The Armed Forces Institute of Pathology
Department of Veterinary Pathology
WEDNESDAY SLIDE CONFERENCE
2000-2001
CONFERENCE 1
6 September 2000
Conference Moderator: COL William
Inskeep, II
Chair,
Department of Veterinary Pathology
Deputy
Director, The Armed Forces Institute of Pathology
Washington,
DC 20306-6000
CASE I – 00-017 (AFIP 2736228)
Signalment: 12-year-old, castrated male, soft-coated wheaten terrier canine
History:
The dog had signs of osteoarthritis and had been on treatment with carprofen
for several months. It developed
vomiting and diarrhea, at which time carprofen treatment was discontinued. It also developed anorexia, had intermittent
vomiting and diarrhea and lost 10-12 lb over a 30-day period. Serial blood tests indicated a
nonregenerative, normocytic, normochromic anemia, leukocytosis, hypoproteinemia
and hypoalbuminemia. He received
prednisone, cimetadine, misoprostal, sucralfate, metronidazole, amoxicillin,
azathioprine and oral Tylan during various stages of treatment for the
inflammatory bowel disease and gastritis.
Approximately 12 hours before his death, he developed a fever,
hyperventilation, and became moribund.
Gross Pathology: External exam - The dog was thin and had a decreased amount of body
fat.
Internal
exam - There was approximately 50 ml of clear fluid in the abdominal
cavity. The thoracic cavity contained
approximately 100 ml of tannish-colored fluid.
Respiratory
system - There was fibrin deposition on the right parietal pleura and
hemidiaphragm. The right caudal lung
lobe was congested, with fibrin deposited on the pleural surface. The left caudal lung lobe was hemorrhagic
and exuded clear fluid on cut surface.
There were multiple organized thrombi in the pulmonary vessels of the
right and left caudal lung lobes.
Urogenital
system - There was a fluid-filled cyst, approximately 3 cm in diameter,
involving the cranial pole of the left kidney.
Both kidneys had multiple small, depressed areas involving the
subcapsular surface.
Digestive
system - There were prominent chyle-filled, dilated lymphatics involving the
serosal surface of the small intestine.
In addition, there were multiple small nodules arising from the
lymphatics. The wall of the duodenum
was thickened and there was marked submucosal congestion in the duodenum and
extending into the jejunum. The
pancreas had several small nodular areas and an area with adhered omentum. The liver had multiple small to medium-sized
areas which were pale in color and extended deep into the parenchyma on cut
surface.
Laboratory Results: Data not included. A summary was provided in the history, and in addition, E. coli was isolated from blood and lung
at necropsy.
Contributor’s Diagnoses and Comment: Marked intestinal lymphangiectasia and mild
granulomatous lymphangitis.
Marked focal duodenal
crypt dilatation and mild epithelial cell metaplasia.
Intestinal
lymphangiectasia with lymphangitis has been associated with protein losing
enteropathy in dogs. This syndrome has
been associated specifically with the soft-coated wheaten terrier (SCWT) breed
ranging from 6 months to 12 years of age.
There are strong indications that there may be a genetic predisposition
for the disease in SCWT. Thromboembolic
complications leading to death have also been associated with this syndrome in
SCWT. The thrombo-embolic complications
may have been related to disseminated intravascular coagulation, with resulting
lesions within the lung and liver.
Marked focal dilatation of the duodenal crypts and
metaplasia/regeneration of the crypt epithelium suggest a chronic, toxic
irritation of the duodenum and may be related to focal concentrations and
toxicosis of carprofen and/or prednisolone.
AFIP Diagnoses: 1. Small intestine:
Lymphangiectasia, multifocal, mild to moderate, with granulomatous
lymphangitis, soft-coated wheaten terrier, canine.
2. Small intestine: Crypt ectasia, multifocal,
mild, with necrosis and neutrophilic and histiocytic inflammation.
Conference Comment: The soft-coated wheaten terrier is predisposed to
the two syndromes of protein-losing enteropathy (PLE) and protein-losing
nephropathy (PLN). Although the precise
mode of inheritance of these diseases is unknown, pedigree analysis has shown
these dogs to be related to a common male ancestor. PLE and PLN in this breed have unique features that include the
common concurrence of PLE with PLN (PLE often seen prior to PLN signs), a
female predisposition and a variable age range for the onset of clinical
signs. The genetic defects involved in
PLE and PLN in this breed may be complex and may include an immunoregulatory
dysfunction, an altered response to an environmental trigger, and an
ultrastructural or developmental defect of lymphatics, vasculature, epithelia,
and/or basement membranes.
