Cat Respiratory Infections

Feline Herpes Virus

• Double stranded RNA virus.
• Glycoprotein lipid envelope.
• 1 serotype.

Generic 'flu' like symptoms. Also conjunctivitis and hypersalivation. Low mortality rates. Turbinate damage can lead to chronic disease. 

Pathogenesis:

• Oronasal infection.
• 2-6 day incubation period.
• Multiplication in oral/respiratory tissue. 

Diagnosis:

• Serology.
• PCR.
• Histopath.
• Viral isolate- OP swab in VTM cultured in cells can take up to two weeks.

Feline Calicivirus

• ssRNA with no envelope.
• Many strains.

Clinical Signs:

• 'Flu like symptoms.'
• Oral ulceration and chronic stomatitis- 80-100% cats shed coronavirus with acute faucitis with experiment infection.
• Pneumonia.
• Shifting lameness in young cats- pneumonia and respiratory disease. Spontaneous resolution.
• Virulent systemic disease. Vaccinated cats not protected. Clinical signs include:

1. Facial/paw oedema-> necrosis/ulceration.
2. Respiratory disease/pyrexia.
3. Haemorrhagic nose and faeces.
4. Jaundice.

Diagnosis:

• OP swabs-> viral isolate.
• Serology.
• PCR.

Epidemiology of Both

• Short lived outside the cat. Herpes <1 day. Calici < 1 week.
• Transmission- direct contact with infectious discharge and fomites. Aerosol transmission not major.
• Carriers. 

1. Herpes- Latency and reactivation. 100% carriers after infection. Latency and recrudescence after stress with shedding for 4-11 days. Latency again.
2. Calicivirus- persistent infection. Most cats shed for 30d post infection with 50% still shedding 75 days post infection. Colony and show cats biggest shedders. Long life infection/self limiting. 

Feline Retroviruses

Feline Immunodeficiency Virus

• Lentivirus.
• Five subtypes-> A in the UK.
• Most common in older males, outside cats or sick cats. 

Pathogenesis:

1. Bite wound.
2. Replication in leucocytes.
3. Tissue localisation e.g. CNS.
4. 6-8 weeks. Lymphadenopathy, neutropenia and decreased CD4:CD8 ratio.
5. Prolonged asymptomatic period.
6. Immunosuppression.

Clinical signs-> Immunosuppression resulting in secondary bacterial infections. Direct virus effects e.g. CNS disease. May also result in tumours.

Epidemiology:

• Persistant infective antibody positive.
• Uninfected antibody positive.
• Test-> 90% sensitivity and 98% specificity, not used well for positive tests at low prevalence hence in house tests should be repeated by an independent test. 

Diagnosis:

• PCR- problems as not all strains recognised and problems with sensitivity.
• Diagnosis- viral isolate.
• Antibody e.g. western blotting. 
• All kittens may be virus positive and retest as there is the MDA to consider. 

Transmission:

• Virus in saliva- bites/fights. 
• Transplacental.
• Birth- milk.
• Does not survive well in the environment.

Prevention and control:

• Isolate infected cats.
• Vaccine-> killed vaccine with 2 FIV strains/adjuv vaccine. 
• Prevent cats fighting.

Feline Leukaemia Virus

• RNA genome with P27 protein core. Envelope and GP70 spikes. Only group A transmitted. 

Clinical Signs:

• Neoplastic disease of myeloid and lymphoid. Results in lymphomas- mediastinal (90% FeLV positive), multicentric, ailmentary and extranodal e.g. spinal/renal. 
• Leukaemia-> erythroleukaemia, and reticuloendotheliosis.
• Anaemia, immunosuppression, infertility and neurological disease.

Transmission:

• Inactivated in the environment.
• Congenital infection.
• Oronasal- virus shed in saliva. 
• Prolonged intimate contact e.g. grooming.

Pathogenesis:

• Transient viraemia- neutralising antibody limits the spread of infection. Up to 8 weeks and infection may spread to bone marrow. Normally mounts effective immunity.
• Latent infection- bone marrow, short lived. Blood tests are FeLV negative.
• Persistent viraemia- grave prognosis. Ineffective immunity mounted. Replicates in bone marrow cells. Virus and P27 ag in bood. <16 week old cats, high viral dose, previous infection, vaccination or maternal antibodies.

