Canine infectious disease

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Canine Adenovirus (CAV-1)

CAV-1 is the cause of infectious canine hepatitis and may cause acute upper respiratory tract disease.

Clinical signs

Infectious canine hepatitis is most common in dogs <1 year of age. Clinical signs include fever, lethargy, abdominal discomfort, tonsillar enlargement, cervical lymphadenopathy, respiratory signs, vomiting, diarrhoea, hepatic encephalopathy and haemorrhage secondary to DIC. Jaundice is uncommon despite hepatic necrosis.

Diagnosis

A tentative diagnosis is based on the presence of hepatic necrosis in an unvaccinated dog. Virus isolation and serology may be useful; inclusion bodies may be observed on histological examination of liver biopsies. Virus isolation from the liver is often not rewarding.

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Canine Adenovirus (CAV-2)

Clinical signs

CAV-2 causes respiratory disease and is a potential cause of canine infectious tracheobronchiti (kennel cough).

Diagnosis

  • Susceptibility to infection is suspected in a non-vaccinated dog and diagnostic tests are not routinely performed in clinical cases. Radiography is unremarkable unless there is secondary bronchopneumonia due to coinfection with other respiratory pathogens or preexisting disease
  • Virus isolation (pharyngeal swab in viral transport medium). Detects CAV1 and CAV2. Ideally samples should be collected early in the course of disease and asymptomatic in contact animals may also be sampled (may be actively shedding). Samples should be collected into viral transport medium, which restricts growth of bacterial contaminants, refrigerated and submitted to the laboratory without delay. Freezing at -20˚C may reduce virus viability
  • Demonstration of a rising antibody titre in acute and convalescing serum (paired samples, 2 weeks apart) could confirm infection but since infection is short-lived this often has no clinical utility for the individual patient

Is booster vaccination necessary?

Little is published about protective titres in vaccinated dogs. A titre >40 is usually associated with protective immunity. It is possible that lower titres are actually protective since local and systemic immunity are involved in protection.

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Babesia

Clinical signs

The presentation is variable, depending on the infecting species and host factors; there may be a peracute, acute or chronic clinical course. Clinical signs include anaemia, lethargy, weakness, fever and haemoglobinuria with tachycardia, tachypnoea, splenomegaly and possibly lymphadenopathy, on clinical examination. Concurrent anaemia and thrombocytopenia is common. A more severe form of the disease may be associated with severe acid-base disturbances, hypoglycaemia, hypotensive shock and secondary organ failure, for example acute renal failure.

Diagnosis

  • Classical clinical presentation along with identification of organisms on blood smear examination. Babesia merozoites within erythrocytes are most commonly identified in smears made from capillary blood (ear vein) rather than venous blood. Organism may also be identified in bone marrow and splenic aspirates
  • PCR. In chronic cases with less virulent species for example, B canis canis, B canis vogeli then the infection may be below the limit of detection of microscopy. PCR is a sensitive and specific technique which amplifies the protozoal DNA for detection
  • Serology: not routinely available in the UK

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Distemper

Clinical signs

Signs are most common after maternal immunity has waned between 3-6 months of age. Mild disease is common with anorexia and upper respiratory tract signs, progressing to oculonasal discharge and coughing. Severe generalised infection is characterised by conjunctivitis (serous to purulent), coughing, anorexia, vomiting and diarrhoea. Nasal and digital hyperkeratosis, keratoconjunctivitis sicca and neurological signs may be noted following infection.

Diagnosis

  • Diagnosis is usually based on the presence of clinical signs in an unvaccinated puppy
  • Antibody titres may be determined in paired samples, collected at a 2-3 week interval. This test is also suitable for investigation of infection in ferrets and phocid (seal) distemper
  • PCR may be performed on CSF, whole blood, deep pharyngeal swabs (with organic material) and conjunctival swabs. A quantitative PCR is available for respiratory samples which may help to differentiate between recent vaccination and infection

Is vaccination necessary?

Studies in this area have used different methods and it is difficult to formulate a consensus view of the literature. A titre >40 is normally associated with protective immunity. It is possible that lower titres are actually protective since local and systemic immunity are involved in protection.

