VET-125 - Ch. 9 - Pansystemic

Effusion

Escape of fluid into a body cavity

Hyperkeratosis

Overgrowth of the cornified epithelial layer of the skin

Hyphema

Hemorrhage into the interior chamber of the eye usually from trauma

Immunocompetence

The ability of an immune system to mobilize & deploy its antibodies & other responses to stimulation by antigens

Mucopurulent

A combination of mucus & pus

Oocysts

Stage in the development of a sporozoan in which a zygote develops enclosed within a cyst wall after fertilization

Panleukopenia

Decrease in all white blood cells

Pansystemic

Involvement of all body systems

Peritonitis

Inflammation of the lining tissues of the abdomen (peritoneum)

Perivasculitis

Inflammation of the tissue surrounding large blood vessels

Pyogranulomatous

Inflammatory process in which polymorphonuclear cells infiltrate into a more chronic area of inflammation characterized by mononuclear cells, macrophages, lymphocytes, & possibly plasma cells

Tachyzoites

Fast multiplication stage of zoites in the life cycle of Toxoplasma gondii or Neospora caninum; found in tissues

Pansystemic diseases

Involve multiple body systems in addition to the primary target organ; causes may be viral, bacterial, or parasitical, & secondary infections are common

Examples of pansystemic diseases

FeLV, FIV, FIP, toxoplasmosis, anaplasmosis, feline distemper (panleuk), canine distemper, canine parvo, ehrlichiosis, Lyme’s (Borreliosis), leptospirosis, & RMSF

Feline panleukopenia

Aka feline distemper; caused by a DNA virus of the family Parvoviridae, which is closely related to canine parvo

Feline panleukopenia risk factors

Primarily seen in young unvaccinated or feral cats

Feline panleukopenia transmission

Direct contact or from a contaminated environment, as the virus sheds in the environment & may remain infectious for years

Virus multiplies within actively dividing cells of the neonatal brain, bone marrow, & lymphoid tissues

Incubation period = about 4-5 days

Feline panleukopenia signs

Fever, depression, vomiting, fetid diarrhea, dehydration, anorexia, fetal death, spontaneous abortion, fetal reabsorption in the queen, & cerebellar or retinal defects in neonates

Feline panleukopenia diagnosis

Moderate to severe panleukopenia, positive canine parvo SNAP test, serum antibody titers, PCR for detection of viral DNA in feces

Feline panleukopenia treatment

Aggressive supportive therapy, such as IV fluids, force-feed after vomiting is controlled, broad-spectrum AB for secondary infections, & isolation to contain spread

Feline panleukopenia prevention

Vaccines; generally start at 8-10 weeks, then booster every 3-4 weeks until 16 weeks old

Cats that survive an infection acquire lifelong immunity

Why do puppies & kittens need booster vaccines?

Maternal antibodies reduce efficacy of vaccines (protects against vaccine) & maternal antibodies fade over time, so boosters fill the gap in this time

Incubation period

Time from exposure to the causative agent until the first symptoms develop & is characteristic for each disease agent

Period between the infection of an individualy by a pathogen & the manifestation of the illness or disease it causes

Polymerase chain reaction (PCR)

Lab technique for rapidly producing millions to billions of copies of a specific segment of DNA, which can be studies in greater detail

How did the parvo vaccine get established?

In the 1980s parvo was rapidly killing dogs & there was no vaccine. Some vets would weekly vaccinate dogs with the feline panleukopenia vaccine, which worked in many cases. Until the parvo vaccine, this was the best & only way to protect dogs from parvo

FIP

Feline infectious peritonitis

FIP risk factors

Primarily catteries, shelters, & multiple cat households

FIP transmission

Does not occur without exposure to feline enteric coronavirus (FECV), which is highly contagious through feces, urine, & saliva, & mutates into FIP

Virus enters macrophages & spreads throughout the body

Dry (non-effusive) FIP signs

Signs less clear than other form

Fever of unknown origin (FUO), anorexia, depression, weight loss, enlarged kidneys (uncommon), ocular lesions, & neurological lesions/signs

45% will have ocular or neurological lesions
— ocular = iritis, retinitis, uveitis, hyphema, corneal edema, retinal hemorrhage, & retinal detachment
— neurological = ataxia, seizures, behavioral changes, paresis, & hyperesthesia

Wet (effusive) FIP signs

Perivasculitis results in accumulation of a protein-rich fluid in the thoracic cavity, abdominal cavity, scrotum, pericardial cavity, & renal subscapular space

Inflammatory process may also involve liver & pancreas

Ascites, pleural effusion, anorexia, depression, weight loss, dehydration, & fever

FIP diagnosis

FECV & FIP are difficult to differentiate with current testing methods; high antibody titers may be suggestive