Epidemiology:

• Age related resistant to development of persistent viraemia.
• 2-4 years old generally.
• Multicat houshold with prolonged contact. Endemic infection= 30% cats persistent viraemic. 

Diagnosis:

• Non specific tests e.g. anaemia.
• Detect virus/viral antigen P27- ELISA, rapid immunomigratory assay, immunoflourescence.
• Viral plasma isolate.  
• Detect FeLV neutralising antibody- detects immune cats.

Control:

• Pets- vaccinated and not high risk.
• Breeding- vaccination not 100%. Regular test and remove and remove any new cats.
• In house tests, possible false positives, so retest all confirm +ve with a second test and retest any positives on the second test. Tested by viral isolation/IF. 

Vaccination:

• Problems= adverse reactions and lack of efficacy.
• Test before vaccination- high risk cats.
• Protects against persistent infection. 12 months. Not 100%. A, B and C types. Canarypox vector. 
• Inactive/virus particles with recombinant gp70 adjuvinated. 

Feline Viral Infectious

Feline Panleucopenia

• Feline version of parvovirus in dogs.
• Targets actively diving cells resulting in:

1. Enteritis (villous crypt epithelium).
2. Panleucopenia (bone marrow and lymphoid tissue).
3. Cerebellar hypoplasia (neonatal cerebellum).
4. Foetal death in early pregnancy.

Clinical signs:

• Profuse diarrhoea.
• Sudden death.
• Pyrexia, anorexia and depression.
• Panleucopenia.
• Cerebellar hypoplasia.

Diagnosis:

• Post mortem histopathology.
• Faecal samples.
• Serology.

Treatment:

• Fluid therapy.
• Interferons.
• Antibacterials.

Successful vaccination with live/inactivated virus. Long term environmental survival.

Feline Spongiform Encelopathy

• Same as BSE (mad cow disease).
• Signs-> polyphagia/polydipsia. Muscle fasiculations/altered gait. Salivia drooling and behavioural changes.

Feline Infectious Peritonitis.

When I just googled this to find a picture- some pretty nasty looking ones came up! Not really something I want on the front page of my blog!

Organism

FIP is a mutation of feline coronavirus. Feline coronavirus alone generally causes an enteric disease. However, FIP has mutated so that it can multiply in macrophages. This leads to a widespread body granulomatous reaction. The disease is generally sporadic, although isolates of the disease from a singular household are more similar than within a geographical area which has a greater genetic variation.

Coronavirus:

• Enveloped +ve RNA Virus.
• Contains a nucleocapsid and glycoprotein spikes.
• In RNA viruses, RNA polymerase shows no proofreading. This leads to higher mutation rates at base pair level and recombination between coronaviruses as a component of the quasispecies theory. 
• Not all cats with coronavirus develop FIP. Infection with coronavirus is faecal-orally and generally affects cats in groups. Not all cats develop the disease as the virus strain, dose and the cat's immunity varies. 
• FIP is enhanced by antibodies and the main pathogenesis of FIP is by antibody-antigen complexes. This means that pre-existing antibodies to coronavirus increase the disease acceleration. This also means there is problems with developing a vaccine, as antibody responses would have an adverse effect on the disease.
• The Immune complexes act by depositing in the wall of small blood vessels leading to vasculitis. The antigen is already bound to the antibody and hence this enhances uptake by macrophages. Cats with NO antiviral antibodies therefore cannot develop FIP. 

Pathogenesis:

1. A shedding cat infects a susceptible cat ORONASALLY.
2. This leads to replication in the tonsils, URT and intestinal epithelia. 
3. This leads to multiplication in macrophages. 
4. Poor CMI-> wet variation of FIP. Partial CMI- Dry FIP. Good CMI-> recovery. If there is no multiplication in macrophages the cat sheds in the salivia and faeces. A recovered cat also sheds via these routes. 

Clinical Signs:

ALWAYS FATAL.

Wet FIP:

• Fluid in the body cavities.
• Fluctuating unresponsive fever. 
• Hepatomegaly, jaundice and abdomen swelling.
• Inappetence & weight loss.
• Muffling of heart sounds. 

Dry FIP:

• Anorexia, depression and lethargy.
• Signs dependent on the organs involved- CNS, eye or abdominal organs.
• Fluctuating fever.

