AFIP Wednesday Slide Conference - No. 12
December 1, 1999
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- Conference Moderator:
Dr. F.M. Garner, Diplomate, ACVP
4416 Oak Hill Road
Rockville, MD 20853
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- Case I - Y10628-8 (AFIP 2688902 )
- Signalment: 8-week-old, Labrador retriever, male,
canine, Canis familiaris.
- History: The puppy was presented for whining, listlessness,
anorexia, and circling of 1-2 day's duration. The puppy's temperature
was 100 degree F. An abdominal radiograph appeared normal. Blood
and serum were collected and submitted for a CBC and serum chemistries,
respectively. At 6 weeks-of-age, the puppy had received vaccinations
for canine distemper and canine parvovirus. Treatment was initiated
at 8 am the morning of presentation and consisted of IV fluids
(LRS) and IM antibiotics (PenG). Fluids and antibiotics were
repeated throughout the day. The puppy's condition had worsened
by 8 pm, and he died later that night. The puppy was necropsied
the next day.
- Gross Pathology: The brain exhibited moderate, diffuse
malacia, and numerous petechiae were scattered throughout the
midbrain and brain stem. Lymph nodes throughout the body were
moderately enlarged and very hemorrhagic. Numerous ecchymoses
were scattered over the epicardium and endocardium. The liver
was slightly swollen and congested, and the gallbladder was edematous.
The spleen was slightly enlarged and contained prominent lymphoid
foci. A few petechia were scattered over the serosal surfaces
of the stomach and urinary bladder. A small to moderate amount
of mucoid to hemorrhagic fluid was in the stomach and small intestine.
- Laboratory Results: The CBC and serum chemistries
revealed anemia (HCT=22.3%), thrombocytopenia (PLT=23,000/uL),
mild neutrophilia (78%), lymphopenia (10%), elevated liver enzymes
[ALKP=287 (normal range=5-56U/L)], hypoproteinemia (TP=4; normal
range=6-8.4 g/dL), and hypoalbuminemia (ALB=2; normal range=3.5-5.3
Contributor's Diagnosis and Comments: Moderate to severe,
acute, periacinar to midzonal and bridging, necrotizing hepatitis
with hepatocellular intranuclear adenovirus inclusions.
- Etiology: canine adenovirus-1
- Disease: Infectious Canine Hepatitis
- Microscopically, the liver is characterized by moderate to
severe, acute periacinar to midzonal and bridging, coagulative
and lytic, hepatocellular necrosis associated with numerous hepatocellular
intranuclear magenta inclusions consistent with canine adenovirus-1
infection (infectious canine hepatitis). The lesions of infectious
canine hepatitis (ICH) result from the tropism of canine adenovirus-1
for endothelium, mesothelium, and hepatic parenchyma. The reason
for the increased susceptibility of periacinar hepatocytes to
necrosis is unknown. Widespread hemorrhages occur due to leakage
from damaged vascular endothelium, inability of damaged liver
to replace clotting factors, and exhaustion of clotting factors
resulting from accelerated consumption initiated by endothelial
damage (DIC). Vaccination has greatly reduced the frequency of
clinical disease and death due the ICH.
- AFIP Diagnosis: Liver: Hepatitis, necrotizing, acute,
multifocal to coalescing, severe, with hepatocellular eosinophilic
intranuclear inclusion bodies, Labrador retriever, canine.
- Conference Note: Canine adenovirus-1 (CAV1)(Genus
Mastadenovirus, Family Adenoviridae) also known as infectious
canine hepatitis (ICH) virus. Adenoviruses are icosohedral, 80-100
nm, double stranded DNA virus. Most adenoviruses cause enteric
or respiratory diseases that are acute, mild and rarely produce
clinical disease except in the immunocompromised host. CAV1 is
uncommon among adenoviruses in that it can produce severe generalized
disease, including hepatitis, respiratory disease, ocular disease
(blue eye), encephalopathy and interstitial nephritis. CAV1 is
also an important pathogen of foxes, wolves, coyotes, skunks,
raccoons, and bears. This virus was recognized as the cause of
fox encephalitis and was proven to cause ICH-like symptoms experimentally
many years before it was realized that the same virus caused
- Clinically, ICH is often associated with corneal opacity.
Before enzyme immunoassay, hemagglutination-inhibition, neutralization
or polymerase chain reaction tests were available to diagnose
ICH, this was considered an important clinical sign to differentiate
ICH from other acute viral diseases. Although ICH produces relatively
distinctive histologic lesions, clinically it may be difficult
to differentiate from canine distemper, toxoplasmosis, coccidiomycosis,
- Contributor: Diagnostic Laboratory Services, College
of Veterinary Medicine, Mississippi State University, Mississippi
State, MS 39762.