Wet = cytology & chemical analysis of abdominal & pleural fluid = viscous clear to yellow fluid, < 20,000 nucleated cells per microliter, protein-rich > 3.5 g per deciliter, & albumin/globulin ratio > 0.81

Rivalta test = positive result consistent with FIP in kittens, but less specific in older cats

Definitive diagnosis = presence of viral antigen or RNA within macrophages from effusions or lesions by PCR or immunohistochemistry (HCA)
— can be difficult, expensive, & PCR or IHC may show false negatives up to 30% of samples

FIP treatment

Supportive = aspirate fluid to increase cat’s comfort, steroids or immunosuppressive drugs daily, & broad spectrum antibiotics

Immunotherapy = only 2 classes of antivirals effective
— inhibitors of RNA synthesis Remdesivir & Molnupiravir
— viral protease inhibitors (Nirmatrelvir); much less efficient crossing blood-brain or blood-eye barriers, so not advised for ocular or neurological forms

New treatment options are available beyond supportive care, but are expensive & require owner involvement in extended treatment

FIP prevention

Isolate pregnant queens by 2 weeks before birth & remove kittens from queens by 5 weeks old

Vaccinate seronegative cats with Primucell FIP (intranasal) at 16 weeks
— although there is still ongoing research for vaccine development

FIP other info

A large number of infected cats die

Virus is inactivated in the environment by most household disinfectants

What are clinical signs of FIP related to?

Granuloma formation in the target organs (CNS, eyes, vessels, etc.)

Hyperesthesia

Excessive physical sensitivity, especially of the skin

Ascites

Abnormal accumulation of intraperitoneal fluid high in protein & electrolytes

Which form of FIP progresses more rapidly?

Wet (effusive), also more easily diagnosable

Rivalta test

Inexpensive & readily performed in-clinic test with an extremely high negative predictive value for FIP (highly reliable indicating absence of disease being test for)

Positive with high protein content (drop retains shape), negative in pure transudates (drop dissolves)

** A positive result is consistent with FIP * in kittens, but is less specific in older cats, as septic peritonitis & neoplasia can result in a positive test, however these can be ruled out with cytology

FeLV

Feline leukemia virus; caused by a retrovirus that is associated with both neoplastic & non-neoplastic immunosuppressive diseases

FeLV transmission

Virus is unstable in the environment, so close contact between cats is required for infection

Virus can be isolated from saliva, urine, tears, & milk, & can be spread through fighting, grooming, & contaminated food, water, bowls, & litter pans

Transplacental & transmammary

What can happen to FeLV exposed cats?

A regressive infection = transient infection, followed by no virus

A progressive infection = persistent viremia (contagious)

An active infection with clinical signs

FeLV signs

Fever, anorexia, weight loss, anemia, secondary infection, vomiting, diarrhea, renal disease, neurological signs, & formation of cancers primarily lymphoma

FeLV diagnosis

Positive SNAP, non-regenerative anemia, positive immunofluorescent antibody (IFA), & clinical signs of recurring infections

FeLV treatment

No cure

Immunomodulator & antiviral drugs for symptoms, broad-spectrum antibiotics for secondary infections, & appetite stimulants

FeLV prevention/other info

Test kittens & adults new to the household before allowing contact with current cats, keep positive cats indoors, isolate from other cats if possible, UTD on vaccines, & watch for clinical signs

FeLV prognosis

Can live really great lives & don’t have to be euthanized

Most common FeLV associated neoplastic disease

Lymphoma; tumors can occur in thymus, alimentary tract, & various lymph nodes throughout the body

FIV

Feline immunodeficiency virus; lentivirus associated with immunodeficiency in cats, which is very similar to human HIV but antigenically distinct

FIV transmission

Highly species specific

Male, outdoor, sexually intact cats are at greater risk, because fighting & bite wounds appear to be the major route of transmission

Little or no sexual transmission

Neonatal kittens can be infected by infected queens, although antibodies may be passed in colostrum

FIV signs

History of recurrent bouts of illness, cachexia (wasting syndrome), anorexia, gingivitis, stomatitis, chronic nonresponsive ear or skin infection, chronic URI, vomiting, diarrhea, neurological signs, ocular disease, pale mucous membranes (aka anemia), & chronic fever

FIV diagnosis

History of recurrent disease, positive SNAP triple test (or Elisa & PCR tests), anemia, & lymphopenia

FIV treatment

No cure exists

Immunomodulating & antiviral drugs (Zidovudine) may alleviate symptoms; if chronic stomatitis & gingivitis, whole mouth teeth extractions may be necessary to alleviate pain

FIV prognosis

Cats can survive for long periods before developing severe illness & advanced disease

FIV prevention

Contagious from cat to cat, especially through fighting, but not to other animals or humans

Isolate aggressive cats from others, & spay/neuter to reduce aggression

There is currently no vaccine commercially available in North America, so best to keep cats indoors & test all cats in household

FIV SNAP triple test

Test checks for circulating antibodies; positive result indicates likely infected

Kittens should not be diagnosed using these tests until after 6 months of age, as maternal antibodies may take up to 6 months to clear (can be tested early, but re-test after 6 months old)

Which one of the following has been demonstrated to result in improved quality of life for FIV–infected cats with clinical signs?