Diagnosis:

• Definitive diagnosis-> histopath.
• FIP fluid- viscous and straw coloured, high protein content (globulins), froths when shaken and clots when standing.
• Blood chemistry-> neutrophilia, lymphopaenia, mild non regenerative anaemia, hyperproteinaemia (increased IG), albumin:globulin ratio decreases, and increases liver enzymes, bilirubin and urea. 
• Serology- 

1. Ab via ELISA.. +ve result does not mean the cat has FIP with certainty and shoudl be used in conjunction with other diagnosis.
2. Ag via PCR. Detects infection not disease. Needs single molecular deletion that predicts FIP for absolute diagnosis. 
3. Ab with IF-> results vary as different strains/techniques used. Goat anticat ab where cat ab adheres to cells infected with feline coronavirus. Experimental error so needs a four fold difference to be different. 

Treatment:

• Interferon.
• Always fatal. 

Transmission:

• Faeces.
• Salivia.
• Transplacental (1 in 3 queens). 

Epidemiology & Control:

• 75% breeding catteries and 25% pets positive for coronavirus. 
• Sporadic FIP- peak between 6 months to 2 years old.
• Asymptomatic carriers in seropositive healthy cats- faecal excretion for between 14 days to 7 months possibly cyclical. 
• In endemic breeding households kittens seroconvert by 10 weeks after loss of the MDA-> therefore isolate the queen 1-2 weeks prepartum, wean the kittens early with strict isolation, and check kittens still seronegative at ten weeks old. Appropriate hygiene should be ensured with an adequate number of litter trays, less cat and kitten numbers (max 8-10 adults) and keep groups stable to not introduce the disease.
• In rescue centres control encompasses batching cats, decreasing stress and thorough hygiene. 

Bacterial Infections of Dogs and Cats

There are many infections of the dog and cat of bacterial origin. The most well known ones will be leptospirosis and bordatella bronchiseptica. Bordatella as a respiratory pathogen will not be covered in this blog post. However, there are many other bacterial pathogens that we do not naturally associate with disease in dogs and cats.

Salmonella

Primarily a disease we associate with chickens. 

In dogs, infection is more common than disease. 25% dogs are carriers below 6 months old, and 1-5% cats. They will shed the virus for around 4-6 weeks. The most common species isolate is salmonella typhimurium. 

• Typically of salmonella the route of transmission is faecal oral/direct contact. 
• Clinical signs, if any, generally appear subclinically. Therese vary from non specific signs such as vomiting and diarrhoea to bacteraemia, abortions and stillbirths. 

Diagnosis generally requires faecal isolation. For GI disease the use of antibacterials is NOT reccomended, although bacteraemia in the blood needs to be treated with antibacterials. Sensitivity tests should be done on antibiotics such as sulphonamides or trimethoprims. 

Campylobacter

Another disease we generally associate with chickens. Zoonosis. C.Upsaliensis most common pathogen. Opportunistic/secondary pathogens include C.Jejuni in conjunction with Canine Coronavirus which can result in severe GI disease 

Diagnosis requires fresh material, and special transport in growth media. Treatment involves supportive therapy.

Leptospirosis

Three species- canicola, icterohaemorrhagiae and grippotyphosa.

Wild and domestic subclincial reservoirs.

Pathogenesis:

1. Entry via mucous membranes/abrasions.
2. Leptospiraemia.
3. Kidney, liver, CNS, spleen, eyes and genital tract localisation.
4. Persists in the renal tubules.

Clinical Signs:

• Peracute sudden death.
• Pyrexia/anorexia.
• Vomiting.
• Icterus.
• Acute renal failure (anuria/oliguria). 

Diagnosis:

• Serology- titre about 1/800.
• Spirochetes in urine- flourescent ab.
• leptospira PCR detection.

Treatment:

• Supportive fluid.
• Penicillin- bacteraemia. 
• Doxycycline- eliminates carrier status.
• Zoonotic.

Prevention:

• Prevent contact with reservoir hosts.
• Eliminate infection from carrier animals.
• VACCINE- does not protect against all serovars. 

Other Disease Affecting Dogs

E.Coli- Enteropathogenic E.Coli Toxins.

