Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
69 Cards in this Set
- Front
- Back
|
Endemic area of Histoplasma capsulatum
|
Eastern US (CA, some mid-southern states recently)
|
|
|
Endemic area of Blastomyces dermatitidis
|
Eastern US (some southern Canada)
|
|
|
Endemic area of Coccidioides immitis
|
Southwestern US, Central/South America
|
|
|
Endemic area of Cryptococcus neoformans
|
Internation (now includes Inland NW)
|
|
|
Transmission of systemic fungal diseases
|
Inhalation
|
|
|
Primary species affected by Histoplasma
|
Cats more affected than dogs
|
|
|
Primary species affected by Blastomyces
|
Dogs more affected than cats
|
|
|
Primary species affected by Coccidioides
|
Dogs more affected than cats
|
|
|
Primary species affected by Cryptococcus
|
Cats more affected than dogs
|
|
|
Organs affected by Histoplasma
|
Liver, spleen, lungs, lymph nodes, bone marrow, bones, eyes, GI tract (especially colon in dogs)
|
|
|
Organs affected by Blastomyces
|
Lungs, bones, lymph nodes, skin, eyes, CNS, testes
|
|
|
Organs affected by Coccidioides
|
Lungs, bones, lymph nodes, skin, eyes, pericardium, CNS
|
|
|
Organs affected by Cryptococcus
|
Respiratory (lungs, nasal cavity), skin, eyes, CNS (nasal disease is most common manifestation of feline infection; single organ involvement is also common)
|
|
|
Diagnosis of Histoplasma
|
Demonstration of organism in aspirates or biopsies of affected organs; demonstration of organism in macrophages (blood smear); TTW or BAL
|
|
|
Diagnosis of Blastomyces
|
Demonstration of organisms in aspirates, exudates (skin lesions in dogs), or biopsies of affected organs; TTW or BAL; serum antibodies are supportive
|
|
|
Diagnosis of Coccidioides
|
Demonstration of organisms in aspirates or biopsies; TTW or BAL; serum antibodies are supportive
|
|
|
Diagnosis of Cryptococcus
|
Demonstration of organisms in aspirates, exudates (nasal in cats), or biopsies; detection of antigen in serum, CSF, or aqueous humor; TTW or BAL
|
|
|
Clinical signs common to fungal diseases (depending on organ involvement)
|
Anorexia, depression, weight loss, lethargy, fever (often antibiotic-unresponsive; NO fever common in cryptococcus)
Skin: draining or granulomatous lesions Eyes: Chorioretinitis, blindness, anterior uveitis Neuro: signs from brain, spinal cord, meninges; diskospondylitis Liver: hepatomegaly, icterus Bone, joints: lameness Lymph nodes: lymphadenomegaly GI: diarrhea, vomiting, weight loss Respiratory tract/pericardium: cough, tachypnea Nasal cavity/respiratory tract: nasal discharge |
|
|
Most important piece of history in case of fungal disease
|
Travel history
|
|
|
Clinical pathology results in fungal disease
|
Variable: (often normal in cats with cryptococcus)
Neutrophilic leukocytosis Hyperglobulinemia (often polyclonal, uncommon in cryptococcus) Hypercalcemia +/- hyperphosphatemia (granulomatous) Elevated liver enzymes (AP also if bone lesions) Hypoalbuminemia (GI/renal losses, more common than vasculitis/proteinuria) |
|
|
Radiographic results in fungal disease
|
VARIED thoracic (diffuse interstitial: nodular or unstructured; alveolar; consolidation); bones may be proliferative (rarely lytic)
|
|
|
Definitive diagnosis for cryptococcus
|
Antigen - positive serology
|
|
|
Urine antigen detection assay for Blastomyces, Histoplasma
|
More sensitive than serum, but may be cross-reactive; positive is still supportive of indication to treat
|
|
|
Types of treatment for fungal diseases
|
Ketoconazole: $$$, hepatotoxic, vomiting/diarrhea
Itraconazole: less hepatotoxic, dermal side affects Fluconazole: less hepatotoxic, drug of choice for ocular/CNS disease Amphotericin B: used in severe disease (quickest kill of organism), nephrotoxic Fl |
|
|
Length of treatment for fungal disease
|
>60 days, one month beyond resolution of clinical signs (in cryptococcus, one month beyond negative antigen titer); relapse is common. Anti-inflammatory doses of corticosteroids may be necessary.
