53 | How to take the panic out of caring for your parvovirus patients

PodcastGastroenterologyEmergency and Critical Care
Written By Laura Jones

Today, we’re talking about quite possibly the worst GI disease of them all - parvovirus.

 

Yep, these patients are often a winning combination of tiny, horrifically behind on fluids, poorly tolerant of nutrition and dealing with severe gastrointestinal signs. We need to do a lot to support these patients, and we’re diving into all of it in this episode.

Giving great care to these patients starts with understanding how this common infectious disease affects the body—so let’s get straight into what parvo is and what it does to our patients!

So let’s talk about parvo…

Parvovirus, or canine parvovirus-2 (CPV2), is a highly contagious and resilient virus which rapidly attacks the gastrointestinal tract in dogs. There are actually three strains of CPV2 - a, b, and c. All are highly virulent; types a and b are predominantly found in the UK, whereas type c is the predominant strain throughout Europe.

Regardless of the strain, the transmission route and the effect on our patient are the same.

What happens when a patient gets parvo?

CPV is transmitted either directly or indirectly, via the faeco-oral route. It is a highly resistant virus that can survive in the environment for up to a year, including in the soil and in both extremes of heat and cold.

Once our host ingests the virus, it travels to local lymphoid tissue, where it replicates before travelling to its target organs and exerting its effects.

CPV targets rapidly dividing cells, which are located in the bone marrow, lymphoid tissue, and intestinal crypts (small glands between each villi in the GI tract). It can also affect the myocardium, particularly in neonates.

If we think about how this impacts our patients, parvovirus causes:

  • Destruction of the immature blood cells in our bone marrow - particularly causing leukopenia, which in turn causes immunosuppression and predisposes our patient to sepsis

  • Immune dysfunction due to lymphoid tissue damage as well as leukopenia

  • Severe gastrointestinal signs due to intestinal crypt cell damage, in turn, causing changes to fluid, electrolyte and acid-base balance, risking hypoglycaemia and increasing the risk of bacterial translocation across the damaged GI tract.

  • Myocarditis, progressive cardiac injury or sudden death in puppies. This tends to happen in very young puppies <2 weeks old.

So, how do these patients present to the clinic?

CPV is most commonly seen in young dogs between six weeks and six months old. Most adult dogs are immune due to vaccination (assuming they are up-to-date with vaccinations) or have some immunity from a previous mild or subclinical infection.

The signs each individual patient presents with depend on, among other factors, their age, vaccination status, whether they have maternally derived antibodies and the presence of concurrent gastrointestinal disease.

Young puppies under 18 weeks of age are particularly at risk due to weaning, dietary changes, stress and lifestyle changes, and rehoming, which all occur during this time.

What signs do they come in with?

These patients typically present as an emergency with acute onset anorexia, lethargy and pyrexia, alongside vomiting and severe diarrhoea. In most cases, this is haemorrhagic - though it isn’t always, so the absence of haemorrhagic diarrhoea does not exclude CPV!

The combination of anorexia, vomiting and profuse diarrhoea means these patients are severely dehydrated on presentation. Often, their dehydration is so severe that they are hypovolaemic on presentation, too. Signs such as:

  • Bradycardia

  • Weak pulses

  • Pale MMs

  • Prolonged CRT

  • Hypotension

  • Hypothermia

  • Tacky or dry MMs

  • Severe skin tenting

  • Acute weight loss

Are commonly seen. Alongside this, the anorexia we see in these young patients quickly leads to hypoglycaemia, in turn causing neurological signs - including dull or obtunded mentation and even seizures in severe cases.

These patients are also at a high risk of sepsis due to bone marrow cell destruction, lymphatic dysfunction and leukopenia. When we combine this with the severe intestinal cell damage CPV causes, the risk of sepsis in these patients increases even more.

Because the lining of our GI tract acts as a barrier (keeping the bacteria and normal GI flora in the GI lumen and stopping it from crossing into the bloodstream) and CPV compromises this barrier, we can get movement of those GI bacteria into the bloodstream and endotoxic shock.

Septic and endotoxic shock cause similar signs to hypovolaemia, with the exception of MM/CRT. Because these patients get vasodilation due to their sepsis, blood pressure and cardiac output drop. As the vessels in the peripheral tissues dilate and blood flow to them increases, these patients have bright red MMs and a rapid (almost immediate) CRT.

All of this means that our parvovirus patients commonly come in collapsed, with significant changes to fluid balance, hypothermia and (possible) hypoglycaemia and sepsis.

So, how do we diagnose these patients?

The first clues we have lie in our patient’s signalment and clinical signs. From here, we’ll perform standard bloodwork (and possibly imaging) to determine the severity of our patient’s condition and guide treatment, and perform confirmatory testing to make our diagnosis official.

Let’s start by looking at bloods

Common tests performed on these patients include haematology, biochemistry and a venous blood gas or emergency blood panel.