Borrelia Burgdorferi- reverse zoonosis. Lameness with lymphadenopathy. 

MRSA- zoonotic. Commensal in the nasal and skin passages. Prevent spread and decolonise EMRSA 15+16. Treat via culture and sensitivities.

Ehrliciosis- monocytic. Travelled dogs- R.Sanguineus. Coinfection with babesia and leishmania. Doxycycline treatment. 

Bacterial Infections of Cats

Mycobacterium

• Zoonotic.
• Cutaneous nodules, draining sinuses and panniculitis.
• Culture diagnosis.
• Treatment with rifampicin/enrofloxacin.

Feline Infectious Anaemia

• MYCOPLASMA HAEMOFELIS
• Transmitted by fleas or vertically.
• Usually asymptomatic but can cause anaemia through stress/immunosuppression.

Clinical Signs:

• Anaemia.
• Splenomegaly.
• Pyrexia.
• Severe haemolysis= jaundice.
• Cyclical- 3-8 week replication.

Diagnosis:

• Haematology- regenerative anaemia, polychromasia and nucleated RBC.
• Giemsa smear- red dots adherent to RBC. (Smear can appear negative with antibiotics). 

Treat:

Oxytetracycline/doxycycline. 

• 3 weeks- does not eliminate infection.
• Prednisolone as some cats can develop autoimmune haemolytic anaemia.
• Check for underlying inmunosuppression e.g. FeLV (trigger). 

Just another week...

I wish I was .. I could do with a beach holiday right about now. The sun is shining outside, it looks glorious and I'm stuck inside revising public health legislation, one resounding sad face :(. A brighter note- only ONE WEEK until freedom!

One bit of sefton park.

Another thing to look forward to tonight is pizza with the housemates :D. I've definately been bad for the junk food through revision so my healthier eating habits have gone a bit down the pan. My recent array has been jelly babies, white milk chocolate, 3 creme eggs and some marshmellows. They all went in about 4 days.. whoops. 

I went out running the other day. It's been a week since, and with all the junk eating and exams it was one of my harder runs. I go running in sefton park which is a really lovely place. If you ever visit liverpool, you should have it on your list of places to go :). I did 25 minutes which was good, even though my muscles are feeling the pain today.

Exams have been fine so far although I wasn't feeling my best at all through the first 2 exams. Although it all turned out alright in the end and I was very happy with the turnout of the pathology written exam. I hope I can do better in the practical element this time around though!

My exams left are public health and infectious disease. They're both about even... I know public health better but it will be the harder exam. Pros and cons I think...

One week until I get to see my gorgeous padawan Pippa dog. :). I also have the summer ball and canal boat trip in the next two weeks. So excited for exams to be over. 

Adrenal Gland

Function 

Mineralcorticoids:

• Loss of potassium and conservation of sodium. Acts on cells of the kidney DCT and sweat gland. 

Glucocorticoids:

• Intermediate glucose metabolism.
• Acute effect- within 15-30 minutes before the compensatory effects of insulin. 
• Increased glucose production- hyperglycaemia due to:

1. Overall decreased glucose uptake.
2. Increased glucose catabolism in tissue and muscle.
3. Increased gluconeogenesis (liver).
4. Decreased lipogenesis, increased lipolysis in adipose tissue-> glycerol and ffa. 
5. Increased protein catabolism. 

Hypoadrenocorticism

• Primary (addison's disease). Idiopathic cortical atrophy. All zones affected. Non specific symptoms. 
• Secondary- due to hypopituitary. 

Hyperadrenocorticism 

Hyperaldosterone:

• Dogs and cats.
• Nodular hyperplasia, adenoma or carcinoma.
• Zona glomerulosa. 
• Metabolic acidosis and oedema are the consequences. 

Hypercortisolism:

• Generally seen in the dog.
• Adenoma/carcinoma of the zona fasiculata.
• Iatrogenic- prolonged use of glucocorticoid therapy.
• Paraneoplastic- ectopic ACTH production in non pituitary tumours e.g. bronchial carcinoma, thymoma. 

General features:

1. Increased appetite and food intake.
2. Weak and atrophic muscles- extremities and abdomen. 
3. Gradual abdominal enlargement, lordosis and muscle trembling.
4. Temporal muscle atrophy.
5. Skin alterations.