|
|
|
Zoonotic potential in fungal disease
|
Low, except for lab personnel in cases of Blastomyces
|
|
|
FIP viral characteristics
|
Enveloped (easily inactivated), arises from spontaneous mutations of feline enteric coronavirus (FeCoV), can live and replicate in macrophages
|
|
|
Transmission of FIP
|
Fecal-oral; can be transmitted by queens in utero (rare) or soon after weaning (common); asymptomatic carriers exist
|
|
|
Shedding of FIP
|
If viral RNA is detected in stool, can document shedding, but not possible to reliably detect shedders; cats may shed continuously or intermittently
|
|
|
Epidemiology of FIP
|
A disease of multi-cat households and catteries
|
|
|
Age peaks for clinical disease of FIP
|
3 months to 3 years; older than 10 years
|
|
|
Pathogenesis of FIP
|
Mutants can replicate in macrophages --> disseminate to sites rich in macrophages (ln, CNS, liver, kidney, uvea, pleura, peritoneum) --> deposited in endothelial lining of small venules
|
|
|
Elimination of FIP
|
If virus not eliminated but dissemination prevented, cats are latently infected but can be reactivated with stress
|
|
|
Three types of cell-mediated immune response in FIP
|
Strong CMI (elimination or latency)
Partial CMI (non-effusive/dry FIP): slowed viral replication = granulomas Weak CMI (effusive/wet FIP): viral complexes, macrophages in venular walls elicit pyogranulomatous inflammation and type III hypersensitivity; complement-mediated vasculitis allows protein and fibrin-rich fluid to escape |
|
|
Onset of signs in FIP
|
Usually slow, rarely rapid
|
|
|
Clinical signs in wet and dry forms of FIP
|
anorexia, depression, weight loss, dehydration, fever unresponsive to antibiotics (be sure to check retinas)
|
|
|
Difference in fever of FIP and cryptococcus
|
Crypto's fever is late or absent
|
|
|
Clinical disease of effusive form of FIP
|
(More rapidly progressive;)
Abdominal distention (from effusion) Respiratory distress: restrictive breathing (pleural effusion) or non-restrictive (pyogranulomatous pneumonia) Scrotal swelling in intact males Vomiting and diarrhea Icterus Pancreatitis, EPI, DM |
|
|
Clinical disease of dry form of FIP
|
(May convert to effusive form)
Hepatic insufficiency Renal insufficiency Pancreatic disease Ocular disease (anterior uveitis, chorioretinitis) Neurologic disease (posterior paresis, ataxia, cerebral/cerebella signs, CN deficits) Mesenteric lymph node enlargement Cough Respiratory distress characterized by non-restrictive pattern |
|
|
Lab abnormalities of FIP
|
(None are pathognomonic:)
CBC: normocytic, normochromic non-regenerative anemia, neutrophilic leukocytosis, lymphopenia, neutropenic when end-stage Chem: azotemia, hyperbilirubinemia (always abnormal, may soon have hemolytic or cholestatic disease), increased liver enzymes, hyperglobulinemia (usually polyclonal) UA: proteinuria, low SG Effusion analysis: high protein (>5 g/dl), neutrophils, monocyte/macrophages, fibrin clots; cell counts low for exudative fluid) |
|
|
Serology of FIP
|
Positive ELISA/IFA detect antibody but cross-react with coronavirus, so only suggestive; rising titers are also suggestive (but exposure only, needs proper context)
Some with FIP have no antibody left to react if end-stage |
|
|
Histopathology of suspect organs in FIP
|
Gold standard of diagnosis; perivascular pyogranulomatous vasculitis tissues
|
|
|
Immunohistochemistry in FIP
|
Can demonstrate viral antigens by tissue from biopsy or post-mortem
|
|
|
RT-PCR for FIP
|
Detects coronavirus, cannot differentiate; may be of use in seronegative cats but have compatible clinical signs and lab abnormalities
|
|
|
Differential diagnoses for FIP
|
Toxoplasmosis (lung, liver, CNS, pancreas)
FeLV/FIV (via secondary infection of neoplasia) Neoplasia (lymphosarcoma) Systemic fungal infection Hepatic disease (cholangiohepatitis, hepatic lipidosis) Renal disease IBD/pancreatitis |
|
|
Diagnosis of FIP
|
Presumptive by exclusion of other causes
|
|
|
Prognosis of FIP
|
Fatal disease (form dictates progression)
|
|
|
Therapy for FIP
|
Supportive (fluids, abdominocentesis, thoracocentesis), palliative (immunosuppressive/anti-inflammatory drugs: glucocorticoids; cyclophosphamide, chlorambucil - if these two used with pred, evaluate CBC weekly for myelosuppression; broad-spectrum antibiotics; recombinant human interferon-alpha)
