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Sunday, March 14, 2010

Distemper

Most of us have heard of distemper infection for dogs and gather it is very bad. The basic vaccine for dogs is “the distemper shot,” which vaccinates against distemper, parvovirus and some minor kennel cough agents. Luckily, this is all most people ever hear of distemper. If you are reading this, however, you probably have a dog that is suspected of having this dreaded infection.

The typical distemper suspect is a rescue or pet store dog or puppy, usually with questionable vaccination history or an as yet incomplete vaccination series. The dog or puppy has been housed with other rescue dogs. Symptoms begin with:
  • Gooey eye and nose discharge
     
  • Fever (which often comes and goes unnoticed)
     
  • Poor appetite
     
  • Coughing and the development of pneumonia
The virus is attacking interfaces of the body with the environment (the mucous membranes) and starts with the respiratory tract, hence the pneumonia, but it does not stop there. The virus moves on to produce:
  • Vomiting and diarrhea
     
  • Callusing of the nose and foot pads (hence one of the old names for distemper – hard pad disease)
After completing what is called the “mucosal phase” of infection where environmental interfaces are attacked (as described by the above GI and respiratory disease), the virus proceeds to the central nervous system for its “neurologic phase” leading to:

Seizures (classically starting with snapping or tremoring of the jaws that progress to convulsions of the whole body. This distemper classic sign is called a chewing gum fit.)
  • Seizures are not the only distemper sign by any means. Tremors , imbalance, and limb weakness all may occur. Signs may progress to death or may become non-progressive and permanent. Recovery is also possible.
This means that the dog appears to recover only to break with neurologic disease 1 to 3 weeks later. Younger puppies or individuals with weak immunity often die during the mucosal phase while stronger individuals may have relatively mild mucosal signs and not appear ill until the neurologic phase strikes.

THE VIRUS ITSELF
paramyxoviradeaeThe canine distemper virus is closely related to the human measles virus and, in fact, in older times, puppies were immunized for distemper with vaccine against measles. It has been said that a child in the home of a dog vaccinated with live distemper virus vaccine will become exposed to the virus and immunized against the measles (though we do not recommend such experiments at home).

The distemper virus consists of a single strand of RNA, encased in a protein coat which is again encased in a fatty envelope. This sounds esoteric but the fatty envelope makes all the difference in the world. The fatty envelope is easily disrupted in th e environment which makes it impossible for infectious virus to persist in the environment. Because an intact fatty envelope is required for infection, virus transmission must involve dog to dog contact or at least contact with extremely fresh (less than 30 minutes old at 60 degrees and up to 3 hours oldat room temperature) infected body secretions. As with other viruses, living virus happily freezes and can survive for years if kept frozen and protected from light. Routine disinfection and cleaning readily kills the distemper virus in the kennel setting.

TRANSMISSION AND INFECTION
The infected dog typically infects other dogs via coughing infected respiratory secretions though the virus is shed in most other body secretions including urine. The virus enters the new host via the nose or mouth and promptly begins to replicate. Virus is engulfed by cells of the immune system called “macrophages.” The idea is that the virus will be engulfed, walled off within the cell and then destroyed by enzymes. Unfortunately for the new host, this process does not damage the virus as intended; instead, the virus is able to use the macrophage as a means of transportation through the host’s body. Within 24 hours, the virus has traveled to the lymph nodes of the lung. By the 6th day, the virus has migrated to the spleen, stomach, small intestine, and liver. Fever is developing at this point.
By day 8 or 9 an important crux is reached in the timetable of infection. The host is mounting an immune response during this time and the outcome depends on how fast and how well this is accomplished. A strong immune response begins to clear the virus at this point and has eliminated all traces of virus with no symptoms of illness by Day 14. A weak immune response allows the virus to reach the “epithelial cells,” the cells which line every interface the body has with the outside world. The tender epithelial cells lining the chambers of the brain are infected as well. The host begins to get sick as the virus spreads but as the host’s immune response grows symptoms wane. This phenomenon accounts for the wide variability in symptoms; some dogs get only a few mild symptoms while others get a full lethal combination.

After clearing from most internal organs, the virus is able to “hideout” for long periods of time in the nervous system and skin. Because of this phenomenon, callusing of skin or, much worse, seizures may occur long after the infection was thought to be cleared.

Most victims in the U.S. are puppies. (The colostrum suckled in the first day or so of life will provide them with a solid reflection of their mother’s immunity. This will have waned by age 16 weeks leaving the puppy vulnerable if vaccines have not been administered for further protection. In our society most mother dogs will have received some form of vaccination and thus be able to pass on at least some immunity and will have some ability to protect herself. In societies where vaccination is not common, distemper attacks all age dogs.)

CONFIRMING THE DISTEMPER INFECTION
As if it is not bad enough that this infection has a poorly defined endpoint so one never knows for sure one is “out of the woods,” it is almost impossible to confirm a distemper diagnosis. Because of this, distemper is a “clinical diagnosis” which means that rather than confirming infection with a test that is negative or positive, the veterinarian must look at the whole picture: what symptoms are there, is the history typical, etc. The virus itself remains elusive so that positive test results are meaningful in confirming the infection, but negative results do not rule it out. The following are tests that can be used:

DISTEMPER INCLUSION BODIES – “Distemper inclusion bodies” are actual clumps of virus that are visible under the microscrope within infected cells. Post-mortem inclusion bodies are readily visible in the urinary bladder tissue thus making confirmation of distemper after death relatively easy. In the living patient, we typically have ready access to blood cells and cells of the eye’s conjunctival membranes (the pink park of the eye socket). To enhance the visibilty of inclusion bodies, “immunocytology” is used. In this technique, antibodies against distemper virus are tagged with fluorescent markers. The antibodies bind to virus if it is present effectively dying the inclusion body with glow-in-the-dark fluorescent color. The presence of inclusion bodies confirms distemper infection. The lack of dectectable inclusion bodies does not rule out distemper infection as inclusion bodies ultimately become coated with the host’s own antibodies which in turn block the fluorescent-tagged antibodies used in the test.

distemper inclusion bodies
If callusing of the footpads or nose is evident, a biopsy of this tissue can be tested for inclusion bodies fairly late in infection.

DISTEMPER ANTIBODY LEVELS – Distemper titers (another word of “antibody level”) of either the “IgM” type (produced in early stages of infection) and the “IgG” type (produced in later phases of infection) can be checked. The problem is that distemper vaccination induces these same antibodies and often distemper suspects have had recent vaccination. A high IgM titer indicates recent infection or recent vaccination. There is no way to tell which.

PCR TESTING - PCR testing involves amplification of DNA so as to allow detection of very small amounts of virus. Since the distemper virus is an RNA virus, not a DNA virus, a test called "Reverse Transcriptase PCR" must be used but the amplification concept is the same. Vaccination will interfere with PCR testing for approximately 2 weeks (i.e. the modified virus from the vaccine will be detected creating a false positive).

CEREBROSPINAL FLUID ANTIBODY LEVELS – In neurologic distemper cases, cerebrospinal fluid is often tapped and distemper antibody levels checked. Distemper antibodies in cerebrospinal fluid is highly indicative of distemper infection as vaccine-induced antibodies do not cross the blood-brain barrier into the CSF fluid.
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