Infectious diseases Flashcards
0
Q
What are the clinical signs of feline panleucopaenia virus?
A
Early to mid stage in utero infection can result in foetal death, resorption or abortion. infection in the late stage of gestation or in neonatal kittens may result in kittens with profound and permanent suppresion of their immune system., thymic atrophy and cerebellar hypoplasia, tremors and wide based stnce. Infections in older kittens typically follow incubation period and range from subclinical to peracute death. mild forms include self limiting diarrhoea, panleucopenia. Other kittens may show profound diarrhoea, panluecopaenia, secondary bacterial infection, sepsis/death. Affected kittens often present with a sudden onset of depression, anoreia, pyrexia and apparent thirst - but do not actually drink.
1
Q
Describe the transmission of feline Panleucopenia virus
A
Ubiquitous in the environment and highly contagious, almost all cats exposed, seen most freq in unvaccinated kittens 3-5 mths, may also be seen in kittens from well vaccinated pedigree breeding cats - high levels of environmental contamination, disease results from superinfection with gut bateria. FPV transmitted via oro faecal route, direct contact, envinronmental contamination. Virus very stable and can survive long time in organic material. On entry to the cat the virus repilicates in rapidly dividing cells particularly the lymphoid tissue bone marrow and intestines.
2
Q
How is feline panleucopaenia virus diagnosed?
A
Presumptive based on presence of clinical signs, vaccinal status, age and environment accompanied by profound panleucopaenia, particularly neutropenia. Serology should show a rising titre in a non vaccinated kitten. Virus isolation or PCR tests can be performed in faeces samples, oropharyngeal swabs in transport media or post mortem material.
3
Q
What is the treatment for feline panleucopaenia virus?
A
Treatment relies on supportive care. This includes intensive fluid therapy, broad spectrum antibiotics, anti emetics, gut protectants, B vitains, provision of warm clean environment and good nursing care. Severely panleucopaenia kittens may benefit from a blood transfusion. Parenteral feline interferon omega can be very helpful or oseltamivir.
4
Q
How can feline panleucopaenia be prevented?
A
all kittens should be vaccinated against FPV, beggining at 8-12 weeks of age, with a second dose 3-4 weeks later, and a final dose >16 weeks of age. cats older than 16 weeks of age need be given 1 dose only. colostrum deprived kittens can be vaccinated regardless of age.
5
Q
Describe the aetiology of ‘cat flu’
A
Common name for infectious acute upper respiratory tract disease. Seen freq in unvaccinated cats and kittens when they are kept in large groups. Can be caused by feline calicivirus, feline herpes virus, Other organisms may also be involved, bordatella bronchiseptica, pasturella multiocida and mycoplasma species and chlamydophila felis.
6
Q
Describe feline herpes virus (causing cat flu)
A
FHV-1 is a labile DNA virus of a single serotype and consistent pathogenicity that is readily destroyed outside the host. up to 80% of recovered cats may become viral carriers and excrete virus under stress, concurrent disease or following the use of corticosteroids.
7
Q
describe Feline calicivirus (causing cat flu)
A
An RNA virus with variable virulence and pathogenicity that is more resistent within the environment to disinfection. all affected cats shed this virus for variable periods of time after resolution of the clinical signs. the most important sources of these viruses are clinical cases followed by healthy carriers.
8
Q
What is B bronchiseptica?
A
A gram negative coccobacillus that can act as a respiratory pathogen in a number of species, including pigs, dogs, cats and humans. It can cross species and has potential zoonotic risk Affected cats may remain persistently infected and shed bacteria.
9
Q
What is C felis?
A
It has a special predilection for the conjunctiva. In the Uk up to 30% of cats with conjunctivitis have a C felis infection. It is an obligate intracellular bacterium. Affected cats may remain persistently infected and shed bacteria.
10
Q
Describe the pathogenesis of cat flu
A
Most are transmitted by aerosol and or direct contact of the eyes, noses and mouths. FHV-1 replicated in the epithelial cells of the nasal chambers, tonsils, conjunctiva and trachea. It causes local necrosis of mucosa and leads to a serous then mucopurulent discharge FCV targets similar cells but more often causes ulceration of the tongue, hard palate, soft palate, pharynx and external nares. These ulcers form from vesicles which burst due to tissue necrosis and cellular infiltration with neutrophils. An acute immune complex mediated synovitis can occur occasionally.
11
Q
What are the clinical signs of cat flu?
A
young cats, although any age group can be affected. Incubation period around 6 days. Morbidity is high while mortality should be low with appropriate treatment. Disease more serious in pure breeds. Sneezing first clinical sign, followed by serous occular and nasal discharge which rapidlyy becomes mucopurulent due to secondary bacterial infection. Cats are depressed and pyrexic. Conjunctivitis, keratitis and corneal ulceration may occur. Coughing and dyspnoea seen less comonly. Ulceration of the oral cavity leads to salivation nd loss of appetite. C felis is associated with conjunctivitis. Coughing seen with FHV-1 and b bronchiseptica. FHV-1 causes more severe disease than FCV with more conjunctivitis, perfuse nasal discharge and obvious coughing and FCV tends to be associated with milder signs and oral ulceration.
12
Q
How is cat flu diagnosed?
A
Presumptive diagnosis - clinical signs and history of exposure. Not usually possible to determine which organisms are involved. Nasal or oropharyngeal swabs can be taken for isolation and culture and in the case of fhv-1 and c felis PCR tests. Bacteriology of little value. Serology can test whether a cat has previously exposed to FCV or FHV-1.
13
Q
What is the treatment for cat flu?
A
Antivirals and immune stimulants - Feline IFN omega as antiviral, oral famcyclovir, oral L lysine. Antibiotics - selected by culture and sensitivity or broad spectrum 2-3 weeks. For b bronchiseptica - doxycycline. Nutritional and fluid support - iv fluids, feeding tube. supportive nursing care, multivitamins, ucolytics - ease respiratory tract congestion e.g bromhexine, nebulised air - use of steam or or nebulised air can help clear airways. Decongestants. Do NOT use corticosteroids.
14
Q
How can cat flu be controlled?
A
Suitable vaccination - against C felis, B bronchiseptica. Decrease stockign density a nd increase ai r flow, ensure good sneeze barriers, hygiene, disinfectant, have individual cats and wean kittens in isolation, have suitable quarantine facility, stop breeding.
15
Q
Describe the aetiology of feline infectious Anaemia?
A
The organism that causes - haemobartonella felis ( renamed mycoplasma haemofelis, M turicensis, and mycoplasma haemominutum - non pathogenic. The parasites adhere to red blood cells changing their cell surface and making them antigenic so they are removed by the RE system of the spleen and liver. the replication cycle of this parasite takes 2-8 weeks so clinical disease tends to be cyclic. infection may be subclinical, most likely to result in disease when the cat is coinfected with FeLV.
16
Q
Describe the pathogenesis of feline infectious anaemia?
A
Route of transmission believed to via saliva through biting and fleas. Transmission from queen to kittens either in utero or via milk may also occur. Persistent infections, clinically normal carriers and recurrent infections can all occur.
17
Q
What are the clinical signs of feline infectious anaemia?
A
Cats may be asymptomatic, just show fever or other cats develop acute disease with signs of lethargy, pale mucus membranes, tachypnoea, tachycardia and dyspnoea, splenomegaly is common and pyrexia is variable. Where the anaemia is severe a haemic murmur may be detected and jaundice may develop. Autoimmune haemolytic anaemia usually develops concurrently.
18
Q
How is feline infectious anaemia diagnosed?
