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Diagnosis of effusive FIP has become more straightforward in recent years: detection of viral RNA in a sample of the effusion, by reverse-transcriptase polymerase chain reaction (RT-PCR) is diagnostic of effusive FIP. However, that does require that a sample be sent to an external veterinary laboratory. Within the veterinary hospital there are a number of tests which can rule out a diagnosis of effusive FIP within minutes:
1. Measure the total protein in the effusion: if it is less than 35g/l, FIP is extremely unlikely.
2. Measure the albumin to globulin ratio in the effusion: if it is over 0.8, FIP is ruled out, if it is less than 0.4, FIP is a possible—but not certain—diagnosis
3. Examine the cells in the effusion: if they are predominantly lymphocytes then FIP is excluded as a diagnosis.
Non-effusive FIP is more difficult to diagnose than effusive FIP because the clinical signs tend to be more vague and varied: the list of differential diagnoses is therefore much longer. Non-effusive FIP diagnosis should be considered when the following criteria are met:
1. History: the cat is young (under 2 years old) and purebred: over 70% of cases of FIP are in pedigree kittens.
2. History: the cat experienced stress such as recent neutering or vaccination
3. History: the cat had an opportunity to become infected with FCoV, such as originating in a breeding or rescue cattery, or the recent introduction of a purebred kitten or cat into the household.
4. Clinical signs: the cat has become anorexic or is eating less than usual; has lost weight or failed to gain weight; has pyrexia of unknown origin; intra-ocular signs; icterus.
5. Biochemistry: hypergammaglobulinaemia; raised bilirubin without liver enzymes being raised.
6. Hematology: lymphopenia; non-regenerative—usually mild—anaemia.
7. Serology: the cat has a high antibody titre to FCoV: this parameter should be used with caution, because of the high prevalence of FCoV in breeding and rescue catteries.
Non-effusive FIP can be ruled out as a diagnosis if the cat is seronegative, provided the antibody test has excellent sensitivity. In a study which compared various commercially available in-house FCoV antibody tests, the FCoV Immunocomb (Biogal) was 100% sensitive; the Speed F-Corona rapid immunochromatographic (RIM) test (Virbac) was 92.4% sensitive and the FASTest feline infectious peritonitis (MegaCor Diagnostik) RIM test was 84.6% sensitive.
Diagnosis of FVR is usually by clinical signs, especially corneal ulceration. Definitive diagnosis can be done by direct immunofluorescence or virus isolation. However, many healthy cats are subclinical carriers of feline herpes virus, so a positive test for FHV-1 does not necessarily indicate that signs of an upper respiratory tract infection are due to FVR. Early in the course of the disease, histological analysis of cells from the tonsils, nasal tissue, or nictitating membrane (third eyelid) may show inclusion bodies (a collection of viral particles) within the nucleus of infected cells.
There is a vaccine for FHV-1 available (ATCvet code: , plus various combination vaccines), but although it limits or weakens the severity of the disease and may reduce viral shedding, it does not prevent infection with FVR. Studies have shown a duration of immunity of this vaccine to be at least three years. The use of serology to demonstrate circulating antibodies to FHV-1 has been shown to have a positive predictive value for indicating protection from this disease.
Opportunistic infections caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections can be treated with Lymphocyte T-Cell Immune Modulator.
Individuals at higher risk are often prescribed prophylactic medication to prevent an infection from occurring. A patient's risk level for developing an opportunistic infection is approximated using the patient's CD4 T-cell count and sometimes other markers of susceptibility. Common prophylaxis treatments include the following:
FVRCP vaccines have also come under scrutiny of late due to possible risks to long term health. A study at Colorado State University noted an association between vaccination with parenteral (injectable) FVRCP vaccinations and development of antibodies against feline kidney tissue. Antibody development is hypothesized to develop when the immune system reacts to protein contaminants from the cell line used to cultivate vaccinial viruses. The cell line in question, the Crandell-Rees Feline Kidney (CRFK) cell line, was derived from a cat kidney. It is currently unknown whether this antibody development can lead to renal disease, though a recent follow-up study demonstrated evidence of inflammation on re-biopsy samples from some of the study cats.
