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Zoonoses: How real is the threat? (Proceedings)
In the language of law (at least in the US), the term "zoonoses" has not been defined. In medical terms, it refers to "infectious diseases shared by animals and humans." Of particular importance in both human and veterinary medicine are those zoonoses known to be transmitted directly from animals (vertebrates) to humans.
Legal/Liability Considerations of Zoonotic Diseases
In the language of law (at least in the US), the term "zoonoses" has not been defined. In medical terms, it refers to "infectious diseases shared by animals and humans." Of particular importance in both human and veterinary medicine are those zoonoses known to be transmitted directly from animals (vertebrates) to humans. To date, there are about 250 zoonotic infections known to be transmitted from animals to humans, with about 20 to 30 resulting from contact with cats and/or dogs. Transmission can occur through inhalation, ingestion, bites, or scratches. Arthropod vectors, while certainly capable of transmitting infectious organisms from animals to humans, pose a threat to humans and animals alike, but these infections are likely to occur simultaneously and independently of each other.
The question at hand, therefore, becomes, "How real is the threat of an individual acquiring a pet-associated infection?" From the perspective of the legal profession, the categories of concern for the veterinary profession, arising from the risk of exposure to a known or suspected zoonotic infection, include:
• Failure to warn and individual that a particular disease (in an animal) might be transmitted to a person.
• Improper execution of a health certificate.
• Delegation of duties to assistants without providing appropriate supervision.
• Poor sanitation standards.
• Failure to isolate animals with known or suspected zoonotic infections.
Animal Bites to Humans
Although over 1 million people are reportedly bitten by dogs every year, it has been estimated that this represents only half of the dog bites that actually occur. Accounting for approximately 1% of all emergency room admissions, dog bite wounds cost over $30 million in annual health care costs.
In the last 10 years, a number of significant facts have been learned about animal bites to humans. For example, dog bites to humans are more likely to occur in males (especially young boys) than in females. From one-half to two-thirds of dog bite victims are less than 20 years old and many of these are less than 10 years old. About half of all bites are from dogs owned by neighbors and are inflicted by medium or large-sized dogs. Arms and hands are the most likely part of the body to sustain injury from bite wounds. About 65% of all facial bites occur in children less than 10 years old.
Although dogs appear to inflict more bite wounds than cats, the likelihood of infection developing subsequent to a bite wound is greater in cats than in dogs. Wound infection is most common in those victims who are more than 50 years of age, when wounds are not properly nor adequately cleansed, when there is more than a 24 hour delay in seeking treatment, and when wounds occur on the hands.
While an animal bite to a human is not, per se, a zoonotic disease, the potential for significant injury or infection does exist. Recently, renewed concern has developed over the ability of the dog to cause severe, even fatal, sepsis in humans following the inoculation of resident oral bacteria via bite into human tissue. It is interesting to note that, although infections from dog bites are a major concern, cat bites and human bites are much more likely to become infected. The likelihood of infection following a dog bite is only 3 to 5% (gram negative, aerobes) while infection rates following human or cat bites can be as high as 50% (esp. Pasteurella multocida).
The DF-2 organism, now recognized as Capnocytophaga canimorsus, has surfaced as one of the resident organisms in dog saliva that, following bite-wound contamination, can cause sepsis in humans leading to severe morbidity or death. At particular risk are individuals who have experience splenectomy or are otherwise immune compromised. This group of gram-negative rods has a propensity to cause disseminated intravascular coagulation (DIC) and symmetric peripheral gangrene in asplenic patients. True incidence of bacteremia after dog bite is considered to be underestimated. Penicillin is the treatment of choice in affected patients.
Animal Associated Opportunistic Infections
With almost 60% of US households having pets, it is not surprising that the risk, and the incidence, of opportunistic infections among immune suppressed individuals (cancer patients and HIV-positive) has increased. While the risk has increased, levels of pet ownership remain the same. This fact alone is of particular significance to the companion animal practitioner: risk awareness/risk assessment, on behalf of the pet owner, is becoming an increasingly important part of private practice.