A
Parasitaemia waxes and wanes but giemsa or acridine orange stained blood smears can be used for detection of the organism attached to red ccells. the organism may appear as rods, cocci or chains. detection of the organism is variable and repeat smears may be required. Small peripheral vein best. Regenerative anaemia should be present with polychromasia and normoblasts. AIHA is often present (autoimmune haemolytic anamia) resulting in autoagglutination or positive coombs test.
19
Q
What is the treatment for feline infectious anaemia?
A
Doxycycline or oxytetracycline - which may actually be able to clear the infection. Where AIHA is present give prednisoline tapering over 8 weeks. Use of steroids may lea to increased risk of generating a chronic carrier. Blood transfusion in severe cases of anaemia. no vaccine available.
20
Q
Describe Feline leukaemia virus
A
a retrovirus with an RNA genome surrounded by a protein core and an external envelope. The most abundant of the core proteins is p27 which is the antigen detected in the FeLV test. The envelope has glycoprotein spikes which contain the antigens which induce production of the viral neutralising antibodies. Three subgroups of FeLV exist - A,B and C - dependent on the type of glycoprotein spike present. Subgroup A is found in all infected cats and is important in the generation of B and C in vivo by gene recombination and mutation.
21
Q
Describe the transmission and pathogenesis of feline leukaemia virus?
A
FeLV is transmitted by cat to cat contact with the virus being excreted in saliva (biting, licking and mutual grooming), urine, faeces and milk. Congenital infection can also occur. FeLV is labile and indirect spread of the virus is not thought to occur.
22
Q
What are the possible outcomes of infection with feline leukaemia virus?
A
30% progressive infection, 40% latent infection, 30% regressive or abortive infection. Progressive and latent infection may show FeLV related disease.
23
Q
Describe abortive infection of feline leukaemia viirus
A
Following infection the virus is eliminated by an effective early immune response so there is no viral replication and no FeLV infection of cells. These cats test PCR negative.
24
Describe regressive infection cased by feline leukaemia virus?
The virus replicates in the cats oropharynx. In these cats the antigebaemia is only transient since the virus is then reduced to very low levels by an effective immune response. the duration of the transient viraemia which can be detected by p27 elisa/rim test is variable and can last from a day to 12 weeks. These cats may maintain low levels of viral replication for protracted periods of time before eventual elimination and conversion to abortive status.
25
Describe latent and focal infections of feline leukaemia virus?
In about a third of cats which appear to eliminate the virus the infection is maintained in bone marrow or other tissues such as the intestines or mammary tissue. This is because moderate initial proviral load and viral replication leave a residual viral infection. Inadequate virus is present to reslt in a viraemia and these cats are usually n egative on conventional FeLV elisa/ RIm and IFA tests. In latent infections the virus can sometimes be identified on bone marrow samples. Cats are not thought to excrete virusa.
26
Describe progressive infections of feline leukaemia virus?
Where the immune response is inadequate the virus is transferred to the bone marrow via the blood. Following replication in the bone marrow large amounts of virus are released into the plasma and from here can gain access to other organs. Multiplication of the virus in the salivary glands allows excretion of the virus in saliva. the incubation period between infection and the appearance of virus in the blood can vary between 4 and 30 weeks.
27
What is the epidemiology of Feline leukaemia virus?
The outcome of infection depends upon a number of factors, particularly the age of the cat and the dose of the virus. the younger the cat the mroe susceptible it wil be to persistent infection and therefore development of clinical disease. Cats <16 weeks of age are most likely to develop persistent viraemia. Prolonged or recurrent exposure to the virus aids effective transmission of FeLV making transfer likely in large multicat households. With increased use of FeLV screening and vaccination FeLV infection is now less common in multicat households and infection is being seen more common in older adult males related to fighting.
28
describe immunosuppression related to FeLV?
Many of the diseases due to FeLV are related to its immunosuppressive actions. FeLV can result in immunosuppression by numerous mechanisms including cytopenia, neutrophil and lymphocyte dysfunction, Thymic atrophy. this may result in non specific infections; predispose to opportunist infections, exacerbate pre existing disease and ,make treatable disease slower to respond to appropriate treatment.
29
Describe anaemia caused by feline leukaemia virus?
Anaemia in association with felv is seen commonly. Regenerative anaemia can occur due to FeLV associated immune mediated haemolytic anaemia or due to M haemofelis infection whilst marrow disorders can result in non regenerative anaemia. A pure red cell aplasia can result from FeLV subgroup C infection but this is quite rare.
30
Describe the neoplastic diseases seen with FeLV?
Lymphoma most common, infection may have occured years before but left damage,LSA can be generalised or localised. Generalised can b e multicentric or disseminated. multicentric form is seen as LSA affecting several separate sites, such as kidneys, nose and nervous system. Disseminated form occurs in young to middle aged cats with up to 60% being feLV positive. Localised LSA involving the thyymus + intrathroacic lymph nodes. Most cases are now FeLV negative and typically seen in young siamese or oriental cats.
31
What other disorders can feline leukaemia virus cause?
FeLV can cause severe Haemorrhagic enteritis similar to FPV infection, a progressive deforming polyarthritis in young male cats, infertility in queens, plus foetal resorption and neonatal death, and neurological signs such as ataxia and pupil changes.
32
Describe the ELISA test for detection of FeLV infection
Snap, cite test, commercial labs - detects the FeLV p27 antigen detected in the plasma.
33
What is the prognosis for cats infected wwith FeLV?
High risk of developinig FeLV related disease. In one study 85% of viraemic cats died within 3.5 years of diagnosis compared to 15% of recovered or uninfected cats.
34
How should FeLV be controlled?
Testing in a household for all cats for FeLV. Negative and positive cats should be separated and the house qarantined with no new cats. good hygiene measures regardng litter trays, feeding bowls etc should be followed and cats then retested 3 months later. Cats positive on both occasions are considered to be persistently viraemic and should be kept in isolation permanently. Cats which are neative on both occasions are considered to be FeLV negative. If any previously negative cats are now positive they are retested 3 months later.
35
What treatment considerations must be used for cats with FELV or FIV
Isolate the cat to reduce exposure to pathogens and to reduce the risk of it transmitting its infection to other cats. Ideally the cat should be kept on its own and not allowed to roam freely outside. it that is not possible then feed cat separate. if access is permitted outside, instigate a night curfew. avoid overcrowding, vaccinate regularly, feed separately, give essential fatty acids, control parasites especially fleas, have regular health and weight checks., do not use griseofulvin in FIV cats.
36
Describe feline immunodeficiency virus?
Prevalent in cat populations throughout the world and is important cause of disease, FIV belongs to lentivirus family of retrovirus group. Increase in Prevalence with age and a higher prevalence in male cats compared to females. It is the older male cat free to roam outdoors. Major route of transmission is via saliva, biting, and territorial aggression most at risk. Vertical transmission can also occur. Venereal transmission not been reported. level of infection variable.
37
Describe the pathogenesis of FIV
FIV falls into four phases - the acute primary phase occurs as the virus replicates rapidly in lymphoid tissue. This begins approx 3 weeks after infection. This phase may be subclinical. more typically > pyrexia, malaise and lymphadenopathy. Most infected cats then become asymptomatic, levels of circulating virus are low but viral replication continues within infected tissues. Immunosuppression develops as the virus causes a reduction in CD4+ T helper cells. Both cell mediated immunity and humeral immunity become defective as T and B lymphocyte function is suppressed. Initial signs of immunosuppression are usually seen as secondary infections, skin and mucosal surffaces. OVer time infections become repeated and chronic.
38
What are the clinical signs Of Feline immunodeficiency virus?