Feline infectious anemia (FIA) is an infectious disease found in felines, causing anemia and other symptoms. The disease is caused by a variety of infectious agents, most commonly "Mycoplasma haemofelis" (which used to be called "Haemobartonella"). "Haemobartonella" and "Eperythrozoon" species were reclassified as mycoplasmas. Coinfection often occurs with other infectious agents, including: feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), "Ehrlichia" species, "Anaplasma phagocytophilum", and Candidatus "Mycoplasma haemominutum".
A Vaccine-associated sarcoma (VAS) is a type of malignant tumor found in cats (and rarely, dogs and ferrets) that has been linked to certain vaccines. Concern about VAS has resulted in changes in recommended vaccine protocols to limit the type, frequency, and sites of vaccinations. Owners are advised to monitor injection sites for signs of tumors and contact their veterinarian immediately if one develops.
A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.
Preliminary diagnosis is often based on the patient's clinical symptoms, places and dates of travel (if patient is from a nonendemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV.
Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals.
Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.
Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.
Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.
If cases of suspected West Nile virus infection, sera should be collected on both the acute and
convalescent phases of the illness. Convalescent specimens should be collected 2–3 weeks after acute specimens.
It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections.
Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.
In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing.
Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based on testing of amniotic fluid and ultrasound examinations; neonatal diagnosis based on molecular testing of placenta and cord blood and comparative mother-child serologic tests and a clinical examination at birth; and early childhood diagnosis based on neurologic and ophthalmologic examinations and a serologic survey during the first year of life. During pregnancy, serological testing is recommended at three week intervals.
Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific anti-"Toxoplasma" immunoglobulin, serological testing has limitations. For example, it may fail to detect the active phase of "T. gondii" infection because the specific anti-"Toxoplasma" IgG or IgM may not be produced until after several weeks of infection. As a result, a pregnant woman might test negative during the active phase of "T. gondii" infection leading to undetected and therefore untreated congenital toxoplasmosis. Also, the test may not detect "T. gondii" infections in immunocompromised patients because the titers of specific anti-"Toxoplasma" IgG or IgM may not rise in this type of patient.
Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical specimens that include amniotic fluid, blood, cerebrospinal fluid, and tissue biopsy. The most sensitive PCR-based technique is nested PCR, followed by hybridization of PCR products. The major downside to these techniques is that they are time consuming and do not provide quantitative data.
Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic discrimination. This PCR technique utilizes the 5' nuclease activity of "Taq" DNA polymerase to cleave a nonextendible, fluorescence-labeled hybridization probe during the extension phase of PCR. A second fluorescent dye, e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence of the intact probe. The nuclease cleavage of the hybridization probe during the PCR releases the effect of quenching resulting in an increase of fluorescence proportional to the amount of PCR product, which can be monitored by a sequence detector.
Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by "Toxoplasma" have characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B cells, and scattered epithelioid histiocytes.
The classic triad of congenital toxoplasmosis includes: chorioretinitis, hydrocephalus, and intracranial artheriosclerosis.
Cat flu is the common name for a feline upper respiratory tract disease. While feline upper respiratory disease can be caused by several different pathogens, there are few symptoms that they have in common.
While Avian Flu can also infect cats, Cat flu is generally a misnomer, since it usually does not refer to an infection by an influenza virus. Instead, it is a syndrome, a term referring to the fact that patients display a number of symptoms that can be caused by one or more of the following infectious agents (pathogens):
1. Feline herpes virus causing feline viral rhinotracheitis (cat common cold, this is the disease that is closely similar to cat flu)
2. Feline calicivirus—(cat respiratory disease)
3. "Bordetella bronchiseptica"—(cat kennel cough)
4. "Chlamydophila felis"—(chlamydia)
In South Africa the term cat flu is also used to refer to Canine Parvo Virus. This is misleading, as transmission of the Canine Parvo Virus rarely involves cats.
Diagnosis of toxoplasmosis in humans is made by biological, serological, histological, or molecular methods, or by some combination of the above. Toxoplasmosis can be difficult to distinguish from primary central nervous system lymphoma. It mimics several other infectious diseases so clinical signs are non-specific and are not sufficiently characteristic for a definite diagnosis. As a result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine, and folinic acid (USAN: leucovorin)), if the drugs produce no effect clinically and no improvement on repeat imaging.