Haematology reveals a leukopenia in up to 85% of dogs, and biochemical changes can include:

  • Hypoalbuminaemia

  • Hypokalaemia

  • Hyponatraemia

  • Hypochloraemia

  • Increased liver enzymes

  • Hypoglycaemia

  • Hyperglobulinaemia

Acid-base changes secondary to vomiting and diarrhoea are also commonly seen.

What about parvovirus testing?

Once we’ve performed our emergency bloodwork, we must confirm our suspicions with parvovirus testing.

This is most commonly performed via in-house antigen testing (SNAP testing) or faecal polymerase chain reaction (PCR) testing, where we look for viral DNA in the sample.

Antigen testing is highly specific (aka, there’s a reduced risk of a false negative), but we can see false positive results in recently vaccinated dogs, for example.

If you get a negative result in a clinically suspicious patient, there’s a good chance you’ll need to perform a PCR to confirm your diagnosis.

And then there’s imaging.

Now, we usually don’t need to image these patients, which is great, given that the last thing we want to do is spread parvovirus all over our hospitals.

However, if you have a patient with abdominal pain or a patient presenting with diarrhoea and parvovirus is not 100% confirmed, you’ll likely need to perform an abdominal ultrasound.

This can be helpful in looking for intussusception or signs of other underlying gastrointestinal disorders.

Faecal testing may also be performed for parasitology and culture to look for parasitic or bacterial causes of diarrhoea. 

Ok, so you’ve diagnosed your patient. Let’s talk treatment!

The first thing we’ll need to do is stabilise our patient.

Now we know that these patients tend to present as emergencies and severely unwell - meaning that they’ll need rapid triage and stabilisation. We’re not going to be waiting for those diagnostic results - we’ll be placing our IV catheters, pulling bloods for analysis, and stabilising these patients simultaneously.

Stabilisation initially seeks to address life-threatening changes in fluid balance, glycaemic control, and temperature, as well as the risk of sepsis.

So, get crystalloid boluses in to improve their perfusion, treat hypoglycaemia with glucose boluses, and get antibiotics on board due to the risk of bacterial translocation and sepsis.

Then, it’s all about aggressive supportive care.

We can’t treat CPV itself. Instead, we aim to provide aggressive supportive treatment and nursing care while the patient’s immune system works to clear the virus.

Alongside fluid therapy at an appropriate rate based on ongoing fluid losses, we’ll also:

  • Supplement electrolytes (e.g. potassium) as needed to manage hypokalaemia

  • Give analgesia (opioids, not NSAIDs, due to ongoing severe GI disease) to keep the patient comfortable

  • Give antiemetics like maropitant and ondansetron to manage nausea and vomiting

  • Give prokinetics like metoclopramide and cisapride to control ileus

  • Continue antibiotics due to the ongoing risk of sepsis

Other treatments described for managing CPV include antivirals, immunotherapies, and immune plasma, though there is little evidence behind their use.

What about nursing care?

It’s no surprise that these patients need intensive supportive care, and much of that is achieved through the nursing support we give.

These patients need:

  • Intensive and regular monitoring

  • Early nutritional support

  • Careful elimination management and skin and coat care

Alongside general nursing care. 

Nutrition is a particularly important area of nursing. Previously, we were taught to delay the onset of feeding in CPV patients, but we now know that early enteral nutrition significantly improves morbidity and mortality. 

Early enteral nutrition should be prioritised unless the patient has severe ongoing vomiting, which prevents feeding. Place a naso-oesophageal or nasogastric tube (I’m a massive fan of a nasogastric tube in these patients, as we can also use it to aspirate the stomach and drain those horrible parvo-y contents) and start trickle-feeding these patients. Even if you can’t meet all of their calorie needs because they won’t tolerate that much food, getting something in will nourish the GI tract and help prevent bacterial translocation.

In severe cases where patients just won’t tolerate any enteral nutrition (or will only tolerate a tiny amount), parenteral nutrition might be needed. This isn’t without risk, so it is generally only performed in referral settings or facilities with 24/7 hospitalisation.

So that’s treatment—but wouldn’t it be better to prevent all of this?!

Yes! Yes, it would.

Vaccination is a safe and easy way to reduce CPV incidence. It’s a core vaccine recommended for all healthy dogs, regardless of age, lifestyle or location.

Modified-live vaccines are used; these contain a live but weakened form of the virus, which stimulates the immune system to produce antibodies against the virus and protects the host.

Vaccination begins at as early as 6 weeks of age and is repeated regularly until the patient reaches 16 weeks. The frequency and number of vaccinations given depend on the patient’s age at initial vaccination, the presence of maternally derived antibodies, and the risk level in their environment.

The best thing to do is follow either the WSAVA vaccination guidelines or the AAHA vaccination guidelines for core vaccination, depending on your location.

After initial vaccination, a booster dose is given one year later, and then every 3 years thereafter for the rest of the patient’s life.


So there you have it! The lowdown on diagnosing, stabilising, treating and nursing your parvovirus patients. Yep, it’s a horrendous disease but with careful and intensive treatment and nursing, these patients can do very well - and there’s nothing quite like the feeling of seeing a parvo puppy finally go home after weeks of intensive nursing care.

Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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