Lymphangectasia may cause leakage with inflammation, or inflammation may
cause dilation of lymphatics; however, in one study, surgical ligation of
lymphatics did not cause inflammation and granuloma formation. The crypt dilation and abscessation may be
related to toxic mucosal irritation from drug therapy. Similar lesions are described in cases of
inflammatory bowel disease and protein-losing enteropathy.
In
this case, the dog had hypoproteinemia and hypoalbuminemia. The differential diagnosis for
hypoalbuminemia due to decreased production would also include malnutrition,
exocrine pancreatic insufficiency, and chronic liver disease. With exocrine pancreatic insufficiency,
decreased serum trypsin-like immunoreactivity (TLI) and BT-PABA tests would
indicate a deficiency in trypsinogen and chymotrypsin, respectively. High folate and low cobalamin concentrations
could reflect intestinal bacterial overgrowth due to a lack of the
bacteriostatic effect of pancreatic enzymes.
A
loss of antithrombin III through the kidneys due to the PLN was postulated as
possibly contributing to the formation of pulmonary thrombi. Antithrombin III activity also decreases in
hypercoagulative disorders (e.g., disseminated intravascular coagulopathy).
Endoscopic
biopsy sampling of the intestinal mucosa may show an artifactual dilation of
lacteals caused by surgical manipulation.
A deep endoscopic biopsy sample, attained by the collection of a second
sample from the same site, may give a more accurate picture of the underlying
disease process.
Contributor: M.S. Hershey Medical Center, Penn State University, Department of
Comparative Medicine, H054, 500 University Drive, Box 850, Hershey, PA 17033
References: 1. Littman MP: 1999 ACVIM Proceedings: Wheaten terrier PLE-PLN.
(recently published)
2. www.scwtca.org/scwtvmont.htm
3. www.cvm.ncsu.edu/research/SCWT/ple.htm
CASE II – S96-2403 (AFIP 2596318)
Signalment: 8-year-old, spayed female, domestic shorthair cat
History:
This cat was presented to a veterinarian because of a local ulcerative skin
problem of several months duration. Two
other cats lived in the same household, one of them since 8 years of age, the
other since several weeks of age. All
three were kept indoors. Their food
consisted of commercial cat food and occasionally fresh meat. The clinical evaluation and the routine
laboratory blood examination indicated no abnormalities. Serological tests for FIV and FeLV were
negative. An X-ray of the lungs showed
multifocal, ill-defined interstitial densities. Due to treatment failure the cat was euthanized.
Gross Pathology: Several firm, alopecic, partly ulcerated, intracutaneous nodules
(diameter 0.5-1 cm) were found on the inner aspect of the right hind leg. The skin of the outer side of the same leg
was characterized by a large, 5x7 cm, thickened, well-demarcated, alopecic, and
mostly ulcerated area. The cut surface
of all lesions revealed intracutaneous to subcutaneous, firm, gray to pink nodules. All lung lobes contained multiple small, 3-8
mm diameter, irregularly shaped, well-defined, firm, homogenous white to yellow
nodules. The pulmonary and mesenteric
lymph nodes were enlarged and cut surfaces were uniform and pale. The intestine showed no gross lesions.
Laboratory Results: Acid fast bacteria were seen in Ziehl-Neelsen
stained smears of lung and mesenteric lymph nodes. The rod-shaped, medium long, slender and slightly curved bacteria
were single or in groups. Mycobacteria
were cultured in the BacTecT 460TB® system.
The mycobacteria could be classified by “transcription-mediated
amplification” (MTD, Genprobe®) as belonging to the Mycobacterium tuberculosis group.
Unfortunately, the subcultivation did not succeed and further identification
was not possible. No other bacteria
could be isolated in the organs submitted for bacteriological examination
(liver, spleen, kidneys, lungs, pulmonary lymph nodes, intestine, mesenteric
lymph nodes, skin).