Related to secondary infections - including gingivitis, stomatitis, weight loss, rhinitis, diarrhoea, skin disease, occular signs such as uveitis, fever, lymphadenopathy, respiratory disease, otitis, recurrent abscesses, chronic entertis or chronic renal insufficiency. Mild behavioural changes due to meningoencephalitis. Opportunistic pathogens whch healthy cats would usually show greater resistance. such as ; toxoplasmosis, salmonellosis, FIA, demodicosis and dermatophytosis. Evidence tat the incidence of neoplasia is increased in FIV cats. Tumours include lymphoma, scc, mammary gland carinoma, mast cell tumours, bronchoalveolar carcinoma.
39
What are the clinical laboratory findings of FIV?
While clinicopathological abnormalities are common in FIV infected cats, none are pathognomonic. in the acute phase, many cats show neutropenia and lymphopenia. These usually resolve as the cats b become asymptomatic but often recur intermittently. Clinicall ill cats may show neutropenia lymphopenia, anaemia, monocytosis or thromocytopenia. Analysis of serum biochem reveals hypergammaglobulinaemia.also may include azotaemia, raised liver enzymes, hypercholesterolaemia, hyperglycaemia or prolonged coagulation times.
40
Describe why FIV specific testing may be carried out?
There are a number of reasons for a cat to be tested for FIV. the cat has clinical signs suggestive of a retrovirus infection, the cat has been in contact with a retrovirus infected cat, the cat comes from a high risk group (feral, rescue centre), pre breeding testing.
41
How is a definitive diagnosis of FIV determined?
Made by detecting either the virus or FIV specific antibodies in the blood or saliva. In the UK, diagnostic kit to detect anti FIV antibodies are currently based on elisa or rapid immuno migration methodologies. ELISA tests detect antibodies to the core protein FIV p24 while RI tests detect antibodies to the envelope protein gp40. PCR used to detect integrated provirus DNA is used as a confirmatory test by some laboratories as are immunofluorescent antibody tests and western blotting.
42
Describe false positive antibody results that may occur.
since prevalence of infection is low in healthy cats and none f the assays are 100% specific, occasional false positive results will occur. technical error may result in occasional false positive results particularly when whole blood or saliva are used rather than serum or plasma. Equivocal results should not be over interpreted they are unreliable and affected cats should be re tested. Kittens born to an FIV infected queen will gain MDA via the colostrum, they may therefore test positive with tests designed to detect antibodies. while MDA usually declines to undetectable levels by the time the kittens are twelve weeks of age, occasional kittens will test positive beyond this time.
43
Describe false negative antibody results that may occur?
up to 20% of FIV infected cats do not have detectable levels of antibody. this may be due to early infection (it can take up to 8 weeks for antibodies to develop, terminal immune collapse, a relative or absolute lack of antibody, a failure in the test system to identify antibody. these cases must be diagnosed by PCR - available in certain specialist laboratories.
44
describe the management of FIV?
Depends on nature and severity of clinical signs, type of environment it lives, and willingness of owner, cat should be exposed to as few in infectious organisms as possible, ideally should be isolated or kept in small groups, should be fed separately on high quality diet. stress will accentuate immune dysfunction exposure to stressful situations should be minimized. Care must be taken w hen vaccinating. clinically unwell animals should not be vaccinated. Treatment based on managing problems associated with immunosuppresion. Use of corticosteroids appears to be contraindicated.
45
What is the prognosis for FIV?
Long term prognosis is guarded, but some cats will survive for many years following diagnosis. an FIV positive result is not an indication for euthanasia necessarily. it is not possible to give an accurate prognosis but generally/ the more severe and chronic the clinical signs, the worse the prognosis.
46
What is feline infectious peritonitis?
One of the major viral infectious diseases in cats. Although sporadic it is usually fatal. FIP is caused by infection with feline coronavirus. Able to survive in environment under certain circumstances for several weeks. up to 40% of the general cat populatioin have antibodies against FCoV and in catteries and muti cat households this rises. Many FCoV are harmless and only cause mild enteric signs however it is believed that when FCovs are able to replicate rapidly they undergo mutation which can lead to increased pathogenicity. This enables the virus to infect macrophages and in some causes, cause FIP.
47
How does transmission of feline infectious peritonitis occur?
transmission of FCoV occurs via the faeco oral route. there is a higher incidence of FIP in cats housed in colonies and the burmese, persian, birman and bengal reeds appear to be predisposed. F IP is seen most frequently in cats <2 years of age and in geriatrics.
48
What is the pathogenesis of FIP
Immune mediated. Inflammatory lesions occur as small white nodules all over the visceral and parietal peritoneum and various organs. These nodules consist of neutrophils and macrophages in so called pyogranulomatous lesions. These are usuall centred on small blood vessels resulting in a vasculitis. Tw forms are recognised - both wet and dry.
49
Describe the two forms present of FIP
Effusive or wet form, fluid accumulates in the peritoneal or pleural cavities with lesions on the peritoneum and pleua. In the non effusive or dry form small focal lesions develop in the peritoneum, kidneys, liver, and mesenteric lymph nodes and pancreas. In addition, thoracic lesions may involve the pleura, diaphragm, lungs and myocardium. The eyes are often involved presenting as anterior uveitis and posterior uveitis where the CNS is involved inflammation of the meninges may produce ataxia and seizures.
50
Describe the clinical signs of FIP?
While signs of FIP may be acute, they are more commonly chronic and insidious. the History usually includes anoreexia, weight loss, pyrexia and dullness. Int he wet form ascites or hydrothorax are common. in the dry form clinical signs depend on the organs affected and can include renomegaly, jaundice, anterior uveitis and CNS signs. gut involvement may result in vomiting o diarrhoea and a mass at the ileocaecal junction.
51
How is a diagnosis of FIP made?
Clinical signs. Lymphocytic holangitis is a major differential for cats presenting with ascites and jaundice. Haematology most commonly reveals lymphopaenia and Neutrophilia with anaemia. serum biochemistry may reveal Hyperglobulinaemia and or bilirubinaemia. The serum albumin to globulin ratio is often low, tpically <0.4 serum acid 1 alpha glycoprotein. In the effusive form appearance of any ascitic or pleural fluid is characteristic - non septic exudate high in protein and cells which is usually viscous and yellow in nature. Cytology reveals neutrophils. Serology can be used to identify antibody to FcO b ut this is not specific to pathogenic strains. A negative titre can rule out dry fp but not wet FIP.
52
What is the treatment and prognosis of FIP?
Treatment usually ineffective although rFeIFN and steroids and supportive care have been advocated. Prognosis is extremely poor and euthanasia generally recommended once diagnosis has been made.
53
How can FIP be controlled?
Hygiene measures, stress should be m inimised as this may increase a cats susceptibility to FIP. Any concurrent diseases such as FeLV or FIV which may also increase susceptibility should be addressed, no cats should be moved into or out of household for 6 months.
54
Describe Toxoplasmosis in cats?
Toxoplasma gondii is an intracellular coccidian parasite. the definitive hosts are members of the felidae family. Although infection with T gondii is extremely common, t is rarely a cause of significant disease in any species.
55
How do cats become infected with toxoplasmosis?
Cats usually become infected y ingestion of encysted organisms present in the tissues of a chronically infected intermediate host. The cyst wall is digested by the cat, releasing infectious organisms which penetrate the intestinal wall and replicate throughout the body as rapidly dividing tachyzoites. The organisms also invade and replicate in the intestinal epithelial cells where sexual reproduction results in the formation of oocysts which are excreted in the faeces. As the cat develops an immune responce, oocyst shedding stop and tachyzoites become bradyzoites within tissue cysts.
56
What happens to cats after ingestion of cysts?
Cats previously unexposed to T gondii usually begin shedding oocysts between 3 and 10 days after ingestion of infected tissue and continue shedding for around 10-14 days, during which time many millions of oocysts may be produced. once immune, further shedding of oocysts is extremely rare, after oocysts have been passed in the faeces they undergo sporulation which takes 1-5 days: prior to this, they are not infectious. Oocysts are very resistant and may survive in the environment for well over a year.