- 1. Greene CE: Infectious Diseases of the Dog and Cat, 2nd
ed., pp 22-27. WB Saunders, Philadelphia, PA, 1998
- 2. Kelly WR. The liver and biliary system. In: Pathology
of Domestic Animals, eds. K.V.F. Jubb, P.C. Kennedy, and N. Palmer,
4th ed., Vol 2, pp. 319-406, Academic Press, Inc., San Diego,
- Case II - 98-9138 (AFIP 2694721)
- Signalment: Six-year-old castrated male Labrador retriever
- History: The dog was diagnosed with pemphigus foliaceus
via biopsy and treated for one month with Triamcinolone and 10
days with Imuran. The dog developed diarrhea two weeks after
Triamcinolone therapy began and became anorexic and lethargic
3 days after Imuran treatment began. The dog presented with weakness,
icterus, generalized lymphadenopathy, and bilateral harsh respiratory
sounds. Clinical signs progressed despite supportive care, and
the animal died while in the hospital.
- Gross Pathology: There was cutaneous ulceration over
the bridge of the nose and ulceration of the hard palate. There
were multifocal raised, granular yellow 0.1 cm coalescent perivascular
foci on the pericardial surface of the heart. The myocardium
of the left ventricular free wall had poorly delineated yellow/red
foci. The lung contained randomly scattered 0.2-0.3 cm red rimmed
target lesions in all lobes. The parietal pleura was granular
and reddened. There was focal softening and yellow/red discoloration
of the left renal crest and yellow radial streaks in the medulla
and cortex of both kidneys. The liver was enlarged and friable
with multifocal 0.1-0.3 cm soft red foci.
- Laboratory Results:
- CBC abnormalities included: macrocytic (1+), hypochromic
(1+) anemia (HCT 26.6%, normal 37.0-56.0%) with polychromasia
(1+) anisocytosis (1+) and poikilocytosis (1+). Mild neutrophilic
leukocytosis (10.4x103/mm3, normal 3.0-9.5) with a left shift
(bands- 3.5x103/mm3, normal 0) was also present.
- Serum chemistry abnormalities included markedly elevated
alkaline phosphatase (>3750 u/l, normal 11-174), alanine aminotransferase
(2326 u/l, normal 19-136), aspartate aminotransferase (636 u/l,
normal 21-41) and total bilirubin (10.3 mg/dl, normal 0.1-0.6).
There was also hypoproteinemia (5.2 g/dl, normal 5.7-7.3) and
hypoalbuminemia (2.8 g/dl, normal 3.1-4.3).
- Urinalysis abnormalities included low specific gravity (1.010,
normal 1.015-1.045), high pH (8.0, normal 6.0-7.0), proteinuria
(2+), bilirubinuria (3+), hematuria (3+), and many yeast forms
within the sediment. Urine culture yielded a pure culture of
Candida albicans (>100,00 colonies/ml).
Contributor's Diagnosis and Comments: Heart: Severe acute
multifocal necrosuppurative myocarditis and fibrinosuppurative
epicarditis with intralesional fungal spores and pseudohyphae
consistent with Candida spp. Etiology: Candida albicans.
- Candida albicans is a commensal organism commonly found as
part of the normal flora of the gastrointestinal tract. Candida
albicans can cause superficial infections of the skin and mucous
membranes and, less commonly, systemic infections in hosts whose
resistance has been lowered due to prolonged antibiotic therapy,
chronic illness, or immune suppression. Systemic candidiasis
is very rare and has been reported in humans, nonhuman primates,
mice, cetaceans, birds, pigs, foals, calves, cats and dogs.
- AFIP Diagnosis: Heart: Myocarditis and epicarditis,
necrotizing, acute, multifocal, moderate, with numerous yeast,
hyphae and pseudohyphae, Labrador retriever, canine, etiology
consistent with Candida sp.
- Conference Note: The presence of budding, 3-5 mm diameter
yeast cells (blastospores), pseudohyphae and hyphae in tissue
is diagnostic of candidiasis, but the particular species cannot
be identified by histologic examination. Although conference
participants readily identified the etiologic agent in the H&E
stained sections, the organisms were also strongly positive by
the GMS method for fungi.
- Candida infections must be differentiated from Aspergillus
sp., Histoplasma capsulatum, and Torulopsis glabrata. Aspergillus
in tissues is identified by its septate, uniform width (3-4 mm)
hyphae with acute angle dichotomous branching and occasionally
conidia or fruiting bodies. Histoplasma capsulatum does not form
pseudohyphae and hyphae are rarely encountered in tissue. Torulopsis
glabrata is very similar to Candida but does not produce hyphae.
- Most cases of systemic fungal infection are the result of
a compromised immune system, as in this case in which the dog
was treated with immunosuppressive drugs.
- Contributor: Department of Pathology, Angell Memorial
Hospital, 350 S. Huntington Avenue, Boston, MA 02130.