Contributor’s Diagnoses and Comment: 1. Skin:
Dermatitis, granulomatous, multifocal to coalescing, severe.
2. Lungs: Pneumonia, granulomatous, multifocal,
moderate.
3. Lymph nodes (pulmonary, mesenteric) [not
submitted]: Lymphadenitis, granulomatous, severe.
Etiology: Mycobacteria,
tuberculosis group. The detection of
few intracellular, acid fast, rod-shaped bacteria in the above-mentioned organs
is consistent with the etiological diagnosis of tuberculosis.
Histological examination of the skin reveals ulceration
(not on all sections) and a dense nodular to coalescing cellular infiltrate in
the dermis and subcutis which expands and spreads to the surrounding
tissue. The nodules consist mainly of
histiocytes and epithelioid cells accompanied by a proliferation of
fibroblasts. A considerable number of
lymphocytes and few neutrophils and plasma cells are scattered in the
granulomas. Small foci of necrosis are
surrounded by few neutrophils and lymphocytes.
Within lung lesions, there are nodules consisting of histiocytes,
epithelioid cells, proliferating fibroblasts and scattered inflammatory
cells. In both organs, single
intracellular acid fast bacilli could be detected with Ziehl-Neelsen stain
(transparency).
Feline mycobacterial infections can be divided into three
forms: classical tuberculosis (caused
by M. bovis, M. tuberculosis, the recently described variant that has
characteristics of M. bovis and M. tuberculosis, and M. microti), feline leprosy (caused by M.
lepraemurium) and atypical
mycobacteriosis (caused by M. avium, M. fortuitum, M. thermoresistible, M.
xenopi, M. phlei and M. smegmatis. Members of the first group are considered
obligate pathogens.
Tuberculosis in cats is mainly caused by M. bovis. The cats were believed to be infected by ingestion of
contaminated fresh milk or meat. Since
tuberculosis in cattle has been eradicated, those forms have nearly
disappeared. Being a primary human
pathogen, feline infections by M.
tuberculosis are considered an inverse zoonosis. Recently, several cases of tuberculosis were described, where the
organisms isolated had cultural characteristics of M. tuberculosis and M. bovis. There are only very few reports concerning
the isolation of M. microti. M.
avium, an opportunistic organism belonging to the atypical mycobacteria
causes lesions indistinguishable from those of the tuberculosis complex. Cats are highly resistant to M. avium and reports of infections are
rare.
In this case, the organisms were identified as members of
the tuberculosis group. The health
status of the persons in contact with this cat was checked. The owner, the treating veterinarian and one
of his technicians had a positive tuberculin reaction of 10 mm or more. None of them showed signs of active
tuberculosis in the clinical examination or in the thoracic X-ray. Nevertheless, preventive chemotherapy for 6
months was prescribed.
The incidence of human tuberculosis in Switzerland is
generally low and slowly decreasing.
Nevertheless, an increase of tuberculosis in immigrants and
immunocompromised patients is evident.
In some countries of central Europe (e.g., Italy, Denmark, the
Netherlands), the number of newly infected persons has even increased by 30-40%
between 1990 and 1994. In our case, the
origin of the organism remains unclear.
The owner had no known contact with an infected person. The cat had no contact to other animals than
those in the same household, apart from a one-week stay in an animal boarding
establishment 7 years previously. The
other two cats showed no sign of illness at clinical examination and they were
radiographically negative.
AFIP Diagnoses: 1. Haired skin: Dermatitis
and panniculitis, granulomatous, focally extensive, severe, domestic shorthair,
feline.
2. Lung: Pneumonia, granulomatous, multifocal,
moderate.
Conference Comment: Although often present in low numbers, as in this
case, intracellular tubercle bacilli are recognized by their clubbed shape and
beaded appearance. Evidence of lesion
encapsulation is often characterized by densely packed fibroblasts in a thin,
fibrous connective tissue capsule.
Mycobacteria have the distinctive property of retaining hot
carbolfuchsin stain after treatment with acid or alcohol. This acid-alcohol fastness is due to the
high lipid content of mycolic acid in the cell wall. Cord factor and Wax D, also part of mycobacterial cell wall,
contribute to the host’s granulomatous response to the organism. Pathogenic mycobacteria are slow growing,
often requiring several weeks to establish visible colonies, and their growth
is inhibited unless enrichment media are used.
