-killer’ and hydrillicola is Latin for ‘lives on hydrilla.’ This novel toxic cyanobacterium is a new threat associated with exotic, invasive species. This is another reminder that invasive species continue to wreck havoc in environments where they do not belong. I would direct people’s attention to the “Get Habitattitude” campaign of the US Fish and Wildlife Service/ NOAA’s Sea Grant/ Pet Industry Joint Advisory Council. Non-native plants and animal pets should not be released into the environment or flushed down the toilet (a la Nemo, the fish star of the Disney film). And boaters need to clean all recreational equipment of potential exotic hitchhikers. See this MN DNR website for helpful instructions.

Ominously, the A. hydrillicola toxin has been shown to not only affect birds but also fish (grass carp) and herbivorous turtles. And it is expected to continue to expand its range across the south. Time will tell what impacts it will have on waterfowl and raptors.

REFERENCES AND FURTHER READING:
Dodder, NG, B Strandberg, T Augspurger, & RA Hites. 2003. Lipophilic organic compounds in lake sediment and American coot (Fulica americana) tissues, both affected and unaffected by avian vacuolar myelinopathy. Science of the Total Environment 311: 81-89.

Fischer, JR, LA Lewis-Weis, & CM Tate. 2003. Experimental vacuolar myelinopathy in red-tailed hawks. Journal of Wildlife Diseases 39: 400- 6.

Wilde, SB, et al. 2014. Aetokthonos hydrillicola gen. et sp. nov.: Epiphytic cyanobacteria on invasive aquatic plants implicated in Avian Vacuolar Myelinopathy. Phytotaxa 181(5): 243- 60.

How vultures, cattle, and a minority religious sect are interconnected.

Posted on February 12, 2015 | 2 comments

Work with me here. I need to tell a circuitous story.

Gyps indicus vultures in the nest, Orchha, Madhya Pradesh.
Source: Yann (talk), Wikipedia.
Creative commons Attribution Share-alike.

Gyps vultures belong to a genus of Old World vultures that, depending on species, range from south Asia across southern Europe and northern Africa. Beginning in the 1990s, researchers noted a significant decline in Gyps species in India. And when I say significant, I am talking about a major loss in population: 95% or more of the birds disappeared over a decade. Ten million vultures were gone. Ecologically this was unprecedented.

I became aware of the loss of these vultures when the story was reported May 30, 2000 by ProMED. (See comment on ProMED in endnote.) Andrew A. Cunningham, a veterinary pathologist with the Zoological Society of London, reported his findings:

“I recently spent three weeks investigating vulture mortality in India at
the request of the Bombay Natural History Society (BNHS) and in
collaboration with, and funded by, the Royal Society for the Protection of
Birds (RSPB). Over the past ten years, populations of Gyps spp. vultures
have declined catastrophically – in at least some areas their numbers have
been reduced by about 96% – and the decline is still continuing.”

Ill vultures were noted to sit on tree branches with drooped necks. Deborah Pain of Britain’s Royal Society for the Protection of Birds, described, ”you see them slumped on tree branches everywhere. And then they just fall off, dead.”

The cause of the disease was unknown, but both a toxicologic cause (a pesticide?) and an infectious cause (a virus?), were theorized. A novel avian virus, perhaps introduced due to the expansion of the Indian poultry industry, was thought to be a possible cause. But no one knew, which was extremely frustrating given the consequential impacts the outbreak was having on the population.

Indian white-rumped vulture (Gyps bengalensis).
Image: Goran Ekstrom, Gross L, PLoS Biology Vol. 4/3/2006, e61 http://dx.doi.org/10.1371/journal.pbio.0040061
Creative Commons.

Birds affected included the Indian white-rumped vulture (Gyps bengalensis) which was previously the world’s most common bird of prey.

Indian Vulture (Gyps indicus) in flight, Ramanagara, Karnataka.
Image: Vaibhavcho. Wikipedia.
Creative Commons.

Additional vulture species affected included the Indian Vulture (Gyps indicus) and the slender-billed vulture (Gyps tenuirostris). Imagine birds as common as our American Crow suddenly disappearing from the skies. And disturbingly, ornithologists had no idea why.

Range map of three Gyps species in South Asia.
Image: Shyamal. Wikipedia.
Common domain.

Whatever the cause, the problem was spreading. Vulture population declines were soon noted in Pakistan and Nepal as well. The griffon vulture (Gyps fulvus) has a range that spans the Indian subcontinent across the mideast and into parts of southern Europe and west Africa. Would it be infected by the same presumed virus? Ecological implications of the epidemic spreading into Europe and Asia were horrifying.

Vulture declines triggered two sets of cascading ecological and cultural impacts. Normally, vultures provide an essential ecological service, scavenging and disposing of animal remains. Animal carcasses that would have been consumed by vultures now lay rotting in the sun. Loss of the major scavenger species led to a surplus of food (and I use the term loosely) for other scavenger animals. Of greatest concern was the potential for a population explosion of south Asia’s feral dogs, many of whom carry rabies. More rabid dogs, ultimately, means more people being bitten and subsequently dying of rabies. Too few know that once a person has symptoms of rabies, the disease is essentially universally fatal. Thanks to a robust veterinary and public health infrastructure, rabies is under good control in the United States. However, rabies remains the 10th most common infectious disease cause of death worldwide. An estimated 50,000 to 60,000 people die of rabies annually, with 20,000 to 30,000 deaths in India alone. A 2008 study (Markandya, et al) estimated that excess rabies cases attributable to the vulture decline cost the Indian economy $34 billion over the 14 years 1993–2006.