57
How do intermediate hosts become infected?
Intermediate hosts ( rodent, birds, sheep, pigs, cattle). become infected by ingestion of sporulated oocysts. An extra intestinal cycle of infection occurs and results in encysted bradyzoites which are infectious to cats and other intermediate hosts. T gondii may also be acquired by a foetus in utero if the host acquired infection during pregnancy.
58
Describe Clinical feline toxoplasmosis
Clinical disease rare, but may develop following primary ifection where inadequate immune response fails to arrest the invasive tachyzoites or as a result of reactivated infection where compromised immunity allows the reactiation of infection from encysted bradyzoites with the formation of invading, multiplying tachyzoites. Clinical disease most common in young cats less than 2 years old may be due t poorly developed immune response. reactivation of infection in older cats may be linked to co infection with FV or felv.
59
What are the clinical signs of feline toxoplasmosis?
Anorexia, weight loss, lethargy, dyspnoea, occular signs, pyrexia. other less common features include - gastrointestinal signs, neurological signs, lymphadenopathy, jaundice, myositis and abortion.
60
How is diagnosis of feline toxoplasmosis made?
Diagnosis is problematic and a definitive diagnosis rests on demonstration of the organism in tissues taken at PM examination or in biopsy samples. Faecal samples may be examined for T gondiii oocysts but this is technically difficult and requires experience to correctly identify the oocysts. Clinical signs do not usually develop until after oocyst shedding has ceased.
61
How may serology be used to diagnose feline toxoplasmosis?
following infection, igG seroconversion occurs after 2-4 weeks, with peak titres by 4-6 weeks. Titres are then maintained at high levels for many months or years. recent infection is seen as a fourfold rise in antibody titre over weeks 2-4. In many cases clinical signs will develop either before seroconversion occurs or not until after peak titres have developed. IgG serology is therefore often difficult to interpret and a single antibody titre is rarely of any value. IgM titres rise more rapidly following infection and are normally maintained for only a limited period of time so a single high IgM titre demonstrates recent or reactivated infection with T gondii.
62
What is the treatment of feline toxoplasmosis?
Clindamycin treatment of choce. Azithromycin good second choice espeically with pneumonia. Combining clindamycin with pyrimethaminne may be needed in severe cases effective therapy. If uveitis is present apply topical glucocorticoids.
63
Describe the zoonotic potential of T gondii?
Congenitally acquired toxoplasmosis is of most concern which can occur when a previously unexposed woman acquires toxoplasmosis during pregnancy in this situation - 40% of foetuses will be infected and 10% will develop neurological or occular disease which is present at birth. Infection is correlated with eating undercooked meat - not owning a cat.
64
What is feline cowpox virus infection?
Infection is seen in domestic cats, rodents, h umans, cattle, dogs elephants and foals. Although cowpox virus infects cattle they are not implicated as a source of infection for cats. Cats infected with cowpox are usually hunters or bank voles, field voles and wood mice which are known to carry the infection. Infection can be found in house mouse occasionally. Affected rodents do not usually show signs of infection. N o age or breed /sex predilection.
65
What are the clinical signs of feline cowpox virus infection?
Virus enters skin through a bite wound usually on the cats head, neck or limb. Infection becomes apparent after a few days as a small ulcerated nodule. the may be followed by secondary bacterial infection causing cellulitis or abscessation. The virus multiplies in the lungs, nasal passages and lymphoid tissue. the mouth nasal passages, lungs and gut may be affected with oral and gastrointestinal ulceration, nasal discharge, pneumonia and diarrhoea. Numerous skin lesions appear 10 days to several weeks later - oval circulated ulcerated papules and plaques up to 1cm in size any part of the body. Infection usually resolves 6-8 weks later.
66
How is diagnosis of feline cowpox virus infection made?
A positive antibody titre is supportive of recent infection (previous 6 moths) titres ay be positive 7-14 days after initial exposure. Crust material from skin lesions can be sent in a sterile container for analysis, PCR, viral culture or electron microscopy. skin biopsies show characteristic changes on histopathologic examination.
67
What is the treatment for feline cowpox virus infection?
The lesions usually heal without intervention. Secondary bacterial infection may require broad spec antibiotics. Severe cases may require hospitalisation and fluid therapy. Severe cases with respiratory involvement have a poor prognosis unless treated with interferon, covering antibitoics, analgesia and potentially inhaled steroids. Avoid glucocorticoids.
68
How is feline cowpox virus spread?
Cat to cat transmission may occur and cowpox can be an occasional zooonosis, to very young or elderly immunosuppresed people, or individuals with severe atopic skin disease. the virus can survive for months at room temperature and is resistant to many disinfectants. Hypochlorite based products are effective.
69
Describe the aetiology of tuberculosis.
tuberculosis can be caused by a number of different, but closely related bacteria. Most feline tuberculosis is now cutaneous although iin chronic cases the infection may spread to the lungs and cause dyspnoea. Most affected cats are keen hunters, regularly catching small roodents. Mice and voles can carry M microti. Cats become infected frequently on the face and legs.
70
Which cats are predisposed to developing tuberculosis?
Adult male cats, most cats are FIV and FeLV negative.
71
What are the clinical signs of tuberculosis in cats?
affected cats present with localised disease affecting the skin or systemic signs related to the alimentary and or respiratory tracts. They are typically firm, raised, dermal nodules which ay be ulcerated or form non healing wounds with draining sinus tracts. Extension of granulomatous tissue may involve the subcutaneous structures, muscle and or bone Skin lesions commonly associated with either local or generalised lymphadenopathy. Submandibular or prescapular lymphadenopathy may b e only clinical finding. Tubercles arise in the lungs. In the alimentary form tubercles arise in the intestines/mesenteric lymph nodes.a range of clinical signs may be seen with disseminated disease.
72
How is tuberculosis diagnosed?
Changes in srum biochemistry and haeatology are non specific and vary with severity of disease. Hypercalcemia > poorer progosis. Radiographic changes variable and include tracheo bronchial lymphadenopathy, interstitial or miliary lung infiltration, localised consolidation, hepato or splenomegaly, abdominal masses, mineralised mesenteric lymph nodes or ascites. Specific tests with IFn gamma test good at detecting members of the tuberculosis complex. Cats do not react strongly to intra dermally administered tuberculin so unreliable. Tests for specific serum antibody responses have also proved unhelpful. Aspirates/biopsy should be stained ziehl n eelsen stain. Acid fast bacilli seen in affected macrophages. Culture organism to determine exact species.
73
How is tuberculosis managed?
Necessary to know w hich mycobacteria resonsible. Deciding to treat a case is contentious. Consider potential zoonotic risk. Treatment is long term and difficult to maintain. Uncomplicated cutaneous disease carries most favourable prognosis. Surgical excision of small cutaneous lesions may be considered Pending a definitive diagnosis interim therapy with a fluoroquinolone has been recommended, but this should only be considered in cases of localized cutaneous infection. It is better to recommend double or triple therapy.
74
What is the treatment of choice for tuberculosis?
Ideally treatment should consist of an initial and a continuation phase. The inital phase reqires 3 drugs and lasts 2 months, while continuation phase lasts a further 4 months depending on the type and extent f the disease. Fluoroquinolones have potential in the treatment. Inital treatment with rifampcin-pradofloxacin-carithromycin/azithromhcin followed by a continuation phase of rifampicin and either pradofloxacin or clarithromycin. For ease of administration all medications can be given as liquids placed in single syrine or tablets put together in single gelatin capsule.