The
differential diagnosis for granulomatous reactions in the skin and lung of a
cat might include nocardiosis, actinomycosis, fungal infections and foreign
body reactions. M. tuberculosis has had a higher prevalence of infection in dogs
than cats. Aerosolized droplet
transmission from respiratory secretions is the primary means of infection for
other people or pets. In general,
tubercle bacilli are not as infectious as other bacterial pathogens since
prolonged frequent exposure or large inocula are usually required. In contrast to the sparse numbers of
organisms within the cutaneous lesions in this case, cats infected with M. lepraemurium often have very large
numbers of acid fast bacilli noted on histology or impression smears.
Unlike
many species, cats do not react strongly to intradermally administered
tuberculin but still have adequate immunity to tuberculosis. Cats sensitized to bacille Calmette-Guérin
(BCG) have responded to intradermal injections in the pinna; unfortunately, the
response is inconsistent, infrequent, or transient.
Contributor: Institute of Veterinary Pathology, University of Zurich,
Winterthurerstrasse 268, Zurich, Switzerland, CH-8057
References: 1. Anonymous: Schweizerische
Vereinigung gegen Tuberkulose und Lungenkrankheiten (SVTL): Richtlinien fur die
preventive Chemotherapie der Tuberkulose (Therapie der Tuberkulose-Infektion).
Bull BAG, Beilage, 4, 36-37, 1991
2. Blunden AS, Smith KC: A pathological study
of a mycobacterial infection in a cat caused by a variant with cultural
characteristics between Mycobacterium
tuberculosis and M. bovis. Vet
Rec 138:87-88, 1996
3. Drolet R: Disseminated tuberculosis caused
by Mycobacterium avium in a cat. J
Amer Vet Med Assoc 189:1336-1337,
1986
4. Greene CE: Mycobacterial infections. In: Infectious diseases of the dog and
cat, ed. Greene CE, pp. 558-572. WB Saunders Co., Philadelphia, PA, 1990
5. Gunn-Noore DA, Jenkins PA, Lucke VN: Feline
tuberculosis: A literature review and discussion of 19 cases caused by a unusual
mycobacterial variant. Vet Rec 138:53-58,
1996
6. Isaac J, Whitehead J, Adams JW, Barton MD,
Coloe P: An outbreak of Mycobacterium
bovis infection in cats in an animal house. Aust Vet J 60:243-245, 1983
7. Loddenkemper R: Tuberkulose - ein immer noch
drängendes problem. Spektrum der Wissenschaft Dossier 3, 106-107, 1997
8. Orr CM, Kelly DF, Lucke VM: Tuberculosis in
cats. A report of two cases. J Small Anim Pract 21:247-253, 1980
9. Wynne Jones J, Jenkins PA: Is tuberculosis
in domestic cats hazardous to human beings? Lancet 346:442-443, 1995
10. Zellweger JP: La tuberculose en Suisse en
1996: Prévention et traitement. Schweiz Med Wochenschr, 126, 1112-1118, 1996
CASE III – H98-1202 (AFIP 2651778)
Signalment: 4-year-old, Texel-cross, female, ovine, Ovis aries
History:
Intravenous inoculation of Chlamydia
pecorum at 85 days gestation.
Normal lambing at term (single live lamb 4.75kg). Localized placental lesion observed.
Gross Pathology: Approximately 25% of placental surface was affected. There was pale soft thickening of the
periphery of cotyledons with adherent cheese-like debris and marked edema of
the adjacent intercotyledonary placenta.
Laboratory Results: Chlamydial organisms were isolated from the
vaginal discharge and from the placenta.
Serology revealed seroconversion of the ewe (anti-chlamydial antibody
titers assessed by complement fixation and indirect immunofluorescence).
Contributor’s Diagnosis and Comment: Placentitis, acute, necrotizing, multifocal with
leucocytoclastic vasculitis; Chlamydia
pecorum
Enzootic abortion of ewes caused by Chlamydia psittaci infection is the most frequently diagnosed cause
of infectious ovine abortion in Britain and is becoming increasingly prevalent
in Ireland. Affected ewes may abort
close to term or deliver lambs of varying vitality at term. Many intestinal
chlamydial isolates of ruminants, formerly designated as non-abortion strains
of C. psittaci, have been recently
assigned to a new species, Chlamydia
pecorum, on the basis of genetic analyses. Mid-pregnancy ewes were
challenged with one such isolate to establish its abortifacient potential. Two of four ewes parenterally inoculated
with C. pecorum had placental lesions
(one aborted and the other lambed normally); chlamydiae were isolated from the
placentae.