The second set of cascading impacts was cultural. We should pause and discuss the religious and ethnic Parsee of India who practice Zoroastrianism. This is a monotheistic faith that originated in Persia (now Iran) in the 6th century BCE. The faith influenced the beliefs of other monotheistic religions including Islam, Judaism and Christianity. Zoroastrians fled Iran after invasion by Islamic armies and the first Caliphs. In the 9th Century CE, a group of Persian Zoroastrians fled to India. Parsee means Persian in the Farsi language and thus Persian Zoroastrians became known as Parsee. They survive as a tiny minority in India, though this is the largest population in any country in the world. Within India, the Parsee population is centered in Mumbai.

Parsee Tower of Silence, Bombay (Mumbai), India.
Note vultures perched on the wall of the tower.
Image: Frederic Courtland Penfield, Wikipedia.
Common domain.

According to Zoroastrian beliefs, fire, water, earth, and air are sacred elements to be preserved. As a result, burial or cremation of the dead is considered unclean. The Zoroastrian funerary practices instead involve disposing of the dead in a dakhma or ossuary where the body is laid out to be cleaned of the flesh by vultures. The feeding of one’s body to birds is the final act of charity before leaving this world for the next. In India, these funeral sites were built as towers and came to be known as “Towers of Silence.” A dakhma that serves the needs of India’s largest single Parsee population in Mumbai is located in Doongerwadi – 54 acres of forest surrounded by urban sprawl.

But what happens when the birds who facilitate one’s passage to the afterlife have disappeared? A three thousand year old burial tradition was upended in a decade. In some dakhma, nonexistent vultures have been replaced by solar concentrators which desiccate the corpse consistent with the prohibition on defiling fire, water, earth, and air. In other dakhma, the solar solution is reported not to have worked. The cultural impacts of this sudden change on a central rite of one’s faith are hard to overstate.

Meanwhile, in 2002, J. Lindsay Oaks, a veterinary pathologist at Washington State University- Pullman, investigated the population decline impacting Gyps bengalensis in Pakistan as part of a project supported by the Peregrine Fund and the Ornithology Society of Pakistan, with logistical support from Bahauddin Zakariya University and the Pakistani National Council for Conservation of Wildlife. He reported to ProMED grim findings from Pakistan troublingly similar to those in India:

“Field studies over the last 2 years in the Punjab Province indicate significant population declines (up to about 80 percent) associated with high adult mortality rates (11-27 percent).”

An intriguing pathologic finding noted in three-quarters of the examined vultures was the presence of urate crystals on the birds’ internal organs consistent with visceral gout. Either an infectious agent or a toxic chemical was killing the vultures. Examining the kidneys, the birds had acute kidney failure with uric acid crystals in the tubules. Inflammatory changes were not consistently present. This suggested a toxic-metabolic rather than infectious cause. Additionally, an infectious work-up did not identify pathogens associated with avian kidney disease. Multiple chemical agents were ruled out based on testing.

The research team hypothesized veterinary drugs might be the cause. Vultures ingested the meat from dead cattle – perhaps the birds were exposed to pharmaceuticals administered to cattle prior to their death. The team surveyed local veterinarians regarding what drugs they used to treat cattle and identified a single drug commonly associated with kidney toxicity: diclofenac. Diclofenac belongs to the group of pharmaceutical drugs known as the nonsteroidal anti-inflammatory drugs or NSAIDs. This drug class includes common medications used by both medical and veterinary practitioners, such as ibuprofen. Oaks and his colleagues tested 25 birds for diclofenac and all 25 had significant concentrations of the drug. Furthermore, by testing Gyps bengalensis birds that had been injured and could not be returned to the wild, they confirmed a dose response of the exposure.

Diclofenac was identified as the principle cause of the vulture declines. Oaks presented his group’s research findings at the World Conference on Birds of Prey and Owls, held on 18-23 May 2003 in Budapest, Hungary. Eventually, in 2006, the governments of India, Pakistan and Nepal banned the manufacture of diclofenac. Pharmaceutical firms are instead promoting an alternative NSAID, meloxicam, which is safe for vultures. Unfortunately, decline in vulture populations continues, though at a slower rate. Three species of Gyps vultures are critically endangered and may still go extinct in the wild.

Fortunately, North American vultures appear to suffer none of the toxicity that Gyps vultures experience. (Ref: Dr. Pat Redig, Raptor Center, University of MN, per. comm. 2/11/2004.)