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Ehrlichia

Clinical signs

The clinical signs seen with Ehrlichiosis depend on the infecting species. The signs reported with Ehrlichia canis, which infects monocytes and macrophages, include fever, anorexia, weight loss, bleeding disorders (petechiation, ecchymosis, mucosal haemorrhage), lymphadenopathy and neurological signs. Clinical signs of chronic monocytic Ehrlichiosis may develop some months after importation from an endemic region. Infection is reported in Europe, USA and Africa but has been reported in a dog in SE England with no travel history (J Small Anim Pract. 2013 54(8):425-7). Anaplasma phagocytophilum which infects granulocytes is endemic in the UK. Signs include fever, anorexia, depression, lameness and lymphadenopathy. In addition, anaemia, thrombocytopenia and DIC have been reported in some patients.

Diagnosis

  • Clinical pathology: anaemia, leucopaenia, thrombocytopenia, hyperglobulinaemia and proteinuria are possible with E.canis infection. Thrombocytopenia, anaemia and DIC have been reported in A.phagocytophilum infections
  • Blood film examination (or buffy coat exam): demonstration of Ehrlichia morulae in leucocytes
  • PCR testing (EDTA peripheral blood, splenic or bone marrow aspirate). PCR testing for Ehrlichia spp detects A.phagocytophilum but a specific PCR is available for the latter if required

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Herpes virus

Clinical signs

Infection in bitches can cause abortion, stillborn or fading pups. Pups infected after birth develop an acute, fatal condition between 1-3 weeks of age. There is depression, anorexia, vocalisation, petechiation and the development of an erythematous rash (sometimes with oedema) on the ventral abdomen and inguinal region. Primary genital infections in adult bitches may show vaginal hyperaemia and submucosal haemorrhages. Vesicular lesions are reported during pro-oestrus, but regress in anoestrus. Infected male dogs may have similar lesions over the penis, sometimes with a preputial discharge.

Diagnosis

The following options could be considered but the first two are preferred:

  • Post mortem of affected puppies: reveals typical multifocal haemorrhages and characteristic kidney lesions
  • Virus isolation from genital lesions: a genital swab in viral transport medium is required
  • Serological testing: antibodies rise after infection but are only high for approximately 2 months. Low titres may be detected for some years after infection. The presence of antibodies only indicates exposure and not active infection, although latent infection might be inferred

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Leishmania

Clinical signs

Clinical signs may develop many months or years after infection. They are very variable but include exercise intolerance, weight loss, lymphadenopathy, skin disease (often an exfoliative dermatitis but also periorbital alopecia), anorexia, diarrhoea, lameness, epistaxis, melena and coughing.

Diagnosis

  • Clinical pathology: hyperglobulinaemia, hypoalbuminaemia and proteinuria are common (>80% of cases). Thrombocytopenia is reported in approximately 50% of infections
  • Organisms may be identified in smears made from lymph node aspirates or bone marrow
  • PCR on EDTA blood, bone marrow aspirate, lymph node aspirate, fresh biopsy material and conjunctival swab. Sampling of tissues most likely to be infected (as judged by the clinical presentation) is recommended but the sensitivity of the test is higher for lymph node and bone marrow aspirates. A negative result, particularly in peripheral blood, does not exclude infection. Fresh biopsy material should be placed on saline soaked gauze in a sterile container to keep moist. Formalin fixed specimens are not recommended. Conjunctival swabs should be moistened with sterile saline before use. After collection, the end should be cut off and placed in a sterile container. PCR may be used for diagnosis and generally the quantity of DNA correlates with the severity of clinical disease. In addition, qPCR can be used to monitor therapy and sampling at 1, 4, 6 and 12 months after the start of treatment is recommended. Correlation with serology may be useful in some patients, particularly if the PCR result is negative despite strong clinical suspicion of disease or the test is positive, despite only mild clinical signs. Testing for Leishmania may be combined with PCR tests for other arthropod borne infections such as Ehrlichia and Babesia
  • Serology. Given the long incubation period, dogs with clinical disease are expected to demonstrate antibody production and high titres are noted in dogs with active disease. Low titres imply infection but are less likely to indicate active disease and correlation with qPCR and further serological monitoring in 2-6 months is recommended to check for a rising titre. Serology is also used to determine the response to therapy but titres only start to decline at 4-6 months after initiation of successful therapy

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Leptospirosis

Clinical signs

Infection should be considered in dogs with acute renal or hepatic disease. It has also been proposed that infection may play a role in the development of chronic hepatopathies. Signs are more severe in young animals and include pyrexia, muscle tenderness, vomiting, dehydration, vascular collapse, increased thirst and coagulation defects. Icterus and renal failure are commonly noted but some animals may die per acutely, prior to development of typical clinicopathological changes.