75
What is feline leprosy syndrome/ disease caused by non tuberculosis mycobacteria ? (NTM)
disease is believed to be caused by infections from rodents or by saprophytic usually non pathogenic organisms from soil, water and decaying vegatation contaminating cutaneous wounds. Cats appear at greater risk than most other domestic species. adut cats with a hunting or fighting lifestyle most ilkely to be affected. Siamese and abysinnian cats appear to be predisposed.
76
What are the clinical signs of feline leprosy syndrome?
Granulomatous panniculitis is seen where multiple punctate draining tracts occur with a salt and pepper shaker appearance these are associated iwth subcutaneous nodules and coalescence produces large areas of ulcerated non healing tissue. Inguinal fat pads, flanks and tail base are affected most frequently. Feline leprosy syndrome or feline leprosy like disease is seen as single or multiple cutaneous or subcutaneous nodules which may be haired, alopecic or ulcerated on head limbs and ocassionaly trunk.
77
How is feline leprosy syndrome diagnosed?
Histopathology - granulomatous nodules or pyogranulomatous panniculitis . culture is the diagnostic test of choiice. some of the organisms grow easily, but molecular techniques are being used more commonly to identify those that are more difficult to grow
78
Describe the treatment of feline leprosy syndrome
Minimum of pradofloxacin is suggested while waiting for culture. Surgical removal of small nodules is recomended. antimicrobial therapy should be determined by culture and sensitivity. extensive cases may require a combination of fluoroquinolone, clarithryoycin or azithromycin and or rifampicin. May be needed for prolonged periods 6-12 weeks for simple cases, or 6-12 months for extensive ones.
79
What is the prognosis for feline leprosy syndrome?
Depends on extent and severity of disease. For single cutaneous nodules it is good while for panniculitis and systemic disease it is poor to guarded. the prognosis deteriorates further when there have been previous unsucessful attempts at surgery.
80
What is distemper?
A large RNA vrus of the morbilivirus genus. The CDV single stranded RNA is surrounded by a lipoprotein envelope composed of viral glycoproteins. Different strains of virus exist and account for variation in pathogenicity. These may have tropisms for pulmonary, neural or epidermal tissues. Virulence is likely determined by variations in viral glycoproteins. CDV is most comoonly spread by aerosol or droplet exposure reflecting its high concentration in respiratory secretions. It is also spread in urine and faeces. It is extreely labile and susceptible to heat and drying and UV light.
81
Describe the pathogenesis of CDV.
Following exposure CDV multiplies in tissue macrophages and spreads via the local lymphatics to tonsils and bronchial lymph nodes. Widespread virus replication within lymphoid tissue results in pyrexia and leukpenia approximately 4-6 days post infection. Within 8-10 days of infection CDV spreads haematogenously to epithelial cells and the CNS tissues. The clinical outcome depends on the level of CDV antibody titres and adequacy of the cell mediated immunity. Individuals with adequate antibody titres and cell mediated cytotoxicity clear virus from most tissues and show no clinical signs, although they can still shed virus. Intermediate levesof CMI with delayed antibody production results in infection of the epithelial tissues ad development of clinical signs.
82
What are the clinical signs of canine distemper virus?
Bilateral serous to mucopurulent oculonasal discharge with concurrent coughing and dyspnoea due to bronchopneumonia. Ocular serous to mucopurulent bilateral conjunctivitis, keratoconjunctivitis sicca, mild anterior uveitis, damage to intestinal epithelium results in vomiting and diarrhoea - anorexia, dehydration, weight loss, pustular dermatitis, nasal and digital hyperkeratosis, may include seizures, vestibular disease, ataxia or myoclonus, acute meningoencephalitis. Neonatal infection prior to eruption of permanent dentition results in damage to enamel and dentine resulting in distemper rings.
83
How is diagnosis of CDV made?
characteristic clinical signs in an unvacciated dog, especially 3-5 month old puppies once MDA levels have fallen.Absolute lymphopenia may be present, distemper inclusions on peripheral blood smears, false negative results are comon, non specific biochemical changes relating to dehydration and polyclonal gammopathy, csf may show increased protein content and cell count. Immunofluorescent antibody on cojunctival smears or on tonsilar tissue, leukocytes or respiratory epithelium. ELISA to detect anti CDV IgG and IgM. demonstration of a rising antibody titre may be useful for confirmation of infection. Interpretation may be difficult in vaccinated individuals. In dogs with neurological signs increased anti cdv antibody may be present within the CSF. PCR can be performed on various tissues e.g csf.
84
What is the treatment of canine distemper virus?
IVFT, anti emetics, antibiotics for secondary infections, coupage and nebulisation if bronchopeumonia is present, anticonvulsants for seizures. Prognosis - mortality estimated at 30%. development of neurlogical signs carries a guaded prognosis.
85
DEscribe infectious canine hepatitis
ICH is caused by canine adenovirus, a dsDNA virus with haemagluttinating surface antigens. CAV-1 is closely related to, although antigenically distinct from cav-2 which causes resp tract diseease. CAV-1 is transmitted via the oronasal route from infected urine, faeces and fomites. Urinary excretion of virus may persist for 6-9 months following active infection. CAV-1 is resistant to environmental inactivation, surviving for days on soiled fomites at room temperature. Inactivation occurs at 5-60 degrees C or using p henol, sodiu hydroxide or iodide based disinfectants.
86
What is the pathogenesis f infectious canine hepatitis?
After oronasal infection CAV-1 initially localises in the tonsils b efore progressing along the lymphatics to regional lymph nodes and via the thoracic duct tot he blood. viraemia results in dissemination to various tissues, with hepatic parenchyma and vascular endothelium being the primary targets. Viraemia persists for 4-8 days and is associated with pyrexia. CAV-1 is cytotoxic and results in cellular injury of affected tissues. Liver - widespread centrlobular to panlobular necrosis may occur, clinical outcome depends on various factors including level of pre existing immunity and viral load/dose.
87
What happens to the vascular endothelium, kidney and eye in infectious canine hepatitis?
Damage to vascular endothelium results in bleeding diathesis, including vasculitis and disseminated intravascular dissemination. Kidney: localised in the glomerular endothelium results in glomerular injury and glomerular deposition of circulating immune complexes results in transient proteinuria, persistence of virus in renal tubular epithelium results in prolonged viral excretion. eye - direct cytotoxic damage and deposition of immune complexes within the cornea and uveal tract result in corneal oedema and uveitis.
88
What are the clinical signs of infectious canine hepatitis?
Peracute - rapid death. Acute- pyrexia, anorexia, vomiting, abdominal pain, diarrhoea, bleeding, lymphadenopathy, pharyngitis, abdominal pain, hpeatomegaly, abdominal distension, jaundice, petechiation, ecchymoses, epistaxis, leeding from venipuncture sites, cns signs, harsh lung sounds.
89
How is diagnosis of i nfectious canine hepatitis made?
Leukopenia, lymphopenia, neutropenia, initially followed by leukocytosis and neutrophilia on recovery, raised ALT, AST and SAP with reduced hepatc function, hyperbilirubinaemia, hhypoglycaemia may occur with acute hepatic necrosis, poteinuria, coagulation abnormalities, thrombocytopenia, demonstration of a rising antibody titre, typical findings of centrilobular necrosis on liver biopsy, nuclear inclusion bodies from impression smears of liver, viral isolation from body tissues or secretions of IFA of tissues may be necessary to make a definitive diagnosis.
90
What is the treatment of infectious canine hepatitis?
Treatment is symptomatic and supportive - IVFT, IV glucose, blood plasma transfusion, anticoagulant therapy for DIC, therapy for hepatic encephalopathy, lactulose and antibiotics, anti emetic therapy, s adenosyl methionine as a glutathione precursor. Prognosis guarded.
91
Describe the aetiology of rabies
It is a rhabdovirus, neurotropic - characterised by neuronal degeneration and encephalitis, it is invariably fatal, all mammals are susceptible but some are much more susceptible than others, primary route of transmission is through the saliva of an infected animals. Classic rabies is characterised by furious aggression.