Several bacterial, fungal, and protozoal infections of animals are now being confirmed as secondary infections among immune suppressed humans, including: Toxoplasmosis, Cryptosporidium, Microsporidia, Salmonella, Campylobacter, Giardia, Rhodococcus equi, Bartonella sp. (previously called Rochalimaea), Bordetella bronchiseptica (yes! "kennel cough"), and Listeria monocytogenes. Among the animal-associated opportunistic infections, Bartonella — the cause of Cat-Scratch Disease — is perhaps the most important. Still, it is important to appreciate the fact that pet-associated zoonoses present a small risk to even the immune suppressed client; risk awareness combined with practical suggestions for avoiding exposure can significantly reduce any risk. The benefits of animal companionship far outweigh the risks to human patients. Prohibiting pet ownership by immune suppressed individuals is generally NOT warranted.
Cat-Scratch Disease (CSD)
A number of recent studies have prompted us to do a complete turn-around on this disease we call CSD. As it turns out...Cat Scratch Disease (CSD) is one of several infectious disease syndromes of humans caused by Bartonella sp...a member of the family Rickettsiaceae. In fact, CSD, caused by Bartonella henselae, is the most common of these persistent syndromes associated with necrotizing inflammation in lymph nodes. While people are susceptible to at least 9 species (or subspecies) of Bartonella, 7 are considered zoonotic! Bartonella hensleae and B. clarridgeiae are the most likely to be transmitted to humans from domestic cats. The spectrum of Bartonella infection in domestic and feral animals is remarkable...in fact, it has been estimated that Bartonella infection occurs in 22,000 people in the US annually! Given newer isolation techniques and an increasing number of immunocompromised people, it is likely that the reported incidence of Bartonella-associated diseases in humans will increase substantially. It appears that the domestic cat serves as the reservoir for the CSD causative organism (especially B. heneslae) and may, in fact, be a principal source of human infection.
Human Infection...is it really "cat SCRATCH disease"??? Most of the cases of CSD occur in persons under 21 years of age. The disease does appear to have a predilection for males, but is not known to be transmitted human to human. CSD has characteristically been reported to develop following a scratch, lick (on abraded skin or in the eye), or very rarely a bite from a young cat. Furthermore, cats capable of transmitting CSD were not thought to become ill as a result of carrying the infectious organism. However, studies now show that Bartonella bacteremia does occur in up to 40% healthy and ill cats in the United States alone. Just how humans become infected is less clear. It's NOT just the claws. In fact, there is no evidence to support that de-clawing will prevent transmission from cats to humans. Fleas (and to a lesser extent, ticks) are particularly implicated. When it comes to preventing human infections, emphasis should be on flea control in cats, rather than attempting to identify infected carriers through blood tests or declawing.
Following inoculation into a human, the patient first develops tender and moderately enlarged regional lymph nodes near the inoculation site. In many patients, swollen lymph nodes are the only clinical sign observed in CSD. One third of the patients have fever. Less than one third have fatigue, anorexia, vomiting, or weight loss. Occasionally, a headache and/or sore throat develops.
The incubation period in humans is three to ten days. On the skin, one or more papules or pustules will develop. Skin lesions may last from one to three weeks; some may persist for up to ten weeks. Lymph nodes usually swell about two weeks after the inoculation. Rarely, infected humans develop CNS involvement characterized by meningitis, polyneuritis and/or myelitis with paraplegia. Neurologic signs are sudden in onset and occur from one to six weeks after the swelling of lymph nodes. Rarely, patients have been reported to have seizures followed by coma persisting for one to four weeks. The most severe clinical manifestations occur in immunocompromised individuals, especially those with advanced HIV infection. Human deaths have been reported.
The diagnosis of CSD in humans is confirmed on lymph node biopsy. Laboratory studies are otherwise not diagnostic for CSD in people (or in cats!). Blood culture studies in cats have demonstrated significantly high recovery (from 5% to 40%) of Bartonella.
Prognosis: The prognosis for CSD in humans is excellent with the exception that immunocompromised individuals are at significant risk of developing severe disease subsequent to infection. Lymph node swelling usually regresses within two to four months. Humans are reported to develop lifelong immunity following infection. Fatal complications and irreversible clinical findings are almost nonexistent.Prevention: CSD does not require isolation nor quarantine since it is not transmitted from one human to another. Specific preventative management strategies for individuals who are considered at risk of exposure (eg, veterinarians/veterinary technicians) have not been defined. However, sufficient evidence does exist to warrant the recommendation that individuals (humans) known to be immunocompromised should take measures to avoid contact with cats.