Zidovudine aka AZT (made in Research Triangle Park in NC)

Toxoplasmosis

Caused by Toxoplasma gondii, a coccidian parasite with worldwide distribution

Toxoplasmosis risk factors

May be especially severe in very young or immunocompromised animals

Don’t give immunosuppressive drugs to seropositive cats

Toxoplasmosis transmission

Felines are the only definitive host, but other warm-blooded mammals, including humans, can serve as intermediate hosts

Routes = eating meat from infected intermediate host, fecal-oral, & transplacental

Once sporulated oocysts are ingested, tachyzoites form & invade any tissue in the body

After infection, the cat sheds oocysts in feces for about 1-2 weeks, which it takes as little as 24 hours for oocysts to sporulate into infective stage

Toxoplasmosis signs

Clinical signs related to whatever tissue is involved
— cats = mainly lungs & eyes
— dogs = rarely infected, but mainly GI, neuro, & respiratory tissues

Anorexia, lethargy, fever, weight loss, vomiting, diarrhea, icterus, respiratory disease, lameness, pancreatic disease, anterior uveitis, glaucoma, CNS disease, & sudden death

Toxoplasmosis diagnosis

Nonspecific CBC changes

Elevated ALT, ALP, bilirubin (liver is affected), & creatinine kinase

Thoracic radiographs = possible diffuse lesions with or without pleural effusion

ELISA test, PCR (ocular or CNS), & paired titers

Toxoplasmosis prevention

Keep cats from hunting (keep indoors), don’t feed raw or undercooked meat, follow good hygiene around feces, & immunocompromised people should avoid contact with infected cats

Infection in pregnant women can lead to serious birth defects
— have yourself checked for antibodies before getting pregnant
— while pregnant have someone else coop the litterbox daily & thoroughly clean litter box at least weekly
— don’t need to give your cat away

Anterior uveitis

Inflammation of the eye’s uvea, specifically the iris & ciliary body

Signs = irregular shaped pupil, opaque smoky material obscuring the pupil, & dark discoloration of the uvea (notably iris) caused by accumulation of inflammatory cells

Glaucoma

Eye disease in which aqueous humor just behind the lens is unable to drain normally, causing increased intraocular pressure that damages the optic nerve

May affect one or both eyes & can result in partial or total blindness if untreated

What is the most likely main route of toxoplasmosis transmission for humans & cats?

Ingestion of uncooked or undercooked meat (NOT oocysts in feces aka litter box)

How long does it take Toxoplasma gondii oocysts to become infective?

Sporulate in as little as 24 hours

Is it likely to be infected with Toxoplasma gondii by touching an infected cat or through cat bites or scratches?

No

What are the forms of Toxoplasma gondii? And which forms are infectious?

(3) Tachyzoites, tissue cysts, & bradyzoites; all are infectious, including separate sporulated oocyst stage

About how many adults are seropositive for toxoplasmosis exposure?

30-60%

Glaucoma

Uveitis (anterior?)

Canine distemper virus risk factors

Greatest incidence in dogs 3-6 months

Canine distemper virus transmission

Highly contagious

Aerosolized body secretions (coughing, sneezing, drooling?, etc.)

Canine distemper virus signs

Hallmark = immunosuppression followed by secondary infections

Predominantly GI, respiratory, & neuro signs = fever, cough, mucopurulent nasal & ocular discharge (conjunctivitis), pneumonia, vomiting, diarrhea, anorexia, dehydration, abdominal pustules, hyperkeratosis of foot pads, chewing gum seizures, muscle twitching, ataxia, circling, & blindness

Canine distemper virus diagnosis

Physical exam, history/risk factors, rising titers in paired serum samples, & FA test

Canine distemper virus treatment

No specific treatment

Supportive = fluids, nutrition, vitamins, & antibiotics

Canine distemper virus prognosis

Fatality rate may be as high as 90%

Canine distemper virus prevention

Vaccinate; prevention is key

Relatively labile (easy to destroy) in the environment
— Most routine cleaning agents, disinfectants, & heat will destroy virus

FA test

Fluorescent antibody; detects canine distemper virus in epithelial cells collected from the conjunctiva or other mucous membranes