Histopathologically, there was focally extensive loss of
the trophoblast layer that was replaced by aggregated nuclear debris. Fibrinoid necrosis of superficial arterioles
was apparent; these vessels were encircled by dense aggregates of degenerate
leukocytes. An infiltrate of neutrophils
and fragmented nuclei occurred in the tunica media and adventitia of deeper
arterioles; fibrin thrombi were present in the lumens of some blood
vessels. Congestion and edema of the
chorionic stroma was accompanied by a light to moderate, diffuse infiltrate of
neutrophils. In some sections,
intracellular clusters of basophilic bodies were seen in trophoblasts.
The ovine placenta is classified as being villous,
cotyledonary, (syn)-epitheliochorial and nondeciduate. Some normal histological features of ovine
placentation which may be observed are hematomas in the spaces between
chorionic villi, hemosiderin deposits in adjacent trophoblasts and the presence
of binucleated giant cells in the trophoblast layer. Other infectious agents which cause necrotizing placentitis in
sheep in the British Isles include Toxoplasma
gondii, Campylobacter foetus, Listeria monocytogenes, Salmonella dublin and
Coxiella burnetti. However, the marked vasculitis which
develops with chlamydial infection is not usually a feature of placentitis due
to any of these agents. Furthermore,
histochemical stains (modified Ziehl-Neelsen, Giemsa or Gimenez) or an
immunoperoxidase technique can be used to demonstrate chlamydial organisms in situ.
AFIP Diagnosis: Chorioallantois: Placentitis, necrotizing, acute, multifocal,
moderate, with severe vasculitis, crossbreed, ovine.
Conference Comment: Chlamydiae are obligate intracellular organisms,
larger than viruses (200-1000 nm), possess DNA and RNA, form their own cell
wall, and are susceptible to some antibiotics much like bacteria. Chlamydiae have two morphological forms:
elementary and reticulate bodies; an intermediate body is sometimes described
as a transitional stage. These
organisms can play an active role in the internalization process by inducing
phagocytosis in cells that do not normally engulf particles.
Chlamydiae
have a strong affinity for the placenta.
After entering via the digestive or respiratory tract, or after
activation of latent organisms, there is hematogenous spread to the placenta. Organisms traverse capillary walls of
maternal septa and enter extravasated blood in the lacunae. Chlamydiae spread in periplacentomal
chorioallantoic membrane by infecting syncytiotrophoblasts and forming colonies
of elementary bodies in cytoplasmic vacuoles.
Chlamydiae, unlike Brucella, also replicate in endometrial
epithelium. Within endosome-bound
inclusion bodies that fail to fuse with host lysosomes, elementary bodies
transform to reticulate bodies and multiply to as many as 500 organisms per
host cell. Because of their inability
to synthesize ATP, the organisms induce host cell mitochondria to closely
appose the inclusion body. After about
20 hours into the cycle, some of the reticulate bodies condense and mature,
forming new elementary bodies. Cells
lyse and release organisms into chorionic mesenchyme, capillaries, and the
intervillous-septum space. Additional
chorionic epithelial cells are parasitized and chorionic capillaries distribute
organisms to the fetus. Infection
provokes inflammation in both cotyledon and caruncle causing necrosis, thrombosis
and infiltration of neutrophils.
Separation of the placenta occurs with abortion due to a combination of
placental damage and fetal injury.
All organisms of the genus belong to four species: C. psittaci, C. trachomatis, C. pecorum
(known as “enteric” chlamydia that have been isolated from gut, joints, lung
and conjunctiva), and C. pneumoniae. In addition to abortions, chlamydia can also
cause intestinal infections and pneumonia in sheep, goats, cattle and swine;
polyarthritis in calves and lambs; epididymitis in sheep; orchitis in bulls and
mastitis in cows; keratoconjunctivitis in sheep and goats; conjunctivitis in
cats; and sporadic bovine encephalomyelitis (SBE).