Diagnosis

  • Clinical pathology: azotaemia is most common. Leucocytosis and thrombocytopenia may also be noted. Raised ALT, ALP and bilirubin are noted with hepatic involvement
  • Serological testing. A presumptive diagnosis may be made on the basis of a single high titre, with appropriate clinical signs, in a dog which has not been vaccinated recently. However, the titres may be negative in the first 7-10 days and further testing in 2-3 weeks is required to demonstrate a rising titre. Two serological tests are available. The Leptospira antibody screen (immunofluorescent antibody test; Leptospira antibody screen detects antibodies against a genus-specific antigen and is expected to detect antibodies against pathogenic serovars likely to cause clinical disease in the UK. However, it does not allow confirmation of the infecting serovar. A microscopic agglutination test is also available in which the patient sample is tested against serovar pools. If a positive result is obtained then the sample is tested against individual serovars (at an additional cost). Dogs with positive titres often have sera which cross reacts with a variety of serovars and historically the highest titre may be presumed to indicate the infecting serovar. However, this assumption has been questioned since it was found that the highest titre may vary between laboratories, over time, in the same patient
  • PCR on urine. Organism shedding is typically noted from day 7-14 after infection, prior to development of an antibody titre. A positive result confirms infection and urinary shedding

Is booster vaccination necessary?

Vaccination usually only produces a very short-lived humoral response and prevaccination screens are not advised.Serology should be reserved for suspected clinical cases. Annual booster vaccination is recommended for dogs with a reasonable risk of exposure.

Lyme disease

Clinical signs

Lyme disease is caused by infection with the tick-borne spirochaete, Borrelia burgdorferi. Clinical signs may develop from 3-30 days post infection and include fever, lethargy and most commonly an inflammatory polyarthropathy. The characteristic skin rash associated with human infection is rarely seen in the dog. Owners may or may not be aware of a recent tick bite.

Diagnosis

  • A polyarthropathy with neutrophilic (suppurative) inflammation is typically evident on cytological examination of synovial fluid from affected joints
  • Serology. The presence of an antibody titre only demonstrates exposure and does not confirm a diagnosis. Correlation with the clinical presentation and PCR is recommended. If there is no antibody titre early in the clinical course then repeat sampling in 2 weeks is recommended in suspect cases. If there is no antibody production by approximately one month after the onset of signs then Lyme Disease is unlikely
  • PCR on synovial fluid or blood (EDTA)

Neospora caninum

Clinical signs

Neuromuscular signs are most common, particularly in young puppies >6 months of age and include progressive hind limb paralysis and lower motor deficits of the bladder and rectum. Tremors, head tilt, seizure, hepatitis and pneumonia are reported in older dogs (>6 months). Infection of puppies is trans-placental and therefore if one puppy is affected then others are at risk. In addition, subsequent litters may be affected.

Diagnosis

  • Serology. Antibodies are detected by IFA. High titres are likely to be associated with clinical disease
  • PCR on CSF (EDTA)
  • Histology. Cysts may be seen in affected tissue

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Parvovirus

Clinical signs

Parvovirus enteritis produces vomiting, diarrhoea (which may be haemorrhagic), anorexia and dehydration. Infection may be fatal. Parvovirus myocarditis develops after in utero infection or infection of very young puppies (<8 weeks). It is seen in pups born to an unvaccinated, isolated bitch and is now uncommon.

Diagnosis

  • Faecal PCR is a sensitive test which may detect virus shedding for some weeks after infection. This quantitative test allows differentiation between prior vaccination and field infection. A negative result does not exclude infection
  • Serological testing: the presence of a high antibody titre in a single sample collected at least 3 days after clinical presentation, indicates infection. Demonstration of a rising titre in samples at a 14 day interval may be required. The humoral response after vaccination is similar to that of natural infection

Is booster vaccination necessary?

A titre >40 is expected to be associated with protective immunity.

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Toxoplasma gondii

Clinical signs

Clinical signs may be localised to neuromuscular, respiratory or GI systems, or may be generalised (seen most commonly in dogs <1 year old). Neuromuscular signs depends on the region affected but include seizures, cranial nerve deficits, tremors, ataxia, paresis and myositis. Retinitis and uveitis has been reported although is uncommon. Dogs do not support the sexual stages of the parasite and are therefore not a risk to pregnant humans or sheep.

Diagnosis

  • Serology: IgG and IgM. There is no reliable specific data for interpretation of canine serology but it is recommended to broadly follow the advice for interpretation of feline antibody titres. The presence of IgG antibodies indicates exposure, while IgM antibodies may be more indicative of early/active disease
  • PCR on CSF (EDTA)

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Authors & References

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