CPV

Canine parvovirus; common infectious enteritis in dogs, caused by single-stranded non-enveloped DNA virus that is closely related to feline panleukopenia virus

One of the most resistant viruses known, potentially surviving for years in the environment

CPV risk factors

Primarily young puppies that lack sufficient antibody protection

Black & tan breeds, especially rottweilers & dobermans

Intestinal parasites may predispose to infection

CPV signs

Diarrhea**, vomiting**, fever, dehydration, anorexia, lethargy, & depression

CPV diagnosis

Always perform fecal exam

Fecal ag test (parvo snap or witness), PCR test, & high serology titer

CBC = lymphopenia (< 50%), neutropenia, & increased PCV due to dehydration from vomiting, diarrhea, etc.

Chemistry = non-specific; hypoglycemia, hyponatremia, & hypokalemia due to not eating, vomiting, etc.

CPV treatment

IV fluids with additives for hypokalemia (potassium chloride) & hypoglycemia (dextrose) if needed

Antibiotics, such as injectable Convenia (lasts 2 weeks) for secondary infection

Antiemetics (Cerenia)

NSAID for pain & fever only in well-hydrated patients

NPO initially with vomiting, but feed as soon as possible (A/D or EN diets) by recovering diet of small frequent feedings

New treatment = CPV monoclonal antibody

CPV prevention

Vaccinate = begin at 6-8 weeks with boosters every 3-4 weeks until 16 weeks & revaccinate high risk breeds at 22 weeks

CPV other info

Survival is possible, but treatment may be expensive (inpatient vs outpatient)

What is the new CPV treatment?

Canine parvovirus monoclonal antibody, made by Elanco

Proven effective in decreasing mortality associated with parvo & treated dogs showed signs of faster resolution times of the most-adverse effects of parvo, including vomiting

How should dogs with parvo be handled?

Wear proper PPE, put in isolation, & all waste & bedding should be disposed of directly from isolation

What diseases does the canine SNAP 4Dx Plus test for? And SNAP feline triple test?

Dogs = heartworm, ehrlichiosis (2 types), anaplasma (2 types), & Lyme’s (Borreliosis)

Cats = FeLV, FIV, & heartworm

Rickettsiae

Small, gram-negative, obligate, intracellular bacterial organism
— tick-borne pathogens with infection occurring through the saliva when the tick feeds

Distribution & seasonal occurrence of these diseases are related to the life cycle of the corresponding tick
— increasing due to human activity

** Transmission requires the tick to be attached to the host for 5-20 hours

Canine monocytic ehrlichiosis

Rickettsial disease caused by Ehrlichia canis, carried by the brown dog tick (Rhipicephalus sanguineus)

Canine monocytic ehrlichiosis stages/types

Acute:
- lasts 2-4 weeks
- organism multiplies within mononuclear cells & cells of the spleen & liver
- infected cells are transported to other organs, such as lungs, kidneys, & meninges
- vasculitis & subendothelial tissue infection develops

Subclinical:
- appears 6-9 weeks after infection
- may not show clinical signs

Chronic:
- bone marrow is suppressed, resulting in thrombocytopenia, nonregenerative anemia, & pancytopenia
- some dogs will develop glomerulonephritis

Canine monocytic ehrlichiosis signs

Acute = lymphadenopathy, anemia, fever, ocular & nasal discharge, dyspnea, edema of extremities & scrotum, depression, anorexia, & weight loss

Chronic = Severe weight loss, debilitation, anterior uveitis, retinal hemorrhage, CNS signs, secondary infections, & bleeding tendencies due to platelet deficiencies

Canine monocytic ehrlichiosis diagnosis

Indirect immunofluorescent antibody (IFA) test, SNAP test, PCR, pancytopenia (25% of patients), non-regenerative anemia, thrombocytopenia, & hyperglobulinemia

Canine monocytic ehrlichiosis treatment

Doxycycline & supportive care (IV fluids, blood transfusions, etc.)

Canine granulocytic ehrlichiosis

Rickettsial disease caused by Ehrlichia ewingii (lone star tick aka Amblyomma americanum) & E. equi (deer tick aka Ixodes dammini)

Canine granulocytic ehrlichiosis signs

E. ewengii = acute polyarthritis (5 or more joints) & inflammatory joint disease causing lameness & muscle stiffness

E. equi = nonspecific signs of severe lethargy, anorexia, & fever

Canine granulocytic ehrlichiosis diagnosis

SNAP test, proteinuria, & thrombocytopenia

E. ewengii = also eosinophilia & increased ALT

E. equi = also increased ALP

Canine granulocytic ehrlichiosis treatment

Doxycycline & supportive care