Conclusion: One Health
This story illustrates interconnections between human health, animal health, and ecological health. Introduction and widespread imprudent use of a veterinary NSAID for the treatment of cattle (a domesticated species) had cascading, interconnected ecological and cultural impacts. Feeding on cattle carcasses, Gyps vultures (a wildlife species) ingested diclofenac residues and suffered high rates of mortality due to visceral gout. Loss of vultures represented a collapse of species diversity and the near loss of an entire trophic level in the south Asian ecosystem. Feral dogs filled the trophic gap with resulting population growth. Incidence of dogbites increased and cases of humans exposed, infected, and killed by rabies increased. Aside from the immeasurable human costs of suffering and death, the fiscal costs of responding to rabies is notable. And 20 years of diclofenac use forced the Parsee to abandon funerary traditions practiced for 3,000 years.

What is the lesson here?
Development of new pharmaceuticals involves multiple research steps from the basic science laboratory to trials conducted in clinical settings. Even after FDA drug approval, post-marketing research will identify adverse reactions not seen in clinical trials. I have the utmost respect for researchers who navigate these labyrinthine protocols and regulations. Such regulations protect healthcare consumers from adverse drug effects and they have been generally effective in this goal.

Yet pharmaceuticals may impact species aside from the intended human recipient. In the case of diclofenac, the drug was being used for veterinary purposes, yet sickened vultures. Drug manufacturing has been documented to lead to contamination of effluent waters with antibiotics (as one example). And every day millions of people follow their doctor’s orders, ingest medications, and then urinate active drug and drug metabolites into our waterways. The traditional research and regulatory regimes for pharmaceutical drug approval typical do not consider such downstream environmental impacts. I would argue it is time to change that myopic focus.

ENDNOTE:

If you have not heard of ProMed or used the website, I invite you to take a look. ProMED, the Program for Monitoring Emerging Diseases, is a web based reporting system for disease outbreaks and not just for human diseases; ProMed also reports animal and plant disease outbreaks. The site was established in 1994 with the support of the Federation of American Scientists and SATELLIFE, but since 1999, has operated as a program of the International Society for Infectious Diseases.

REFERENCES AND SUPPLEMENTAL READING:

Cunningham, AA, V Prakash, D Pain, et al. 2003. Indian vultures: victims of an infectious disease epidemic? Animal Conservation 6: 189– 97.

Green, RE, I Newton, S Schultz, et al. 2004. Diclofenac poisoning as a cause of vulture population declines across the Indian subcontinent. J Applied Ecology 41(5): 793- 800.

Gross, L. 2006. Switching drugs for livestock may help save critically endangered Asian vultures. PLoS Biology 4(3): e61. DOI: 10.1371/journal.pbio.0040061

Karkaria, B. 2015. Death in the city: How a lack of vultures threatens Mumbai’s ‘Towers of Silence’ Guardian. (Link)

Markandya, A, T Taylor, A Longo, et al. 2008. Counting the cost of vulture decline- An appraisal of the human health and other benefits of vultures in India. Ecological Economics 67: 194- 204. (Link)

Oaks, JL, M Gilbert, M Virani, et al. 2004. Diclofenac residues as the cause of population decline of vultures in Pakistan. Nature 427: 630– 3.

Prakash, V. 1999. Status of vultures in Keoladeo National Park, Bharatpur,
Rajasthan, with special reference to population crash in Gyps species.
Journal Bombay Natural History Society 96(3): 365- 78.

Prakash, V, DJ Pain, AA Cunningham, et al. 2003. Catastrophic collapse of Indian white-backed Gyps bengalensis and long-billed Gyps indicus vulture populations. Biological Conservation 109: 381– 90.

Prakash V, MC Bishwakarma, A Chaudhary, et al. 2012. The population decline of Gyps vultures in India and Nepal has slowed since veterinary use of diclofenac was banned. PLoS ONE 7(11): e49118. doi:10.1371/journal.pone.0049118

ProMed. The Program for Monitoring Emerging Diseases. http://www.promedmail.org

Shultz, S, HS Baral, S Charman, et al. 2004. Diclofenac poisoning is widespread in declining vulture populations across the Indian subcontinent. Proceedings of the Royal Society of London B (Supplement), in press. DOI: 10.1098/rsbl.2004.0223

2 Comments

Posted in Uncategorized

Tagged Cattle, Diclofenac, Ecotoxicology, India, Nepal, One Health, Pakistan, Parsee, Vultures, Zoroastrianism

What are the benefits of immunization?

Posted on February 1, 2015 | 1 comment

The recent outbreak of measles has triggered a number of questions about vaccination, public health, and herd immunity. As I have fielded questions from patients, family, and friends about vaccination, I have come to realize this is an area ripe for a bit more detailed discussion.

What are the benefits of immunization? At first glance this seems like an obvious question, but it is more complex than many realize. Depending on the shot, it may provide one or more benefits.

Let’s review why we vaccinate.

IM Vaccination, 1977.
CDC Public Health Image Library.
Common domain.

1st: Vaccination prevents illness in the vaccinated. I think this is the most obvious purpose of vaccination and what most people assume when we talk about the benefits of vaccination.

Example: You don’t want to get tetanus so you get vaccinated for tetanus.

Tetanus (commonly called lockjaw) is caused by a ubiquitous pathogen, Clostridium tetani, that is found in soil and on rusty nails. It sits in wait to be inoculated into your foot when you step on the nail. OK, so that’s the image that tetanus usually conjures, but one can get it from any contaminated wound.