- 1. Bartram PA, Smith BP, Holmberg C, Mandell CP: Combined
immunodeficiency in a calf. JAVMA 195(3):347-350, 1989
- 2. Chandler FW, Watts JC: Candidiasis. In: Pathologic Diagnosis
of Fungal Infections, eds. Chandler, Watts, pp. 97-99. American
Society of Clinical Pathologists, Chicago, IL, 1987
- 3. Clercx C, McEntee K, Snaps F, Jacquinet E, Coignoul F:
Bronchopulmonary and disseminated granulomatous disease associated
with Aspergillus fumigatus and Candida species Infection in a
golden retriever. JAAHA 32:139-145, 1996
- 4. Dunn JL, Buck JD, Spotte S: Candidiasis in captive pinnipeds.
JAVMA 185(11):1328-1330, 1984
- 5. Foley GL, Schlafer DH: Candida abortion in cattle. Vet
Pathol 24:532-536, 1987
- 6. Fulton RB, Walker RD: Candida albicans urocystitis in
a cat. JAVMA 200(4):524-526, 1992
- 7. Gerding PA, Morton LD, Dye JA: Ocular and disseminated
candidiasis in an immunosuppressed cat. JAVMA 204(10):1635-1638,
- 8. Jones TC, Hunt RD, King NW: Veterinary Pathology, 6th
ed., pp. 238. Williams and Wilkins, Baltimore, MD, 1997
- 9. Jubb KVF, Kennedy PC, Palmer N: Pathology of Domestic
Animals, Vol. 2, 4th edition, pp. 256-257. Academic Press Inc.,
San Diego, CA, 1993
- 10. Merlin TL, Gibson DW, Connor DH: Infectious and Parasitic
Diseases. In: Pathology, eds. Rubin E, Farber JL, pp. 408-409.
JB Lippincott Co, Philadelphia, PA, 1994
- 11. Reilly L, Palmer J: Systemic candidiasis in four foals.
JAVMA 205(3): 464-466, 1994
- Case III - P8-306 (AFIP 2683851)
- Signalment: 22-month-old female New Zealand white
rabbit (Oryctolagus cuniculus)
- History: The rabbit was transgenic for the EJras oncogene,
which had been targeted to epidermal keratinocytes by the upstream
regulatory region of the cottontail rabbit papilloma virus. The
transgene causes development of keratoacanthomas and squamous
cell carcinomas in rabbits, and the model is used to study the
multistep progression of cancer. The doe had been used successfully
as a breeder during the past year and had produced multiple litters.
However, most of the young in the last two litters died before
- Gross Pathology: Hair had been pulled from around
the neck. The fur on the dewlap was green/blue. The underlying
skin was slightly red. The mammary tissue was engorged with milk.
- Laboratory Results: Pseudomonas aeruginosa was isolated
from the cutaneous lesions.
Contributor's Diagnoses and Comments: Moderate acute purulent
dermatitis and hemorrhage - Pseudomonas aeruginosa
- Pseudomonas aeruginosa has been associated with blue/green
discoloration of rabbit fur, exudative moist dermatitis, abscesses,
septicemia, pneumonia, and diarrhea. The organism is commonly
found in soil and is known to contaminate water and aqueous solutions
including alkaline disinfectants. It is of comparatively low
virulence and has been found frequently in suppurative processes
in domestic animals. It also causes severe epidemics of respiratory
disease in mink and chinchillas, and green wool condition in
sheep. It produces a pyocyanin pigment, which is bluish green
and oxidizes to brown. The organism produces lecithinase and
protease, which appear to be responsible for edema and induration
of the skin and for the hemorrhagic and necrotizing skin lesions.
Rabbits are less susceptible to experimental infection than guinea
- AFIP Diagnosis: Haired skin: Dermatitis, subacute,
diffuse, severe, with intracorneal pustules, folliculitis, acanthosis,
and numerous intracorneal bacteria.
- Conference Note: Gram stains performed at the AFIP
demonstrated large numbers of Gram negative bacilli within the
- Other causes of bacterial dermatitis in rabbits include Pasteurella
multocida, Stapylococcus aureus, Fusobacterium necrophorum, Arcanobacterium
(Corynebacterium) pyogenes, Streptococcus sp., and Treponema
Contributor: Department of Comparative Medicine, H054,
M.S. Hershey Medical Center, Penn State University, 500 University
Drive, Box 850, Hershey, PA 17033
- 1. DeLong D, Manning PJ: Bacterial diseases. In: The Biology
of the Laboratory Rabbit, eds., Manning PJ, Ringler DH, Newcomer
CE, p. 162. Academic Press, San Diego, CA, 1994
- 2. Peng X, Griffith JW, Han R, Lang CM, Kreider JW: Development
of keratoacanthoma and squamous cell carcinoma in transgenic
rabbits with targeted expression of EJras oncogene in epidermis.