"T. gondii" may also be detected in blood, amniotic fluid, or cerebrospinal fluid by using polymerase chain reaction. "T. gondii" may exist in a host as an inactive cyst that would likely evade detection.
Serological testing can detect "T. gondii" antibodies in blood serum, using methods including the Sabin–Feldman dye test (DT), the indirect hemagglutination assay, the indirect fluorescent antibody assay (IFA), the direct agglutination test, the latex agglutination test (LAT), the enzyme-linked immunosorbent assay (ELISA), and the immunosorbent agglutination assay test (IAAT).
The most commonly used tests to measure IgG antibody are the DT, the ELISA, the IFA, and the modified direct agglutination test. IgG antibodies usually appear within a week or two of infection, peak within one to two months, then decline at various rates. "Toxoplasma" IgG antibodies generally persist for life, and therefore may be present in the bloodstream as a result of either current or previous infection.
To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using an IgG avidity test, which is a variation on the ELISA. In the first response to infection, toxoplasma-specific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it means that the infection began three to five months before testing. This is particularly useful in congenital infection, where pregnancy status and gestational age at time of infection determines treatment.
In contrast to IgG, IgM antibodies can be used to detect acute infection, but generally not chronic infection. The IgM antibodies appear sooner after infection than the IgG antibodies and disappear faster than IgG antibodies after recovery. In most cases, "T. gondii"-specific IgM antibodies can first be detected approximately a week after acquiring primary infection, and decrease within one to six months; 25% of those infected are negative for "T. gondii"-specific IgM within seven months. However, IgM may be detectable months or years after infection, during the chronic phase, and false positives for acute infection are possible. The most commonly used tests for the measurement of IgM antibody are double-sandwich IgM-ELISA, the IFA test, and the immunosorbent agglutination assay (IgM-ISAGA). Commercial test kits often have low specificity, and the reported results are frequently misinterpreted.
Feline zoonosis are the viral, bacterial, fungal, protozoan, nematode and arthropod infections that can be transmitted to humans from the domesticated cat, "Felis catus". Some of these are diseases are reemerging and newly emerging infections or infestations caused by zoonotic pathogens transmitted by cats. In some instances, the cat can display symptoms of infection (these may differ from the symptoms in humans) and sometimes the cat remains asymptomatic. There can be serious illnesses and clinical manifestations in people who become infected. This is dependent on the immune status and age of the person. Those who live in close association with cats are more prone to these infections. But those that do not keep cats as pets are also able to acquire these infections because of the transmission can be from cat feces and the parasites that leave their bodies.
People can acquire cat-associated infections through bites, scratches or other direct contact of the skin or mucous membranes with the cat. This includes 'kissing' or letting the animal lick the mouth or nose. Mucous membranes are easily infected when the pathogen is in the mouth of the cat. Pathogens can also infect people when there is contact with animal saliva, urine and other body fluids or secretions, When fecal material is unintentionally ingested, infection can occur. Feline zooinosis can be acquired by a person by inhalation of aerosols or droplets coughed up by the cat.
In the United States, forty percent of homes have at least one cat. Some contagious infections such as campylobacteriosis and salmonellosis cause visible symptoms of the disease in cats. Other infections, such as cat scratch disease and toxoplasmosis, have no visible symptoms and are carried by apparently healthy cats.
Some disease-carrying arthropods use cats as a vector, or carrier. Fleas and ticks can carry pathogenic organisms that infect a person with Lyme disease, tick borne encephalitis, and Rocky mountain spotted fever
Definitive diagnosis can only occur with positive identification of the larvae. This involves radiologic imaging (preferably MRI which can reveal larval migration tracks and in some cases the larvae themselves) as well as surgical exploration during which larvae can be removed and examined for identification. Identification of exact species is often impossible as the instars of the various "Cuterebra" and "Trychoderma" spp. exhibit significant resemblance, but identification as a "Cuterebra" bot fly is sufficient for diagnosis as cuterebriasis. Typically, a third larval instar is found and identifiable by its dark, thick, heavily spined body.