Tetanus is not transmitted person-to-person. If you elect not to vaccinate yourself or your child against tetanus, the only person put at risk is yourself or your child. I would still argue that would be a poor medical decision. Tetanus is a horrific disease, but you would not be putting others at risk by your personal decision.

Vaccination.
CDC Public Health Image Library.
Common domain.

2nd: Vaccination serves to reduce severity of the illness in the vaccinated. In this case, the purpose of vaccination is not necessarily to prevent the infection, but rather to blunt the severity of the infection. This occurs with a number of vaccinations.

Example: Even though a child vaccinated against measles has a small chance of still getting measles, the course of illness and severity of symptoms are reduced.

This is a benefit – anyone would want a milder rather than a more severe illness. And this is commonly seen with a number of vaccinations.

Administration of the oral polio vaccine, 1977.
CDC Public Health Image Library.
Common domain.

3rd: Vaccination serves to reduce complications of the illness in the vaccinated. In this case you may still get the infection, but the risk of specific complications are reduced. I want to emphasize the subtle difference between benefit #2 and #3, by again using the measles example.

Example: You don’t want sclerosing subacute panencephalitis, so you get the measles vaccine.

Sclerosing subacute panencephalitis (SSPE) is a rare neurologic complication of measles occurring an average of 7- 10 (though as late as 27) years after initial infection. SSPE symptoms are progressive and include behavioral changes, cognitive deterioration, neurologic deficits, and ultimately, death. Based on the 1989-1991 epidemic of measles in the United States, researchers calculated an estimate of the risk of SSPE of 22 cases per 100,000 cases of measles. Vaccination prevents SSPE.

Vaccination.
CDC Public Health Image Library.
Common domain.

4th: Vaccination serves to reduce transmission of the infectious disease. This is different than herd immunity (see #5 below), here the vaccine results in decreased shedding of infectious virus or bacteria in the infected. Because fewer infectious ‘germs’ are shed there are fewer secondary infections.

Example: You know you don’t want your family to get rotavirus so you vaccinate your new baby.

Infant vaccination for rotavirus was implemented in 2006 and, not surprisingly, the rate of severe gastroenteritis in the targeted age demographic plummeted. Remarkably though, gastroenteritis rates also fell in kids older than 5 as well as adults. This suggests a reduction in rotavirus infections originating with neonates that spread to older children (siblings) and adults (parents). This larger impact of rotavirus vaccination was a pleasant added benefit.

Parenthetically, I would also note that part of the reason we treat infections is not only to alleviate symptoms and cure the patient, but also to prevent transmission to others. In this case we are using antibiotics or antivirals rather than immunization. Examples include the use of oseltamivir for influenza, antiretroviral therapy for HIV, and azithromycin for pertussis (whooping cough). In all three cases, the treatment has the effect of reducing likelihood of transmission of infection. In the latter case (pertussis), the use of azithromycin is solely to prevent transmission. We treat with antibiotics in an attempt to limit the spread of the bacterial pathogen, Bordetella pertussis, to others. The inexorable whooping cough of pertussis is due to production of a cough inducing toxin elaborated by Bordetella. Unfortunately, once the toxin has been produced and the patient has symptoms, you are stuck. Stuck for six or more grueling weeks of cough. Annoying for adults, life threatening to infants. Better to vaccinate for pertussis and avoid getting it in the first place.

Cattle herd.
USDA.
Common domain.

5th: Vaccination creates herd immunity as a barrier to transmission of the infectious disease.

Now, in the case of measles the vaccine does prevent disease in the vaccinated (#1 above), to the tune of ~99% for someone who has received two vaccinations. And the vaccine also reduces the severity of illness in someone who still gets measles, despite vaccination (#2 above). The vaccine reduces complications (#3 above). And it reduces viral shedding and decreases secondary cases (#4 above). But measles vaccination also provides herd immunity, AKA ‘community immunity,’ in which the overall risk of measles transmission for everyone is reduced when a threshold percent of the entire population is vaccinated and immune.

Herd immunity only applies for certain infectious diseases: Ones in which there is no environmental reservoir (like surface water) and where there is either (1) no alternate host (such as wild animals) or (2) the alternate host can also be a target of prevention efforts. Measles is transmitted person-to-person. The virus can survive outside a human host for a few hours, but has no environmental reservoir. And it infects no alternate, non-human host which can serve as a reservoir of transmission. Other human pathogens that fit this bill for herd immunity include mumps, rubella, and smallpox. These can survive only by a continuous chain of transmission from one human host to the next. That’s pretty amazing when you think about it. The measles virus currently causing disease in a kid in California was spread by a continuous chain of human hosts reaching back 9- 10 centuries (when measles evolved from another virus, rinderpest, discussed in my previous post.)

So, if the virus needs to jump from one human host to the next in order to continue to survive, the obvious strategy to eliminate disease outbreaks (and potentially fully eradicate the disease) is to block that transmission. This creates a ring of immune hosts around any case of illness that occurs. When no secondary cases occur, voila, no outbreak. That’s herd immunity.