Leptospirosis is a gram negative, worldwide zoonotic infection. All mammals are susceptible. Transmission rates are very high with only 10 organisms needed to cause infection and disease. In order to persist, leptospires need a maintenance host, a role that humans do not serve. The maintenance host (typically wildlife) does not become clinically ill despite the fact that organisms are sustained in the kidneys and shed months to years or for the life of the animal. The route of infection of leptospirosis is either direct or indirect through contact with urine (especially through mucous membranes). The actual infectious dose is not known, although the organisms are highly infectious and can spread through tissues rapidly. They can cross the placenta and infect fetuses. Any damaged skin allows entry.
Clinical Infections in Dogs: Clinical presentations of infected dogs typically, although not always, involves young, large breed dogs presented for acute onset lethargy and significant fever (103° to 104° F). Muscle pain, vomiting, and dehydration are common. Acute onset icterus in a young, outdoor dog always places leptospirosis at the top of the differential diagnosis list. Other signs include bleeding diathesis, tachypenia, cardiac arrhythmia, and shock (vascular collapse). A sub-acute form of clinical leptospirosis is reported in dogs presented for renal failure, with no known predisposing cause. Affected dogs will also have high fever, myalgia and even hyperesthesia.
Hematologic findings typically include leukocytosis and thrombocytopenia. Several significant biochemical abnormalities may be detected in the same patient: azotemia (or uremia), elevated ALT and alkaline phosphatase, hyperamylasemia (with concurrent increase in lipase), and hyperbilirubinemia. Abdominal ultrasound exam may be consistent with intussusception, acute renal failure (large kidneys), and pancreatitis.
When in doubt...Consider the patient infected and shedding spriochetes until proven otherwise...HANDLE WITH CARE!
Does zoonotic potential of Leptospirosis justify vaccination?
All of the leptospirosis vaccines currently available today mitigate clinical illness the dog following exposure...vaccination does NOT consistently prevent infection nor shedding! NEW: a recently licensed (4-servar) Leptospirosis vaccine (Merial) is expected to be available Fall 2010 (release date is predicated on developing sufficient inventory). Uniquely, the product label indicates 100% of dogs, following administration of 2-doses, were protected following challenge. Spirochetes were not found in the kidneys of vaccinated dogs following challenge..suggesting this vaccine induces a 'sterile' immunity to leptospirosis.
New: at least it's in the works...currently under development is an ELISA-based rapid assay ('SNAP' test, IDEXX Laboratories) for in-clinic use in diagnosing Leptospirosis infection in dogs. This rapid assay, when available, offers the first opportunity for veterinarians to perform same-day testing for leptospirosis (the test will NOT verify the infecting serovar).
The Bubonic Plague, also called the Black Death, is a bacterial disease carried by fleas that feed on rats. The disease has afflicted humans for more than 1000 years and still exists in this country today. The factors responsible for its alternate rise and fall remain a mystery.
In the 14th century in Europe, Bubonic Plague killed over 20 million people, about one-fourth of the population of Europe, in a four year period. Subsequent to this period of the Great Dying, repeated epidemics occurred in several of the following centuries. During the period of the Black Death, people were inclined to attribute the disease to unfavorable astrological combinations or malignant atmospheres ("miasmas"), neither of which could be translated into a public-health program of any sort. Although the prevalence of Bubonic Plague is considerably less today, pneumonic plague still occurs sporadically in various parts of the world, including the US, especially in the Southwestern states and Colorado. Not until 1894 was it discovered that a gram-negative, rod-shaped bacillus, Yersinia pestis (previously Pasteurella pestis), caused Bubonic Plague.
Clinical Signs: The name, Bubonic Plague, derives from one of the early signs of the disease: the appearance of large, painful swellings (buboes) in the lymph nodes of the arm-pit, neck, or groin of the victim. Three days after the appearance of the buboes, people were characteristically overwhelmed by high fever, became delirious and broke out in black splotches that were the result of hemorrhaging under the skin. As the disease progressed, the buboes continued to grow larger and more painful; often they would burst, a particularly painful, agonizing aspect of the disease. In some cases, blood would become directly infected, leading to massive hemorrhage and rapid death. In others, plague was transmitted as pneumonia (pneumonic plague) that caused hemoptysis and death within a few days.