The causative agent was not observed in sections examined
in conference.
Contributor: University College Dublin, Department of Veterinary Pathology,
Shelbourne Road, Ballsbridge, Dublin 4, Ireland
References: 1. Banks WJ: Female
reproductive system: comparative placentology. In: Applied Veterinary
Histology, 3rd ed., pp. 457-465. Mosby Year Book, St. Louis, MO, 1993
2. Buxton D, Barlow RM, Finlayson J, Anderson
IE, Mackellar A: Observations on the pathogenesis of Chlamydiae psittaci infection of pregnant sheep. J Comp Path 102:221-237, 1990
3. Fukushi H, Hirai K: Proposal of Chlamydia pecorum sp. nov. for
chlamydia strains derived from ruminants. Int J Sys Bact 42:306-308, 1992
4. Kennedy PC, Miller RB: The Female Genital
System. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N,
4th ed., vol. 3, pp. 387-445. Academic Press, New York, NY, 1993
5. Markey B, Basssett H, Sheehy N, Gleeson M, Clements
L: Chlamydial abortion in an Irish sheep flock. Irish Vet J 49:282-286, 1996
6. Stamp JT, McEwan AD, Watt JAA, Nisbet DI:
Enzootic abortion in ewes: transmission of the disease. Vet Rec 62:251-254, 1950
7. Wooding FBP, Flint APF: Synepitheliochorial
placentation. In: Marshall’s
Physiology of Reproduction, ed. Lamming GE, 4th ed., vol. 3, pp. 330-335.
Chapman & Hall, London, England, 1985
CASE IV – 97-10732 AA or BB (AFIP 2594107)
Signalment: 2-month-old, American quarter horse, female, equine
History:
This foal was treated for pneumonia and diarrhea for 1 1/2 weeks by the referring veterinarian. At the Veterinary Teaching Hospital, physical examination
revealed weakness, irritability, dehydration and diarrhea.
Gross Pathology: Many skeletal muscles were pale, gritty in texture, with a chalky appearance
on cut surface. These changes were
patchy to focally extensive and involved major muscle groups in the limbs,
pectoral and neck muscles, longissimus dorsi and glossal muscles. The laryngeal and cardiac muscles were not
affected. Other findings involved
diffusely reddened mucosa in the ventral colon and a thrombosed large colonic
vein.
Laboratory Results: A hemogram revealed a WBC count of 60,800 with 97%
neutrophils and a PCV of 31.7%. Serum
chemistry values included total protein of 3.8 g/dL, creatine kinase (CK) of
7960 U/L and AST (SGOT) of 4496 U/L.
Vitamin E and Trace Mineral Analysis - The foal’s liver
vitamin E (7.16 ppm) and selenium (0.59 ppm) values were considered
adequate. The mare’s blood selenium
value (0.29 ppm) was considered slightly elevated. ICP analyses for liver copper, iron, manganese, magnesium, lead
and zinc were all within normal limits.
Enzyme Analysis - The foal’s blood glutathione peroxidase
(125.27 EU/gHb) value was considered adequate.
Bacteriology - Cultures of the lung, liver, spleen, small
and large intestine failed to grow pathogenic bacteria, including Salmonella.
Contributor’s Diagnosis and Comment: Severe, subacute degenerative polymyopathy.
The distribution, nature and extent of the muscle lesions
observed in this foal, concomitant with a marked increase in serum enzymes
associated with muscle damage (CK, AST) are consistent with changes described
for nutritional myopathy or white muscle disease in foals. Elevated CK values indicated active muscle
damage as this enzyme has a relatively short half-life (6 hours) and should
return to normal within 48 hours after muscle damage has stopped. Serum AST has a longer half-life than CK
and, thus, declines at a slower rate, but AST is less muscle-specific than CK.
In the equine and other species, white muscle disease is
most commonly associated with vitamin E and/or selenium deficiency. Vitamin E and selenium act synergistically
to prevent peroxidation of lipid membranes; vitamin E inactivates oxygen free
radicals while selenium is a component of the enzyme glutathione
peroxidase. Glutathione peroxidase
reduces organic hydroperoxides to alcohols which limits/prevents formation of
oxygen free radicals. In this foal,
however, values for liver vitamin E and selenium, and blood glutathione
peroxidase were considered adequate. In
addition, the mare of this foal had a slightly elevated, rather than reduced,
blood selenium value. Given these
circumstances it is likely that additional factors were involved in the pathogenesis
of the myopathy in this foal.