To better understand herd immunity, we have to talk mathematical modeling of infectious disease. Imagine a virus enters a nonimmune population – a group of people who have never previously been exposed to the infectious agent. In this setting, we can measure how many new cases originate from each case. This number is referred to as the “basic reproduction number” and is given the mathematical symbol R₀.

R₀ has been calculated for many pathogens in different outbreak settings. The number is not absolute: variables that impact R₀ include the duration of infectivity of the sick and the number of susceptible potential hosts the sick come in contact with. For example, imagine a novel viral infection spread by droplets caused by coughing and sneezing as seen in this photo:

Sneeze.
CDC Public Health Image Library.
Common domain.

As a hypothetical example, let’s say the initial R₀ of the virus is 6. This means for any case of infection, there are 6 secondary cases. If the mode of transmission of the illness is determined to be via droplet, public health authorities would encourage the public to use cough hygiene. The public might adopt wearing masks. The effect would be to reduce transmission. In Asia, where wearing masks during the flu season is socially accepted, the R₀ of this fictional viral illness would be less than if the same viral illness appeared intially in the US. So I want to acknowledge that R₀ is not a fixed number in all settings.

A significant implication of R₀ is that if R₀ is < 1, the outbreak will peter out. If R₀ is > 1, the outbreak will continue to spread. The higher the R₀, the greater the difficulty in containing the outbreak. The calculated R₀ for Ebola for the west African outbreak was somewhere between 1.5 and 2.5. This helped reassure those fighting the outbreak that Ebola would not spread widely in the developed world where we have a vigorous public health infrastructure.

Another implication of R₀ is that the higher the value of R₀, the greater proportion of the population needs to be immune in order to prevent the chain of transmission to continue. This is referred to as the “herd immunity threshold” and is calculated:

1 – (1/R₀)

To have adequate herd immunity in the population for a disease with an R₀= 6 would require about 83% of the population to be immune. If the disease R₀= 16, then 94% of the population would need to be immune.

If we are trying to get to the herd immunity threshold by vaccination, one also needs to take into account the efficacy of the vaccine. This is the proportion of vaccine recipients who develop immunity after vaccination. In the case of measles, the vaccine efficacy after one shot is about 94% and after two shots it is about 99%. What proportion of the population, then needs to be vaccinated with a partially effective vaccine to reach the herd immunity threshold? This is described as the critical vaccination level and can be calculated:

(1- (1/R₀) / E

Where E = vaccine efficacy. So if you have a disease like measles, with a herd immunity threshold of 94% and a vaccine efficacy of 99% (after two shots), you need to have 95% of the population fully vaccinated to prevent outbreaks of disease. The efficacy is specific to each vaccine. As another example, mumps has an R₀= 6 with a corresponding herd immunity threshold of ~83%. One would therefore think it would be much easier to prevent mumps outbreaks, but unfortunately the vaccine is not as effective as the vaccine for measles. After two doses of mumps vaccine, 88% of individuals have protective immunity. Thus you still need 94% of the population vaccinated to prevent outbreaks of mumps.

Here is a table of the routine recommended childhood vaccines:

And if all of the above is confusing, the Manchester Guardian has an interactive, computer model that illustrates the concept of herd immunity graphically.

Of course some people should not get vaccinated: vaccination is contraindicated in infants less than 12 months of age and immunocompromised patients. They must rely on the rest of us to get vaccinated for their protection (by herd immunity).

BONUS! 6th benefit: Vaccination reduces reliance on antibiotics to treat infections with resultant decreased antibiotic resistance.

Occasionally, vaccines have unexpected benefits. Reduction in antibiotic resistance in pneumococcal bacteria was one unexpected benefit associated with introduction of the 7-valent pneumococcal conjugate vaccine. The vaccine (also known by its trade name, Prevnar) was added to the recommended childhood vaccination schedule in 2000.

In the decade following the introduction of the vaccine, invasive pneumococcal disease rates fell in the target population. But more surprisingly, hospitalizations for pneumonia dropped, not only in the target population, but also in the elderly. The latter benefit is presumed to be due to a herd effect in which grandpa was not exposed to the grandchild’s pneumococcal pathogens.

Even more exciting was the observation that the rate of antibiotic resistant pneumococcal infections decreased. Antibiotic resistance is of increasing concern, because as pathogens become more resistant to antibiotics we are further limited in treatment options. Most ear infections in kids are viral and antibiotics are not needed. Providers are concerned, however, that they might miss the ear infection that isn’t due to a virus, but rather is due to pneumococcus which can cause severe complications. As a result, a significant number of unnecessary prescriptions for antibiotics are written for kids that had a viral ear infection. This is one driver of emerging pneumococcal antibiotic resistance. With the documented efficacy of pneumococcal vaccination in reducing the risk of ear infections.providders have written fewer prescriptions for these unnecessary antibiotics. The result has been improvement in the rate of resistance in pneumococcus.

In Conclusion:

Immunization has multiple benefits. Our ultimate goal is to improve the health of people. I get the notion that some patients want to limit their child’s exposure to medical risks and they think by avoiding or limiting vaccinations they may achieve that goal. Ironically though, they are increasing the child’s risk of receiving antibiotics, needing hospitalization, and suffering complications related to vaccine-preventable disease. The calculus is simple: the many benefits of vaccination outweigh the risks.