92
What is post exposure prophylaxis in rabies?
Post exposure prophylaxis is very effective at preventing development of the disease even when exposure to rabies has occured. PEP involves local cleansing of the bite wound followed by administration of the vaccine/immunoglobulin > almost 100% effective. Low awareness, cost of PEP and availability of PEP in the developing world makes rabies a socio economic issue in poorer countries.
93
Describe the two different disease cycles of rabies
Sylvatic rabies > wildlife > low risk to human health. may be transmitted to stray/feral dogs via wildlife.
Urban rabies > stray feral /dog population > high risk to human health.
94
Describe the pathogenesis of rabies
Following bite, there is local viral replication in striated muscle spreading to motor nerve endings. The viral load of the bite and distance from the brain will affect how long it takes for clinical signs to appear. Virus spreads in spinal cord neurons- rapid spread to CNS causing progressive paralysis of lower motor neurons. Viral spread through peripheral and cranial nerves into other tissues including salivary glands but also kidneys, eyes, skin, adrenal glands. A t this point there are behavioural changes, the animal secretes massive amouunts of virus in saliva and will be infectious to other animals.
95
What are the clinical signs of rabies?
1) Prodromal phase > lasts around 3 days, subtle behavioural changes, sensitivity to noise/light, iting/licking wound, anorexia
2) dromal phase > furious form: aggresssive, attacking animals, objects, agitation, convulsions, vocalization, drooling. Dumb form: dullness, dysphagia, profuse salivation, dropped jaw, prolapsed third eyelid, beginning of paralysis.
3) Progressive paralysis of hind limbs, staggering gait, paralysis of swallowing muscles, foaming at the mouth, severe despiratory difficulties, lapsin into coma and death. Course of signs usually lasts less than 15 days. only 30% of dogs wil exhibit the furious form.
96
How is diagnosis of rabies madE?
Fluorescent antibody test on brain tissue, increased specificity, increased sensitivty and rapid.
Also rabies tissue culture inculation test for confirmation - examine inoculated tissue after 3-4 days using FAT.
97
What are the control measures put in place for rabies??
IMport controls - pet travel scheme, quarantine, post import checks. Notifiable disease - legal obligation to report suspect cases. Powers to detain and destroy infected animals and restrict the movement of susceptible animals in the event of an outbreak. Compulsory vaccination and seizure of uncontrolled animals, wildlife intervention. Compensation paid for culled animals.
98
Describe the pet travel scheme for EU and listed 3rd countries.
Step 1- identification: animal must be microchipped - record on pet passport or veterinary certificate if 3rd country. step22: vaccination; wait 21 days post vaccination booster or after primary course completed. record on pet passport. stop 3- arrange travel - animal must be transported via an approved route by approved carrier.
99
What is Bat rabies?
Caused by the european bat lyssavirus-2. Evidence suggests that bats can recover from EBLV or assume silent carrier status. method of transmission similar to terrestrial rbaies. clinical signs include incoordination and abnormal behaviour e.g active during daylight hours.bat rabies is notifiable. Bats are a protected species and any suspect cases are risk assessed.
100
What is canine parvoviral enteritis?
CPV-1 and CPV-2 are small non enveloped DNA viruses which require actively dividing host cells for replication. They therefore have a tropism for bone marrow and intestinal epithelial cells, and foetal tissues. The host nucleus is the site for virion assembly resulting in the formation of intranuclear inclusion bodies. Parvoviral enteritis is caused by CPV-1 which is highly contagious, infection usually results from exposure to contaminated faeces. The incubation period is reported to be 4-14 days. Parvoviruses are extremely stable within the environment persistent for several months on fomites.
101
Describe the pathogenesis of caniine parvoviral enteritis
Following oronasal exposure viral replication occurs within the local lymphoid tissue oof the oropharynx. M esenteric lymph nodes and thymus. Viraemia develops 1-5 days after infection with dissemination of virus to the rapidly dividing cell of the intestinal epithelium, lymph nodes and bone marrow. CPV-2 infects the germinal epithelial cells within the intestinal crypts, resulting in impaired enterocyte turnover. The villi become stunted and lose their absorptive capacity and the intestinal epithelial barrier is destroyed resulting in endotoxaemia and bacteraemia. DIC is a common sequelae to CPV-2 infection. CPV-2 also destroys haemopoietic precursors within the bone marrow resulting in neutropenia and lymphopenia. Active shedding of virus occurs within 3-4 days of infection and continues for 7-10 days, at which point local antibody production occurs.
102
Describe in utero infection with canine parvoviral enteritis?
In utero infection results in myocardial localisation of the virus. the resultant myocarditis leads to either death from sudden cardiac arrhythmia in the neonatal period or the development of chronic myocardial fibrosis and myocardial failure. Myocardial failure may also be associated with infection in the neonatal period.
103
Describe the clinical signs of canine parvoviral enteritis?
Gastrointestinal form - severe vomiting and diarrhoea with anorexia and rapid dehydration. Profuse foul smelling bloody diarrhoea, pyrexia initially proceeding to hypothermia, DIC may result from gram negative septicaemia with associated haemorrhage, sepsis or acid base abnormalities. Myocardial form - Myocarditis may occur concurrently with Gastrointestinal signs or in isolation. Myocarditis may result in sudden death or it may have a more chronic progression to myocardial failure - weeks to months after initial infection.
104
How is parvovirus diagnosed?
Should be suspected in young unvaccinated dogs with sudden onset foul smelling foetid diarrhoea, other enteropathogenic organisms such as salmonella and campylobacter shoould also be considered and may occur as co infections. Laboratory findings; leukopenia, hypoglycaemia, coagulation abnormalities if DIC develops, electrolyte and acid base imbalances are common, faecal antigen test - positive results are limited to the period of faecal shedding of the virus. Serology - virus neutralising antibodies (rising antibody titre). Haemagglutination inhibition est - cpv-2 results in haemagglutination of erythrocytes. Inhibition of haemagglutination by CPV2 antisera can be used to demonstrate serum antibody. Test carried out 3 days of clinical signs.
105
What is the treatment for parvoviral enteritis?
Therapy consists of symptomatic and supportive care, the primary goals being restoration of fluid and electrolyte imbalances. IVFT, antiemetic drugs, antibiotics, gastric protectants, interferon, nutrition. Prognosis is guarded and recovery may require hospitalisation. Some dogs will have chronic diarrhoea due to persistent villus atrophy and malabsorption.
106
What is leptospirosis?
An important zoonotic disease with world wide distribution caused by infection with the leptospira interrogans. Subclinicall infected wild and domestic animals act as reservoir hosts with the potential to infect humans and other incidental animal hosts. Clinical signs in incidental hosts tend to be more severe. leptospira interrogans is a thin filamentos, spiral bacteria.
107
How are leptospires transmitted?
Either by direct or indirect contact. Direct via contact with urine, venereal and placental transfer, bite wounds or ingestion of infected tissue. Recovered dogs may excrete organisms in urine intermittently for months. Indirect via exposure to contaminated water sources (slow flowing stagnant water), soil, food and begging. Leptospires do not replicate once outside the host.
108
Describe the pathogenesis of leptospires?
They penetrate mucous membranes and abraded skin and rapidly divide in the blood before spreading to other tissues including the liver and kidneys, lungs, spleen, CNS, eyes and genital tract. The extent of target organ damage depends on the dose of infection, host susceptibility and the virulence of the organism. In addition to hepatic or renal dysfunction, the lungs may be affected and DIc may lead to multiple organ failure and haemorrhage. REcovery is dependent on an increase in serovar specific antibody 7-8 days after infection. In most instances renal colonisation occurs due to replication and persistence of the organism in the renal tubular epithelium even int he presence of serum neutralising antibodies. In surviving reservoir hosts the organism is shed in the urine for months to years.