This
case was further complicated by marked leukocytosis, microscopic pulmonary
thrombosis, severe subacute ulcerative colitis, and colonic vein
thrombosis. Aspiration is likely a
cause of the clinical pneumonia, as there was severe myodegeneration in the
tongue. Failure to isolate pathogenic
bacteria from the colon and other organs is presumably related to the
aggressive use of antibiotics.
AFIP Diagnosis: Skeletal muscle and tongue: Myodegeneration and necrosis, multifocal
and coalescing, moderate, with mineralization and histiocytic myositis,
American quarter horse, equine.
Conference Comment: Electrolyte disturbances in foals with
rhabdomyolysis may be related to the electrolyte composition of skeletal muscle. The musculature comprises 55% of total body
mass and is a major reservoir for potassium and phosphorus. Disruption of the intracellular and
extracellular membrane boundary in cases of severe rhabdomyolysis results in an
efflux of potassium and phosphorus and an influx of water, sodium, chloride,
and calcium into the damaged muscle tissue.
The hyperkalemia, hyperphosphatemia, hyponatremia, and hypocalcemia
coincide with the onset of clinical signs and increased CK activity. The resultant hyperkalemia may be the most
life-threatening electrolyte abnormality in these foals. Treatment with mineralocorticoids, which act
on the distal tubules and collecting ducts to enhance reabsorption of sodium
and increase excretion of both potassium and hydrogen ions, may be used. Diuretics or cation exchange resins can also
be employed.
Myoglobinuria
can be differentiated from hemoglobinuria by the addition of saturated ammonium
sulfate, which will precipitate and remove the color caused by hemoglobin but
not myoglobin.
Many
other species are affected by vitamin E/selenium deficiency with varying
manifestations. Striated muscle
necrosis can be seen in most species.
Other manifestations include mulberry heart disease, hepatic necrosis
(hepatosis dietetica), and hemolytic anemia in pigs; steatitis (yellow fat
disease) in cats, horses, and pigs; an exudative diathesis with cerebellar
hemorrhage in poultry, and intestinal lipofuscinosis in dogs.
In
foals with similar muscle lesions, both vitamin E and selenium values may be
normal. In this case, other factors may
have contributed to the rhabdomyolysis.
Leukocytosis, pulmonary thrombosis, ulcerative colitis and colonic vein
thrombosis raise the possibility of sepsis.
Contributor: University of Minnesota, Department of Veterinary Diagnostic
Medicine, 1333 Gortner Avenue, St. Paul, MN 55108
References: 1. Dill SG, Rebhun WC: White muscle disease in foals. Compend Cont
Educ Pract Vet, 7:S627-S635, 1985
2. Gillian P, Valberg SJ, Madigan JM, Carlson
GP, Jones SL: Electrolyte disturbances in foals with severe rhabdomyolysis. J
Vet Intern Med 12:173-177, 2000
3. Hulland JJ: Muscles and tendons. In: Pathology of Domestic Animals, ed.
Jubb KVF, Kennedy PC, Palmer N, 4th ed., pp. 228-236. Academic Press, San
Diego, CA, 1993
4. Lee J, McAllister ES, Scholz RW: Assessment
of selenium status in mares and foals under practical management conditions. J
Equine Vet Sci 15:240-245, 1995
5. Littman MP, Dambach DM, Vaden SL, Giger U:
Familial protein-losing enteropathy and protein-losing nephropathy in soft
coated wheaten terriers: 222 cases (1983-1997). J Vet Intern Med 14:68-80, 2000
6. Moore RM, Kohn CW: Nutritional muscular
dystrophy in foals. Compend Cont Educ Pract Vet 13:476-490, 1991
Randall L.
Rietcheck, DVM
Major, Veterinary
Corps, U.S. Army
Wednesday
Slide Conference Coordinator
Department
of Veterinary Pathology
Armed Forces Institute of Pathology
Registry of
Veterinary Pathology*
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