REFERENCES AND FURTHER READING:

Althaus, CL. 2014. Estimating the reproduction number of Zaire Ebolavirus (EBOV) during the 2014 outbreak in West Africa. PLOS Curr Outbreaks doi: 10.1371/currents.outbreaks.91afb5e0f279e7f29e7056095255b288. (Link)

Bellini, WJ, JS Rota, LE Lowe, et al. 2005. Subacute sclerosing panencephalitis: More cases of this fatal disease are prevented by measles immunization than previously recognized. J Infect Dis 192: 1686- 93. (Link)

Dagan, R, N Givon-Lavi, O Zamir, & D Fraser. 2003. Effect of a nonavalent conjugate vaccine on carriage of antibiotic-resistant Streptococcus pneumoniae in day-care centers. Pediatr Infect Dis J 22: 532- 40. (Link)

Fine, P, K Eames, & DL Heymann. 2011. “Herd immunity”: A rough guide. Clin Infect Dis 52(7): 911- 6. (Link)

Gastanaduy, P, A Cums, U Parashar, & B Lopman. 2013. Gastroenteritis hospitalizations in older children and adults in the United Sates before and after implementation of infant rotavirus vaccination. JAMA 310 (8): 851– 3.

Griffin, MR, Y Zhu, MR Moore, et al. 2013. U.S. Hospitalizations for Pneumonia after a Decade of Pneumococcal Vaccination. N Engl J Med 369 (2): 155- 63. (Link)

Musher, DM. 2006. Pneumococcal vaccine – Direct and indirect (“herd”) effects. N Engl J Med 354 (14): 1522- 4.

Orenstein, WA, RT Perry, & NA Halsey. 2004. The clinical significance of measles: A review. J Infect Dis 189 (Suppl 1): S4- S16. (Link)

Kyaw MH, R Lynfield R, W Schaffner, et al. 2006. Effect of introduction of the pneumococcal conjugate vaccine on drug-resistant Streptococcus pneumoniae. N Engl J Med 354 (14): 1455- 63. (Link)

Rodrigues, LC, VK Diwan, & JG Wheeler. 1993. Protective effect of BCG against tuberculous meningitis and miliary tuberculosis: A meta-analysis. Int J Epidemiol 22 (6): 1154–8. (Link)

1 Comment

Posted in Uncategorized

Tagged Epidemiology, Immunization, measles, vaccination

What Can Docs Learn about Measles from Veterinarians?

Posted on January 28, 2015 | 2 comments

OK, quick sum-up for those living in a media-free cave: The US has a resurgence of measles related to falling vaccination rates, especially in specific demographic communities. Ominously, 2015 is starting out with a large, multistate outbreak of measles centered on Disneyland theme parks in California – as of this writing at least 65 epidemiologically linked cases have been identified in 7 US states and Mexico. And of local interest (and concern), a University of Minnesota student was diagnosed with measles this week.

Excellent commentary is available on the internet and in other media regarding measles and the need to improve the public’s acceptance of vaccination in general, and the MMR in particular, to prevent an ongoing spiral of worsening outbreaks of vaccine preventable disease. Just to be clear, there is no epidemiological link between MMR and autism. British gastroenterologist Andrew Wakefield published a fraudulent article in the Lancet in 1998 and then essentially pursued a media campaign to suggest a link between MMR and autism. That article has been wholly discredited. The other authors of the paper withdrew their support and it was retracted. In January, 2010, the UK General Medical Council (essentially the United Kingdom’s medical licensing body), struck Wakefield from the medical register, meting out their harshest sanction available. Unfortunately, Wakefield’s influence has continued to discourage some from vaccinating their children against measles. I have little to add on the above sordid tale, though I encourage readers to know this history because of how significant Wakefield’s impact has been on adherence to recommended vaccinations.

For clinicians, I refer you to the CDC Measles page or the MDH Measles page. I encourage providers who (like myself) have never seen a case of measles (yay! let’s hear it for vaccination!), to review the presenting signs and symptoms of measles as well as your clinic or hospital’s isolation procedures in the event you see a case. You don’t want to be the one contacting the family of someone who was inadvertantly exposed to measles in your healthcare setting.

And let’s get the legal boilerplate out of the way: Yes, I am a doc, but I don’t play one on the internet, so none of what I say should be construed as actual medical advice. Whew!

The topic for today, “What can docs learn about measles from veterinarians?” might seem incongruous as measles is a virus that only infects humans, but let’s talk.

Measles virus belongs to the Paramyxoviridae family of viruses. You have to love virology because the name (Para-“beyond” and -myxo- “slime”) equates to the “beyond slime viruses” and conjures up (at least for me) an image of Bart Simpson working with Petri plates. Viruses in this family have a genome composed of a non-segmented strand of RNA. This contrasts with influenza viruses where the genome is made up of 8 segments (or separate strands of RNA). This difference is important because reassortment of RNA segments between different strains of influenza leads to periodic genetic shifts allowing new pandemics of influenza for which people (and animals) have no immunity. This is one reason why your healthcare provider brings up the flu vaccine every fall. So getting back to the Paramyxoviridae, they have one segment, which gives them genetic stability compared to influenza. Which also means vaccination for measles can be more effective.