|
|
|
Prevention of FIP
|
Clean litterboxes, limit number of cats, introduce/identify seronegative cats; vax is contraversial (causes seroconversion, incomplete protection)
|
|
|
Viral characteristics of FIV
|
Lentivirus, enveloped, has subtypes (difficult to develop vax)
|
|
|
Transmission of FIV
|
Contamination of bite and fight wounds with blood or saliva; (experimentally in utero, via milk, AI, etc.; horizontal transmission in multi-cat households is infrequent)
|
|
|
Epidemiology of FIV
|
Worldwide; 2-3 X more prevalent in males; outdoor, free-roaming cats at increased risks; most often adults
|
|
|
Pathogenesis of FIV
|
Target cells are CD4+, macrophages --> viral replication in tissues rich in lymphoid cells, macrophages --> peak viremia (2-4 weeks post-infection); --> infection of other mononuclear cells in non-lymphoid organs (lung, GIT, kidney); --> CD8+ CMI reduces viremia (not in infected tissues); immunologic abnormalities develop: inversion of CD4/8 ratios (loss of CD4); impairment of lymphocyte function (loss of proliferation, altered expression of cell-surface molecules, abnormal cytokine production profiles, hyperglobulinemia; --> impaired neuro function --> become susceptible to opportunistic infections, neoplasms, or wasting
|
|
|
Stages of FIV
|
Acute: (through peak viremia) May be very mild; fever, malaise, acute GI, acute dermatitis, generalized ln enlargement
Chronic asymptomatic (variable duration) Terminal: lymphadenopathy, AIDS-related complex, signs of opportunistic infection/neoplasia |
|
|
Testing for FIV
|
All sick cats should be tested if status unknown
|
|
|
Lab abnormalities of FIV
|
CBC: neutropenia, lymphopenia (acute), normal (asymptomatic), varied (ill)
Chem: increased plasma/serum protein from hypergammaglobulinemia, azotemia UA: none |
|
|
Serology for FIV
|
ELISA/IFA for antibody: positive is usually infection (don't test before 6 months - maternal antibody); confirm by Western.
False +: if whole blood, reactions to other agents, prior vax, or cell culture components in vax False -: if in acute, or loss of antibody in terminal phase (also possible to revert to negative seroconversion). Retest 1-2 weeks. |
|
|
Histopathology for FIV
|
Reflects current disease; lymphocytic inflammation with neuro disease; lymph node hyperplasia in acute, depletion in terminal
|
|
|
Differential diagnoses for FIV
|
FeLV, FIP, neoplasia, systemic fungal disease, IBD
|
|
|
Prognosis for FIV
|
Can live extended lives; treat complications
|
|
|
Therapy for FIV
|
AZT (anti-viral); $$$, Heinz body anemia possible
Treat concurrent diseases (if dermal, not griseofulvin due to neutropenia) Treat cytopenia with growth factors Symptomatic, supportive therapy |
|
|
Prevention of FIV
|
Isolation of infected cats; keep cats indoors; vaccination may not apply to all subtypes, and antibodies are induced (will test positive and be euthanized)
|
|
|
FeLV viral characteristics
|
Oncornavirus, Retroviridae; short survival outside cat; subgroup A always present, B and C mutations occur from A and are more pathogenic
|
|
|
Transmission of FeLV
|
Contact with infectious saliva and/or nasal secretions of cats with persistent active infection; more transmissible than FIV
|
|
|
Seroprevalence of FIV and FeLV
|
Higher in sick cats than healthy cats (diagnostic importance
|
|
|
Cats more commonly affected by FeLV
|
Older cats more resistant to persistent infection than kittens
|
|
|
Pathogenesis of FeLV
|
Viral replication in lymphoid tissues of oropharynx, some lymphocytes --> myeloid/erythroid cells infected --> persistent viremia, infection of mucosal/glandular tissue --> excretion of virus
|
|
|
Role of host immune responses in FeLV
|
High titers of virus-neutralizing Abs associated with resistance, low titers --> persistent viremia; antibodies to FOCMA are protective; antibodies to other FeLV proteins and CMI provide resistance
Cats controlling infection before bone marrow infection don't develop marrow-associated viremia If viremia not controlled, progresses to FeLV-related disease; small portion of cats have atypical, partially protective immune response with virus sequestration |
|
|
Clinical disease of FeLV
|
May die of leukopenia and immunosuppression; most develop FeLV-related disease months to years after infection/persistent virus replication
|