Am J Pathol 155:1-10, 1999
- 3. Samuelson J: Infectious Diseases. In: Robbin's Pathologic
Basis of Disease, eds., Cotran RS, Kumar V, Collins T, 6th ed.,
pp. 376-377. WB Saunders Company, Philadelphia, PA, 1999
- 4. Schoenbaum M: Pseudomonas aeruginosa in rabbit fur. Lab
Ani 15:5, 1981
- Case IV - 1794/98 (AFIP 2681371)
- Signalment: Guinea pig (Cavia aperea porcellus), adult
- History: This animal originated from a colony of guinea
pigs held at the department of food hygiene of the Leipzig University.
No clinical signs were observed. The animal died unexpectedly
after having been experimentally infected with Trichinella spiralis
six weeks earlier.
- Gross Pathology: Necropsy findings revealed loss of
weight. The cecum contained a red-brown liquid.
- Laboratory Results: Histologically, the animal showed
a mild to moderate granulomatous myositis with only very few
eosinophilic granulocytes, affecting many diverse skeletal muscles
and the diaphragm. Within these lesions encysted larvae of Trichinella
spiralis were detectable. Additionally a severe necrotizing typhlitis,
a moderate mononuclear interstitial myocarditis and a moderate
necrotizing hepatitis were diagnosed (slides not submitted).
Contributor's Diagnosis and Comments: Skeletal muscle
(masticatory muscle): focal granulomatous myositis, minimal infiltration
with eosinophilic granulocytes, encysted nematode larvae; guinea
pig (Cavia aperea porcellus). Cavioidea, Rodentia, Mammalia;
Cause: Infection with Trichinella spiralis.
- Trichinellosis is a zoonotic disease. Trichinella spiralis
belongs to a genus of nematode parasites in the family Trichinellidae.
Humans become infected after consumption of uncooked or incompletely
cooked meat of infected pigs, bears, and aquatic mammals. These
animals are the natural sources of infection for human beings.
The parasitic life cycle begins with the ingestion of infected
meat. The activity of digestive juice leads to release of the
encysted larvae, which undergo four molts and mature into adults.
The male parasites die after copulation, while the females penetrate
the crypts of Lieberkuhn, enter the submucosal lymphatics and
deposit large numbers of larvae within the lymphatic spaces.
These larvae migrate into the blood vessels and reach the striated
muscles via the blood stream. They invade muscle bundles, where
they become encysted and stay throughout the life of the host.
The infected muscle cell becomes a "nurse cell". In
this case, the larvae occurred in many striated muscles, including
the humeral and femoral musculature, the diaphragm, and the masticatory
muscles, while the cardiac muscle was not affected. The cause
of the sudden death of this guinea pig is interpreted as a sequela
of the severe necrotizing typhlitis, the moderate mononuclear
interstitial myocarditis, and the moderate necrotizing hepatitis;
no parasites were detectable within these organs.
- AFIP Diagnosis: Skeletal muscle: Myositis, lymphoplasmacytic
and eosinophilic, multifocal, mild, with encysted nematode larvae,
guinea pig (Cavia aperea porcellus), rodent, etiology consistent
with Trichinella spiralis.
- Conference Note: Identification of parasites in tissue
sections requires detailed knowledge of the microanatomy of the
various parasite groups. Nematodes have a cuticle, musculature,
pseudocoelom and gastrointestinal tract. Trichinella sp. belongs
to a group of nematodes classified as aphasmids. Key anatomic
features of aphasmids are the presence of bacillary bands and
- In the United States, trichinosis was maintained in swine
through the practice of garbage feeding. The institution of garbage
cooking in the mid-1950's, as part of the vesicular exanthema
eradication program, greatly reduced the incidence of the disease
in the United States.
- Special thanks to Dr. Chris Gardiner (Captain, USN) for his
consultation on this case.
- Contributor: Institut für Veterinär-Pathologie,
Universität Leipzig, An den Tierliniken 33, 04103 Leipzig,
- 1. Hulland TJ: Muscle and tendon. In: Pathology of Domestic
Animals, Vol. 1, eds. Jubb KVF, Kennedy PC, Palmer N, 4th ed.,
pp. 253-255. Academic Press, San Diego, CA, 1993
- 2. Jones TC, Hunt RD, King NW: Veterinary Pathology, 6th
ed., p. 629. Williams and Wilkins, Baltimore, MD, 1997
- J Scot Estep, DVM
Captain, VC, USA
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
- * The American Veterinary Medical Association and the American
College of Veterinary Pathologists are co-sponsors of the Registry
of Veterinary Pathology. The C.L. Davis Foundation also provides
substantial support for the Registry.
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