Below is a family tree of sorts for this family of viruses – think of it as something you’d find on Ancestry.com, but instead of aunts and uncles, you’ve got viruses that are related to differing degree. The figure here is from an article by Marsh, et al, (looking at a virus not actually that closely related to measles virus, but the image works for our discussion). Take a look at the cluster on the left labeled “Morbilivirus” (sic). Here is where we find measles virus. A number of closely related viruses are in this genus. And except for measles, all the other viruses here are animal pathogens. Very interesting.

Phylogenetic_tree_Paramyxoviruses_based_on_the_N_protein_sequences_of_selected_paramyxoviruses.

This figure shows only the most important morbilliviruses (not all of them). In addition to measles, these include canine distemper (CDV, a pathogen primarily of dogs), peste-des-petits-ruminants (PPRV; I don’t speak French, but obviously it is a pathogen of petite ruminants, i.e., goats and sheep), and then there is rinderpest virus (RPV). Rinderpest virus, the one that strikes terror in animals and people alike. Wait, what? You haven’t heard of rinderpest? Astonishingly, if you are like most folks outside the veterinary or wildlife biology world you’ve probably never heard of it. It’s time to correct that oversight.

One reason for the anonymity of the virus (and the disease of the same name) is that it infects animals, specifically cattle and other members of the Artiodactyla. These are mammals that are even-toed ungulates, including antelope, gazelles, sheep, goats, pigs, and giraffes, among others. The disease has an ancient origin, likely in Asia. As with many diseases, it spread with trade (via the Silk Road) and with human conflicts. The Fifth Plague of ancient Egypt (Exodus 9:1-3) was a cattle plague and may have been rinderpest. The virus is thought to have spread into central Europe in the 13th century with the advancing armies of the Mongols. Starting in the 1700s, multiple well-documented epizootics of rinderpest wracked Europe.

If there ever was an infectious disease candidate for the worst in the world, rinderpest would certainly be in the running. The devastation wrought by the virus seems incomprehensible to us today. Up to 95% of cattle were killed. Famines followed quickly after epidemics of rinderpest because cattle were not only an important source of food (for dairy and meat) but also power (as draft animals used to plow fields).

Rinderpest outbreak in 18th Century Netherlands
Source: Wikipedia
Public Domain

Africa was spared from the disease, until the 1800s. Starting in 1887 the most devastating documented outbreak of rinderpest ensued, when the virus arrived on the continent, home to the world’s largest free ranging population of hooved animals. All essentially susceptible to rinderpest. And then enters the virus. When the Italian military was waging a campaign in Eritrea, they imported cattle from India for food and draft power. Some of the livestock were unfortunately infected with the virus (presumably unbeknownst to the Italians.) The subsequent outbreak in Ethiopia was estimated by contemporary sources to have resulted in 90% mortality of the entire country’s cattle herd. Famine resulted in 1888-1892. A third of the nomadic peoples of East Africa, dependent on hooved animals for milk and protein, are estimated to have died in the viral conflagration.

By 1890, rinderpest had reached Tanzania. In a very small illustration, in the region surrounding Unyanyembe the cattle population fell from a herd of ~40,000 to ~100. Cattle deaths due to the ever-advancing rinderpest were reported in Rhodesia (now Zimbabwe) by 1896 and ultimately the scourge reached all the way to the Cape, killing an estimated 2.5 million head of cattle in southern Africa alone.

And an equal devastation was meted out against wild hooved species. The ecological impacts of rinderpest is a topic worthy of a separate post (and by a guest blogger who is an expert in ecology.) It is hard to comprehend the devastation this plague left in its wake.

Cows dead from rinderpest in South Africa, 1896. Source: Wikipedia. Public Domain.

Luckily, rinderpest was never imported into North America. And now never will be. A multi-decade effort by wildlife biologists and veterinarians to vaccinate against the plague was ultimately successful. In the case of rinderpest, building herd immunity was both metaphorical and literal. Rinderpest has been eradicated as of May, 2011 – one of only two diseases that can claim the distinction, the other is smallpox.

I want to wrap up this discussion by connecting the rinderpest story back to measles. It turns out measles is not only related to rinderpest – it’s basically it’s offspring. (Imagine the B grade horror flick “Son of Rinderpest.”) Measles appears to have evolved from rinderpest and “jumped” species from cattle to humans around the 11th to 12th centuries. A pandemic ensued that has persisted to this day – most recently impacting Mickey Mouse and his friends.

What can docs learn about measles from veterinarians?

First, this tale is a parable. If rinderpest was eradicated, why not measles? In contrast to measles, rinderpest can infect a variety of host species. Biologists and vets slayed rinderpest in extremely difficult circumstances, working in remote bush across multiple cultural boundaries, during peacetime and war. But the tools used to contain and ultimate eradicate rinderpest were ultimately no different than the public health tools we use against measles.