Other Adrenal Gland Disorders

• Hyperaemia/haemorrhage with intoxication or sepsis.

Regressive Changes

• Adrenal cortical insufficiency- stress induced (circulatory, infectious, toxic etc). Often with cortical necrosis. Addison's crisis.
• Adrenal cortical atrophy- prolonged glucocorticoid use. Z.fasiculata. Addison's crisis with sudden cessation of therapy. 
• Idiopathic cortical atrophy- autoimmune disorder. 

All lead to hypoadrenocorticism:

• Reduced mineralcorticoid levels lead to hyperkalaemia and reduced serum sodium and chlorine. Hyperkalaemia leads to vascular disturbances whereas there is progressive haemoconcentration and dehydration due to loss of sodium. 
• Reduced glucocorticoid levels lead to moderate hypoglycaemia due to decreased gluconeogenesis and increased insulin sensitivity. Also leads to skin hyperpigmentation due to increased MSH release. 

Neoplasia & Hyperplasia

• Bilateral cortical (secondary) due to persistent ACTH levels via the pituitary in the zona reticularis and fasiculata.
• Primary cortical hyperplasia in old dogs. Endocrine activity or silent. Atrophy of zona fasiculata in non hyerplastic areas due to negative feedback.
• Nodular hyperplasia of the zona glomerulosa- hyperaldosterone- metabolic acidosis and oedema.
• Cortical adenoma/adenocarcinoma. 
• Medulla phaeochromocytomas- cattle, dogs and horses. Endocrine activity (catecholamines). Malignant= infiltrative and metastasis. Consequences- arterial hypotonia, left cardiac hypertrophy and myocardial necrosis. 

Parathyroid Gland

One of my favourite glands because a) they are so small and b) they cause a wide range of pathological conditions (although in hindsight this makes my exams harder to revise for...)

The normal function of this gland is to regulate calcium and phorphorus homeostasis by the production of parathyroid hormone (easy to remember right). 

It does this by:

• Mobilisation of calcium from bone. Stimulates a cell called an osteoclast to reabsorb bone material which liberates calcium into the blood. 
• Enhances calcium reabsorption in the small intestine via vitamin D. It stimulates the active form of vitamin D in the kidney which induces a synthesis of calcium binding protein in the enterocytes that facilitates the efficient absorption of calcium into the blood.
• Suppresses calcium loss in urine. Stimulates tubular reabsorption of calcium and loss of phosphate ions. Therefore parathyroid hormones acts to counteract hypocalcaemia and hyperpohosphataemia. 

Hypoparathyroidism

• Reduced parathyroid hormone release. 
• Leads to hypocalcaemia-> neuromuscular excitability-> spasms, temors and muscle tetany. Chronically osteomalacia/rickets.

Causes:

• Parathyroid agenesis.
• Inflammation- autoimmune parathyroiditis.
• Surgical excision.
• Tumour.
• Vitamin D intoxication- leads to functional hypoparathyroid due to high calcium levels.

Postnatal Hypocalcaemia in Cattle

• Milk fever.
• Dietary imbalance between parathyroid hormone and calcitonin.
• Paresis.
• Severe hypocalcaemia and hypophosphataemia near parturition. 
• Caused by excessive calcium in the diet- low rate of bone reabsorption and an inactive parathyroid with anorexia and GI stasis near parturition. When there is the switch to lactation the cow cannot cope and bows under the pressure as the net calcium outflow exceeds the inflow. 

Hyperparathyroidism 

Calcium mobilisation from bone results in hypercalcaemia. 

• Primary- hyperplasia, adenoma or carcinoma of  parathyroid gland.
• Secondary- chronic renal insufficiency or Ca/P imbalance. 
• Tertiary- end stage of secondary- non-responsive autonomous hyperplasia. 
• Pseudohyperparathyroidism- humoral malignant hypercalcaemia or dogs with adenocarcinoma of the anal sac which releases PTH-like hormone. 

Secondary hyperparathyroidism and chronic renal insufficiency:

Leads to:

• Fibrous osteodystrophy.
• Metastatic calcification.