109
What are the clinical signs of leptospirosis?
May result in sudden death. Pyrexia, anorexia, shivering with muscle tremors, vomiting, rapid dehydration and rapid cardiovscular collapse. Acute infections result in a combination of clinical signs; pyrexia, anoreia, depression, vomiting , dehydration, polydipsia, olguria, congested mucous membranes, jaundice, petechiation and ecchymoses, reluctance to move, abdominal pain. Unlikely to be chronic or subclinical. Leptospirosis should be considered in dogs with pyrexia of unknown origin, unexplained renal or hepaptic disease or anterior uveitis.
110
How is diagnosis of leptospirosis made?
Clinical presentation in combination with vaccinal history and potential for exposure. Zoonosiis. Routine haematology - leukocytosis, indicators of renal dysfunction, urea, creatinine, electrolyte abnormalities, hepatic damage and dysfunction (ALT, SAP , bilirubin, bile acid elevations), urinalysis may reflect renal tubular damage; glucosuria, tubular proteinuria, granular casts, active sediment. Dark field microscopy for detection of organism in urine. Culture from urine, blood or tissue. PCR in blood or urine. Light microscopy using giemsa or silver staining. Serology - rising naatibody titre, may be negative in first 7-10 days.
111
What is the treatment of leptospirosis?
Penicillins are the antibiotics of choice for terminating leptospiraemia. They immediately stop replication of the organism and reduce fatal complications - give ampicillin or penicillin G IV during acute phase followed by oral amoxycillin. Elimination of the carrier state is achieved by administering tetracyclines, erythromycin or fluoroquinolones. (penicillins, cephalospoorins, chloramphenicol, sulphonamides ineffective at eliminating organisms). Aggressive IVFT to correct dehydration and maintain urine output, antiemetics, blood plasma transfusions, therapy for anuric/oliguric renal failure should include IVFT, diuresis with frusemide and mannitol once dehydration has been corrected.
112
What is canine infectious tracheobronchitis?
primary pathogens - canine parainfluenza virus, cav-2, bordatella bronchiseptica, canine influenza virus. Secondary pathogens - CDV, canine herpes virus, pasteurella, streptococcus, pseudomonas, mycoplasma. Environmental conditions important in epidemiology of KC with high density population environments such as boarding kennels, pet shops - ideal conditions for transmission of these viral and bacterial pathogens resulting in high levels of morbidity. Mortality is uncommon in adult dogs unless concurrent immunosupresion exists. Most outbreaks are associated with direct dog to dog contact or airborne dissemination of infectious respiratory secretions. CAV-2 and PI3 are transmitted for up to 2 weeks post infection, b bronchiseptica and mycoplasma are shed for up to 3 months post infection.
113
Describe the pathogenesis of canine infectious ttracheobronchitis
CPIV infections is restricted to the respiratory epithelium allowing secondary infection with other pathogens. incubation period of 3-10 days. CAV-2 replicates in local epithelia of the nasopharynx, tonsilar crypts, trachea and bronchi, infection of type 2 alveolar cells may be associated with interstital pneumonia, viral replication and shedding peaks at 5-6 days PI. B bronchiseptica attaches to and replicates on the cilia of the respiratory epithelium; production of various toxins which impair phagocytosis and induce stasis of the cilia facilitates colonisation of the respiratory tract by opportunistic pathogens, commonly associated with mixed respiratory tract infections. Mycoplasma are endogonous to the nasopharynx of dogs and cats but not typically found in the lower respiratory tract, colonisation of both ciliated and non ciliated epithelia results in purulent bronchitis, bronchiolitis and interstitial penumonia, Chonic shedding occurs following infection.
114
Describe the clinical signs of kennel cough?
Dogs with KC present clasically with sudden onset paroxysmal episodes of coughing and often associated retching, 3-10 days following exposure to KC agents. Typically there will be a history of a visit to boarding kennels. coughing is often brought on by excitement and tends to be characterised by a dry or hacking cough. expectoration of mucus may occur and should be differentiated from vomiting. usually the dog is otherwise healthy and active. without treatment the clinical course is 2-3 weeks. occasionally secondary opportunistic bacterial infection will result in the development of bronchopneumonia and mucopurulent rhinitis and conjunctivitis.
115
What is the treatment for kennel cough?
Antibiotic therapy may reduce the duration of coughing and reduce risk of developing bronchopneumonia. consider tetracyclines, amoxycillin clavulanate, tmp-s. Antittussives to interrupt the cough cycle, but should not be given if concurrent bronchopneumonia is suspected. Consider codeine or butorphanol. For KC plus bronchopneumonia - appropriate antibiotic therapy ideally based on culture and sensitivity. supportive care; nebulisation and coupage to encourage expectoration of bronchial secretions. oxygen therapy may be required in severe cases. IVFT and nutritional support may also be required. remember that these dogs are likely to be infectious and isolate during hospitalisation.
116
What are the core Vaccinations?
Live attenuated vaccines used for distemper, canne parvovirus and ICF. For ICH, vaccination with CAV-2 confers good neutralising antibody titre without the clinical signs associated with administration of a modified live CAV-1. for canine parvovirus high titre live attenuated vaccines are used to achieve effective immunisation even in the presence of a low to moderate levels of MDA, transient lymphopenia may be observed 4-6days post vaccination. in the UK combined killed vaccine containing the 2 main serovars.
117
Describe the best vaccination protocol
MDA obtained from colostrum protect upt o 6-12 weks of age. MDA absent by 12-14 weeks of aage. @ doses of vaccine at 2-4 weeks intervals, the initial vaccination being given at 6-10 weeks of age and the last vaccine being administered at over 12 weeks of age. All dogs now to be given a 3rd vaccine at 14-16 weeks of age. All should receive a booster at first year of age.
118
What are the non core vaccines?
CPiV vaccine considered to be non core despite recommendations by vaccine manufacturers. Intranasal vaccines vailable for b bronchiseptica and CPiV, conferring protection for up to 12 months. Annual vaccination advised for anticipated exposure. Intranasal vaccine results in both local igA production which reduces colonisation and systemic immunity. Clinical signs may be seen 2-5 days post intranasal vaccine.
119
Describe the Pet travel scheme (PETS)
Pet must be microchipped for indentification purposes. Pet must be vaccinated against rabies at leeast 21 days before travel. They no longer have to have rabies serology performed 21 days after vaccination to confirm successful vaccination. pet Must have a valid Eu pet passport. before re entering the UK dogs must be treated against tapeworms. between 24-120 hours before the pet is checked in with the approved transport company for return journey to the UK. Tick treatments no longer required under the scheme.
120
What is Erlichiosis/anaplasmosis?
Erlichia species has been reclassified some species as anaplasma. Diseases they cause referred to as anaplasmosis. Ehrlichiosis can be subdivided into three groups - monocytic ehrlichiosis caused by ehrlichia canis, granulocytic anaplasmosis caused by anaplasma phagocytophilum previously named ehrlichia phagocytophilia oor thrombocytic anaplasmosis caused by anaplasma platys.
121
What is anaplasmosis?
Anaplasma phagocytophilum are obligate intracellular bacteria, they are transmitted by ixodes ricinus in europe.. Deer and small rodents are thought to be the primary reservoir hosts. Anaplasmosis is an endemic disease of emerging importance in the uk. It is the most important cause of immunosuppression and tick borne fever in sheep and cattle in the Uk and a rare cause of granulocytic anaplasmosis in dogs. There is no evidence of transmission from dogs to humans. It is thought that proonged tick attachment is usually needed for infection to occur. When disease is seen it occurs 1-2 weeks after the tick bite with acute onset fever, anorexia, letharg, lameness due to muscle and joint pain, ocasional cough, pale mucous membranes, rarely seen in cats. Mild to severe immune mediated thrombocytopenia present in about 80% ofcases. Dogs may initially have lymphopenia then a reactive lymphocytosis.