Second, the story of rinderpest evolving from a virus solely infecting animals to one that infected humans is not unique. In over half of human infectious diseases, the pathogens also infect animals. Of emerging human diseases, the majority ‘jump species’ from an animal host. These include ones that make the headlines: Ebola, SARS, avian and swine influenza… And diseases that don’t: Nipah, Hendra, MERS… Addressing the risks of the next pandemic requires interdisciplinary collaboration between docs and vets as well as ecologists, wildlife biologists, public health sanitarians, and anthropologists. These collaborations have started, but we need to invigorate our approach at transdisciplinary thinking.

#IAMTHEHERD

SUPPLEMENTAL INFORMATION:

For those more interested in the clinical manifestations of rinderpest: A clinical description may be found here.

Rinderpest in cow
Source: CDC PHIL
Public Domain

REFERENCES AND FURTHER READING:

Barrett, T, P Pastoret, & WP Taylor (eds). 2005. Rinderpest and Peste des Petits Ruminants: Virus Plagues of Large and Small Ruminants. Academic Press, Elsevier, London, UK.

Holdo, RM, et al. 2009. A disease-mediated trophic cascade in the Serengeti and its implications for ecosystem C. PLoS Biol 7(9): e1000210. doi: 10.1371/journal.pbio.1000210. (Link)

McNeil, Donald G, Jr. June 28, 2011. Rinderpest, Scourge of Cattle, is Vanquished. New York Times. p D1.

Pankhurst, R. 1966. The great Ethiopian famine of 1888- 1892: A new assessment. J Hist Med 21: 95-124, 271- 293.

Schwabe, Calvin W. 1984. Veterinary Medicine and Human Health. Third Edition. Williams & Wilkins; Baltimore, MD. pp 17- 22.

2 Comments

Posted in Uncategorized

Tagged Conservation Medicine, measles, One Health, OneHealth, rinderpest, vaccination, Veterinary Medicine, Wildlife Biology

Hello blogworld!

Posted on January 22, 2015 | 8 comments

I decided to start a blog after enjoying Fall 2014 basically blogging on Facebook about my experiences and frustrations related to the Ebola Outbreak in West Africa. (i.e., what happens when a developing world disease hits a developed world’s media during an election year and, to top it off, we all still have reptilian brains….) I spent a fair amount of time sharing and commenting on content from the web, as well as making a few observations myself. I realized this was all a bit overwhelming for my otherwise accommodating Facebook audience and so a Blog idea was born. By moving commentary here I will give FB friends a needed respite from the blood, pus, and gore of infectious diseases while still satisfying my own morbid need to communicate about these topics.

Who is the intended audience of this blog? That’s where you will help me out. I am envisioning blog posts targeting a general (though scientifically literate) audience, with add-ons and downloads that will provide more details relevant for those in medicine generally or infectious diseases in particular. Please post in the comments section (or email me) any infectious diseases topics that you are interested in hearing more about.

I need to emphasize my interest in all things One Health or Conservation Medicine. I am fascinated by the interactions shared between human health, animal (domesticated and wildlife) health, and ecosystem health.

There is a rich literature that documents the impacts that climate change, land use change, environmental degradation (water and air quality), invasive species encroachment, and habitat degradation have on the health of animals and humans. Starting with the veterinarian Calvin Schwabe who coined the term “One Medicine” there has been a rich tradition of veterinarians understanding the connection between veterinary medicine and human medicine. Ecologists, conservation biologists, and wildlife biologists have shown the interconnections between wildlife and habitats and how the protection of these also serve a utilitarian function of protecting human health.

I became aware of the field with the 2002 publication of the book Conservation Medicine: Ecological Health in Practice, which was eye opening and exciting and posed to me the challenge – “What is the role for me as a physician in this transdisciplinary field?”

In 2003, I was awarded a grant by the University of Minnesota’s Consortium on Law and Values in Health, Environment, and the Life Sciences, “Building a Community of Scholars in Conservation Medicine.” These funds were used for a lecture series, bringing together Twin Cities researchers, educators, veterinarians, and clinicians from across the fields related to Conservation Medicine to discuss One Health topics. Out of that discussion series, rose new connections between practitioners in these respective fields.

I have continued to apply One Health precepts in my everyday practice of medicine, but have continued to look for a role that, I, as a physician, could more actively serve to enhance the connections between veterinarians, ecologists, and wildlife biologists, to the medical community. This blog is a step in that direction.

Welcome to my blog, pull up a chair, have a cup of coffee and let’s chat about infectious diseases and Conservation Medicine.

8 Comments

Posted in Introduction

Tagged Calvin Schwabe, Conservation Medicine, Infectious Diseases, One Health, OneHealth

Jonathan Sellman, MD, MPH

Vietnam War Dogs and an Unknown New Disease

Dogbites: Management of Infections, A Practical Blogpost

Another Month, Another Zoonosis: Plague in Colorado

Glanders

Calvin Schwabe

Bald Eagles and Aquaria

How vultures, cattle, and a minority religious sect are interconnected.

What are the benefits of immunization?

What Can Docs Learn about Measles from Veterinarians?

Hello blogworld!

Archives

Follow me on Twitter

Connect with me on LinkedIn

Share this:

Share this:

Share this:

Share this:

Share this:

Share this:

Share this:

Share this:

Share this:

Share this:

Archives

Follow me on Twitter

Connect with me on LinkedIn