VAS appears as a rapidly growing firm mass in and under the skin. The mass is often quite large when first detected and can become ulcerated or infected. It often contains fluid-filled cavities, probably because of its rapid growth. Diagnosis of VAS is through a biopsy. The biopsy will show the presence of a sarcoma, but information like location and the presence of inflammation or necrosis will increase the suspicion of VAS. It is possible for cats to have a granuloma form after vaccination, so it is important to differentiate between the two before radical surgery is performed. One guideline for biopsy is if a growth is present three months after surgery, if a growth is greater than two centimeters, or if a growth is becoming larger one month after vaccination.
X-rays are taken prior to surgery because about one in five cases of VAS will develop metastasis, usually to the lungs but possibly to the lymph nodes or skin.
As soon as a tumor is detected, diagnosing the type of cancer remains a primary objective, as it helps determine the best possible treatment by the analysis of the structure of the tumor and cancer cells.
New vaccine protocols have been put forth by the American Association of Feline Practitioners that limit type and frequency of vaccinations given to cats. Specifically, the vaccine for feline leukemia virus should only be given to kittens and high risk cats. Feline rhinotracheitis/panleukopenia/calicivirus vaccines should be given as kittens, a year later and then every three years. Also, vaccines should be given in areas making removal of VAS easier, namely: as close as possible to the tip of the right rear paw for rabies, the tip of the left rear paw for feline leukemia (unless combined with rabies), and on the right shoulder—being careful to avoid the midline or interscapular space—for other vaccines (such as FVRCP). There have been no specific associations between development of VAS and vaccine brand or manufacturer, concurrent infections, history of trauma, or environment.
Treatments of cancer in cats usually consists of diagnosis and observation of the tumor to determine its type and size, the development of a treatment plan, the associated goals on the part of the treatment methods, and the regular evaluation of the overall health of the pet.
Subcutaneous cysts may be surgically opened to remove less mature bots. If more matured, cysts may be opened and "cuterebra" may be removed using mosquito forceps. Covering the pore in petroleum jelly may aide in removal. If larvae are discovered within body tissues, rather than subcutaneously, surgical removal is the only means of treatment. Ivermectin may be administered with corticosteroids to halt larval migration in cats presenting with respiratory cuterebriasis, but this is not approved for use in cats. There is not yet a known cure for cerebrospinal cuterebriasis.
Biopsy of affected lymph nodes or organs confirms the diagnosis, although a needle aspiration of an affected lymph node can increase suspicion of the disease. X-rays, ultrasound and bone marrow biopsy reveal other locations of the cancer. There are now a range of blood tests that can be utilised to aid in the diagnosis of lymphoma. Flow cytometry detects antibodies linked to tumour cell surface antigens in fluid samples or cell suspensions. Polymerase chain reaction (PCR) for antigen receptor rearrangements (PARR) identifies circulating tumour cells based on unique genetic sequences. The canine Lymphoma Blood Test (cLBT) measures multiple circulating biomarkers and utilises a complex algorithm to diagnose lymphoma. This test utilises the acute phase proteins (C-Reactive Protein and Haptoglobin). In combination with basic clinical symptoms, it gives in differential diagnosis the sensitivity 83.5% and specificity 77%. The TK canine cancer panel is an indicator of general neoplastic disease. The stage of the disease is important to treatment and prognosis. Certain blood tests have also been shown to be prognostic.
The stage of the disease is important to treatment and prognosis.
- Stage I - only one lymph node or lymphoid tissue in one organ involved.
- Stage II - lymph nodes in only one area of the body involved.
- Stage III - generalized lymph node involvement.
- Stage IV - any of the above with liver or spleen involvement.
- Stage V - any of the above with blood or bone marrow involvement.
Each stage is divided into either "substage a", those without systemic symptoms; or "substage b", those with systemic symptoms such as fever, loss of appetite, weight loss, and fatigue.
Lymphocytopenia is diagnosed when the complete blood count shows a lymphocyte count lower than the age-appropriate reference interval (for example, below 1.0 x 10(9)/L in an adult).
This is a terminal condition and there is currently no specific treatment for the disease.