122
What is Lyme disease?
Borrelia burgdorferi are also obligate intracellular acteria (spirochaetes) transmitted by a number of different ixodes ticks. Most infections are subclinica. When Lyme disease is seen in dogs it can be transient or recurrent and clinical signs include fever, anorexia, swollen painful joints, lethargy and lymphadenopathy and immune mediated renal disease with depression, vomting, anorexia, polyuria and polydipsia. Diagnosis based on history of tick exposure, clinical signs, antibodies to B burgdorferi and a quick response to treatment with antibiotics. Positive antibody test is not enough on its own to make diagnosis as many dogs exposed to B burgdorferi develop antibodies that can persist for a protracted time.
123
What is erlichiosis?
Erlichia are obligate intracellular bacteria and are transmitted b y ticks, in the case of E canis the vector is Rhipcephalus sanguineus. The incubation period is approximately 8-20 days and acute clinical signs typically include pyrexia, anorexia, lymphadenopathy, b leeding diathesiis , glomerulonephrtitis, uveitis, meningiencephalitis and polyarthritis. The acute phase lasts 2-4 weeks, infection may be Subclinical or chronic if treatment is ineffective.
124
How is ehrlichiosis diagnosed?
clinical presentation, hiistoory of recent travel to endemic area, typical haematological changes include thrombocytopenia, leucocytosis, anaemia, if blood loss has occured, hyperglobulinaemia, may be present on serum biochemistry. Chronic ehrlichiosis associated with pancytopenia and often hyperglobulinaemia. Diagnosis is based on demonstration of infection either by serology, PCr or presence of intracellular organism on a blood smear or bone marrow evaluation.
125
What is the treatment of ehrlichiosis?
Treatment consists of anti rickettsial agents and suppooortive care. Doxycycline is the initial drug of choice for 10-14 days. Fluoroquinolone may provide a viable alternative, particularly pradofloxacin. supportive measures include IVFt and blood transfusion for severe anaemia. Due to the immune mediated nature of thrombocytopenia, polyarthritis etc, short term treatment with corticosteroids may be required. Prevention of infection is by vector control using a long acting acaricide which may need to be given monthly or tick colars.
126
What is babesiosis?
In light of increasing pet travel - most likely to be asociated with recent travel to endemic regions. Haemolytic anaemia is caused by babesia canis canis and babesia gibsoni with babesia canis rossi being prevalent in Southern Africa. These protozoa are transmitted by ticks, rhipicephalus sanguineus is the major vector although dermacentor spp ay also play a role in transmission. Causes immune mediated destruction of erythrocytes - following infection sporozoites attach to erythrocyte membrane and undergo endocytoosis. Incubation period 10-21 days.
127
How is babesia diagnosed?
haemolytic anaemia associated with babesia infection has similarities with idiopathis IMHA. Thrombocytopaenia may occur concurrently due either to immune mediated destruction or consumption secondary to DIC and a leukaemoid response may be observed. Diagnosis is by demonstration of organisms on blood smears although many false negatives occur. evaluation of cpaillary blood may improve detection rates. PCR based detection on EDTA anticoagulated blood is the diagnostic test of choice. As concurrent tick borne infections are common, testing for ehrlichiosis also recommended.
128
What is the treatment of babesiosis?
With imidocarb diproprionate on a named patient basis. In addition supportive care may be required such as IVFT or blood transfusiion. babesia gibsoni which is associated with a severe clinical presentation may be resistant to imidocaarb in which case treatment with clindamycin or azithromycin may be effective. PRevention as with other tick associated diseases is by vector control using a long acting acaricide e.g fipronil or by avoidance of exposure. It usually takes 2-3
129
What is leishmaniasis?
It is caused by the protozoan parasite leishmania infantum with dogs acting as the major reservoir from this potentially zonotic infection. Leishmaniasis is transmitted by the phlebotomus sandfly. Protracted incubation period of 3 months to 7 years. Clinical signs tend to arise as a result of hyperglobulinaemia and immune complex deposition and include glomerulonephritis polyarhtritis and uveitis. Epistaxis may occur as a consequence of thrombocytpenia and platelet dysfunction. Glomerulonephritis leads to protein losing nephropathy. Dermatologicl disease also present in 90% of cases with dry desquamation and alopecia affecting the head in particular.
130
How is diagnosis of leishmaniasis made?
by serology to confirm exposure, PCR based detection of leishmania DNA or detection of organisms on cytology especially of skin or bone marrow. Treatment recommendations include the combination of allopurinol and antiomnial drugs, meglumine antimonite, selective inhibition of protozoal enzymes. Combination therapy is more effective in reaching a clinical cure than single agent therapy. It is unlikely that treatment will completely eliminate the organis, relapses may occur once treatment is withdrawn.
131
How is leishmaniasis prevented?
Prevention of infection is again by avoidance of infection by use of deltamethrin impregnated collars to deter biting sandlflies and keeping dogs indoors for 1 hour prior to sunset and 1 hour after sunrise. The risk of infection of people from infected dogs in areas without sandlflies is remote, although children are at greater risk.
132
What is dilofilariasis?
Heartworm infection caused by the nematode dirofilaria immitis and transmitted by mosquitoes. Following infection microfilaria migrate to the pulmonary artery where they mature to the adult nematode. The incubation /prepatent period is 6-8 months. Clinical signs relate to the presence of the adult nematodes in the pulmonary arteries and range from mild excercise intolerance and coughing to dyspnoea due to allergic pneumoniitis and right sided congestive heart failure, pulmonary hypertension and syncope.
133
How is treatment and diagnosis of dirofilariasis made?
Diagnosis is made on the basis of detecting microfilaria; an antigen test which is dependent of the presence of mature female nematodes or an antibody test which can be a useful screening test. Treatment is aimed at killing nematodes with adulticides (arsenicals, melarsomine) and microfilaricidal drugs ( avermectins, milbemycin) in combination with supportive therapy and treatment of congestive heart failure, oxygen therapy. Treatment may be associated with acute clinical deterioration due to anaphylactic reactions or acute thromboembolic disease associated with embolism of dead parasites.
134
Discuss the current core vaccination guidelines for the prevention of canine infectious diseases
The core vaccines are distemper, parvovirus, and infectious canine hepatitis in which a live attenuated vaccine is given for each. the primary vaccination protocol is to generally wait until the maternal derived antibodies that protect puppies from any viruses be as low as possible. the recommended time is roughly around weeks of age before getting their first vaccine. once given their first vaccine the second vaccine should be given about 3-4 weeks later when the first round of antibodies is getting low. the last injection should be given another 3--4 weeks later (16 weeks of age). following this protocol will ensure good levels of virus neutralizing antibodies (humoral) it is now recommended that the animal come for their next vaccine every 2-3 years. Core vaccines every 3 years due to long lived immunity by both humoral and cell mediated immunity. leptospirosis and parainfluenza needed annually due to protection only lasting for 6-8 months. it has been suggested to give it twice yearly in areas where prevalence of infection is high. CpIV is given anually and if a boarding dog should give within 5 days of boarding.
135
What five different organisms may be involved in causing cat flu?
Herpes virus, calicivirus, bordetella, chlamydophila felis, pasteurella.
136
List five of the most common poisons recorded and indicate the target organ involved?
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Raisins/grapes: kidney
Lily: kidney
Aspirin: gastric mucosa and kidneys
Paracetamol: liver and RBC
Ethylene glycol: kidneys and brain
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