Pathogenesis: Plague bacilli are found at low frequency in many wild rodent populations throughout the world and are transmitted from one rodent to another by fleas...in this case, the oriental rat flea Xenopsylla cheopis. When a flea bites an infected rat, it ingests the bacilli, which in turn replicate within the flea's digestive tract forming a solid mass that obstructs the lumen of the gut. The flea, now unable to ingest blood, becomes ravenously hungry. In a feeding frenzy it repeatedly bites its animal host, regurgitating plague bacilli into the host's bloodstream with every attempted meal. These injection sites act as foci for the spread of bacilli. The disease spreads rapidly in this manner. As the number of live rats decreases (they, too, die of the infection), the fleas move to other available warm-blooded hosts on which they would not normally feed, such as humans and their domesticated animals. This is the pathway most responsible for the start of an epidemic. It should be noted that an essential requirement for an epidemic among humans is an outbreak in a rodent population. In addition, the two populations must be in very close proximity for transmission to be successful.
Treatment: Even patients with pneumonic or septicemic disease can be cured if treatment is initiated within the first 15 to 20 hours of infection. In most cases, antibiotic treatment is dramatically effective. Oral tetracycline or chloramphenicol are recommended for individuals who do not require hospitalization. Streptomycin (IM injections) is the drug of choice and is administered for 7 to 10 days. However, streptomycin can be difficult to obtain today. In critical patients, intravenous chloramphenicol or aminoglycosides are recommended for a minimum of 7 days.
Perhaps the coccidian parasite that has caused more concern as a zoonotic infection than any other disease is that of Toxoplasma gondii. The organism is a common environmental organism capable of infecting a very wide range of animals, including fish, reptiles, and birds, as well as mammals. Cats, however, are the only definitive host. The life cycle of toxoplasmosis in the cat is extremely complex and not entirely understood. Nevertheless, the cat is able to excrete unsporulated (NON-infectious) oocysts in the feces. The oocysts are capable of becoming infectious to other animals and humans as early as one day (usually 3 to 5 days) following excretion in the feces.
In the clinical disease in cats, the T. gondii is capable of causing a wide variety of signs since it can localize in a number of organs. The exact type of infection that results and the degree of clinical illness depends on the animal's age at the time of infection, its immune status, the strain of parasite, and the route of infection. In most animals, toxoplasmosis is a subclinical disease. In other words, outward clinical signs are not evident, yet the cat does harbor the organism. Generally, clinical illness in cats is characterized as interstitial pneumonia and is most likely to develop in immune suppressed cats, eg, those with FeLV or FIV infection.
By far the most concern over toxoplasmosis in humans occurs in prenatal infections. Congenital toxoplasma infections are the result of in utero infection of the unborn fetus. The resulting clinical signs depend on the stage of pregnancy at the time that infection occurs. The fetus appears to be most susceptible during the last trimester of gestation. However, the most severe outcomes occur when the human fetus is infected very early in pregnancy. In this country, there are still approximately ten thousand congenital infections reported in humans each year.
The in utero infection in humans results only when acute infection occurs in a susceptible pregnant female. A woman that has become chronically infected, then becomes pregnant, is unlikely to transmit the organism to the fetus. These pregnancies are usually uncomplicated.
Perhaps of most concern to our clientele is the possibility of a cat transmitting toxoplasmosis to a woman during pregnancy. It should be emphasized that, although possible, there has never been a documented case of prenatal toxoplasma infection in a human caused by a cat. Nonetheless, the concern remains, and many pregnant women will present their cat to a veterinary hospital for "testing." It is most important to understand the strict limitations associated with the toxoplasmosis antibody test available today. In all probability, a cat with a positive titer is protected against disease. The only definitive diagnosis test is finding oocysts in the feces or finding evidence of the organism in tissue.
While it is important to advise clients on the potential risk of toxoplasmosis to the unborn fetus, it is only rarely necessary to separate or eliminate a cat from a household.
Despite the association between human infection and exposure to cats, the frequency and risk of human infection is most likely to be associated with ingestion of infected, RARE OR RAW meat (particularly, pork, goat, or lamb). Also, the ingestion of raw goat's milk may be a source of human toxoplasmosis. Risk of exposure and contact of affected meat can be avoided by heating and cooking all meat to greater than 150?F. Freezing of meat, however, is not a consistently reliable method of killing of toxoplasma organisms. Therefore, all meat should be adequately cooked. Good personal hygiene also dictates that hands be washed well after handling raw meat.