This is due to a reduced calcium reabsorption and phosphate secretion, and a reduced vitamin D activation. Hyperphosphataemia and hypocalcaemia in the blood. Due to the reduced intestinal calcium reabsorption the calcium precipitates mineral in the tissues leading to metastatic mineralisation. Reduced blood calcium leads to parathyroid hyperplasia and fibrous osteodystrophy with overlapping osteomalacia. 

Fibrous osteodystrophy:

• Bone pain, loss of teeth, and deformity of the maxilla and mandible. Grossly= soft demineralised bone. 
• Enhanced osteoclast reabsorption of mineralised bone with substitution of normal bone by insufficiently mineralised osteoid and collagenous connective tissue. 

Other Parathyroid Changes

• Regression/inflammation- atrophy due to thyroid goitre/cysts. Diffuse lymphocytic parathyroiditis in old dogs which is rare. 
• Hyperplasia and neoplasia- primary hyperplasia (rare), secondary hyperplasia (consequence of hypocalcaemia), and primary tumours- rare (chief cell adenoma/adenocarcinoma which can be hormonally active). 

Thyroid Function

Other common endocrine conditions include diseases of the thyroid gland. The ones which are most common/heard about are hypothyroidism usually affecting dogs and hyperthyroidism usually affecting cats. 

Hypothyroidism

• Especially seen in old dogs. 

Primary hypothyroidism

Causes include:

• Loss of functional parenchyma (loss of functioning thyroid gland) due to aplasia (organ doesn't develop), hypoplasia (incomplete development), atrophy (decrease in organ size after full growth), inflammation and neoplasia. All of these factors destroy the tissue which results in a decreased capacity for the thyroid to produce the sufficient amounts of the hormones it needs.
• Deficiency of hormone components especially iodine. For hormones to be released into the blood, they are bound in a substance known as colloid in the gland by thyroglobulin. Iodine is needed to bind the tyrosine residues (thyroid hormone) in place for endocytosis (excretion). Therefore a lack of iodine will disrupt the release of thyroid hormones.
• Chemical blockage of production e.g. thioureate.
• Gland resection. 

Canine hypothyroidism is normally due to idiopathic follicular collapse or lymphocytic thyroiditis (inflammation). 

The thyroid gland hormones are responsible for the basal metabolic rate Therefore a reduction in the hormones results in a decreased basal metabolism which results in the following consequences:

• Increased body weight- due to decreased metabolism.
• Dermatological- thin coat, alopecia with hyperkeratosis and hyperpigmentation.
• Reproduction- abnormal oestrus cycles and a reduced sperm count.
• Goitre- enlarged thyroid seen with iodine deficiency. 
• Myxoedema- mucoid oedema in the subcutis/mucosa seen in fetal hypothyroidism.
• Cretinism- dwarfism seen with endemic iodine deficiency or endogenous cretinism (sporadic in the goat). 

Secondary hypothyroidism

• Pituitary gland TSH deficiency. 

Hyperthyroidism

• Common in aged cats with thyroid multinodular hyperplasia and adenoma.

Consequences of increased basal metabolism:

• Weight loss.
• Hepatic lipidosis and necrosis due to glycogen deficiency. 
• Left ventricular hypertrophy. 

Other Thyroid Disorders

• Inflammation- chronic lymphocytic thyroiditis in the dog. An autoimmune disorder.

Hyperplasia

Known as goitre as a consequence of thyroid hormone deficiency. Can also happen after partial gland resection for compensatory mechanism. Occurs due to:

• Hyperthyroid leads to excessive levels of thyroid hormone in circulation which inhibits TRH and TSH secretion leading to atrophy of the normal parenchyma. 
• Hypothyroid leads to functional hyperplasia to try to maintain function. Can also occur in  due to extreme iodine deficiency or with herbivore congenital disease associated goitrogenic plants. 
• Euthyroid is the most common cause of functional hyperplasia. It is due to endemic goitre deficiency. 

Appears diffuse in young animals and nodular in old animals. 

Neoplasia

 

Epithelial Tumours 

• Frequent in areas of endemic goitre.
• Adenoma-> seen in the cat and produce excess thyroid hormone.
• Carcinoma-> early metastasis haematogenously to the lung. Follicular, papillary or solid growth. 

Mesenchymal Tumours

• Fibroma etc. 

C-Cell Tumours 

• Tumour of the cells that produce the hormone calcitonin. Rare and sometimes seen in old animals.