Feline Infectious Peritonitis - Veterinary Pathology

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Feline Infectious Peritonitis : Proteins of Plasma and Ascitic Fluid 

M. Gouffaux, P. P. Pastoret, M. Henroteaux and A. Massip 

Vet Pathol 1975 12: 335 

DOI: 10.1177/0300985875012005-00601 

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Vet. Pathol. 12: 335-348 (1975) 

Feline Infectious Peritonitis 

Proteins of Plasma and Ascitic Fluid 

M. GOUFFAUX, P. P. PASTORET, M. HENROTEAUX and A. MASSIP 

Faculty of Veterinary Medicine, University of Liege, Brussels 

Absrrucr. Electrophoreses of sera, plasma and ascitic fluids of cats with natural or 

experimental infectious peritonitis show important modifications. Special stainings of 

electrophoreses and chromatographic and immunoelectrophoretic technics characterized 

some of the modified proteins. In the experimental disease, fibrinogen, haptoglobin, 

transferrin, and probably orosomucoid are increased; in the natural disease, in addition 

to these modifications, the y-globulins are strongly increased; the immunoglobulins found 

in the often abundant ascitic fluid belong to the IgG class. Increased proteins such as 

fibrinogen, haptoglobin and orosomucoid and decreased albumin are aspecific aspects of 

inflammatory processes, whereas hyperganimaglobulinemia appears in the course of 

immunological response. The rapid evolution of the experimental disease explains the fact 

that immunoglobulins do not increase. 

In a previous paper [ 151, we described the first experimental transmissions 

of feline infectious peritonitis from clinically affected animals. The clinical, 

hematological and anatomopathological aspects and the wide geographical 

spread of the natural disease were stressed ; since then, infectious peritonitis 

has been also reported in Australia [I 1,281, Switzerland [20] and Germany 

1211. 

In the present paper, some of the clinical and anatomopathological aspects 

of the experimental as well as the natural cases are described and compared 

with those previously reported. 

Materials and Methods 

The animals affected by natural disease (NOC) varied in age and sex. They were 

numbered from NOC 01 to 09. At the last stage of the disease, serum, plasma, pleural and 

ascitic fluids were collected. After death, samples were taken for histopathological exami- 



336 GOUFFAUX er al. 

Table I. Inoculations and results 

Cat Age Sex Origin of Nature and quantity Date of 

years inoculums of inoculum' inoculation 

Exp. 10 5 F Noc 05 liver suspension in 

5 ml PBS 

8/5/74 

Exp. 11 3 M exp. 09 organs suspension 

in 10 ml PBS 

8/5/74 

Exp. 12 8 F exp. 08 liver suspension 

in 10 ml PBS 

8/5/74 

Exp. 13 1 F Noc 04 liver suspension 

in 10 ml PBS 

8/5/74 

l PBS = phosphate-buffered saline. 

FIP = feline infectious peritonitis. 

Resul tsa 

dead of FIP 

on 29/5/14 

killed with 

FIP on 29/5/74 

recovered from 

the disease 

no sign of disease 

nations. Liver, spleen, ascitic fluid and urine samples were aseptically taken and stored at 

-20°C to obtain a stock of inoculation material. Soon after abdominal puncture, 5 ml of 

ascitic fluid from cats NOC 06 and 09 were stored in five heparinized (25 mg heparinlml) 

and five nonheparinized tubes, by pairs, respectively, at -20, 4, 20, 37, and 56°C for 16 h. 

All were then brought to 20°C, examined, and submitted to agarose gel electrophoresis. 

Four conventional cats (numbered exp. 10 to exp. 13) of various ages and sex and not 

previously treated were inoculated with infected organ suspensions in phosphate-buffered 

saline (PBS) (table I). Kanacilline@ was added to the virulent material in order to give 5 mg 

of kanamycin sulfate to each cat. Temperature was recorded each day, in the morning, from 

2 days before the inoculation to the end of the disease. Two days before and every day 

after inoculation, blood samples were collected through the ear vein from fasting, tran- 

quillized (Rompunm) cats for a blood count; simultaneously, blood was taken by cardiac 

puncture to obtain serum and plasma. Soon after death, the same samples were taken as 

in natural cases. 

Total proteins of sera, plasma, pleural and ascitic fluids were assayed by the biuret 

method; serum glutamic-oxalacetic and glutamic-pyruvic (SCOT, SGPT) were measured 

by the Sigma Chemical method [19]. 

Electrophoreses were performed on agarose plates in barbital buffer, pH 8.6, ionic 

strength 0.075, stained by amido-black for total proteins and by periodic acid-Schiff (PAS) 

for glycoproteins 1221. Fibrinogen was identified by comparison of serum and plasma 

electrophoreses. Haptoglobin was determined by hydrogen-peroxide and benzidine 191 

after human hemoglobin was added. To determine the saturation capacity of the hapto- 

globin in hemoglobin, serum or ascitic fluid electrophoreses were performed with increas- 

ing amounts of hemoglobin (from 1 to 20 mglml). 

Immunoelectrophoreses were carried out in agarose gel (Immunoagaroslide, Millipore) 

in barbital buffer, pH 8.6, ionic strength, 0. I. Goat serum against normal cat whole serum 

was supplied by Nordic Diagnostic (Tilburg, The Netherlands), and Dr. J.P. VAERMAN 

[23,24] provided the rabbit sera against cat IgG, and IgG2, IgA and IgM, as well as rabbit 

serum against dog transferrine. 



Feline Infectious Peritonitis 337 

Ten milliliters of ascitic fluid were clarified and then dialyzed against 2% NaCl (w/v) 

buffered with 0.02 M Tris-HCI buffer, pH 8.0, containing 0.1 YO NaN,, and then eluted with 

the same buffer on a column (Pharmacia, Uppsala, Sweden; K 26/100) of Sephadex (3-200 

under a 40-cm water pressure. The eluate was divided into five fractions that were con- 

centrated prior to electrophoretic and immunoelectrophoretic analysis in agarose gel. 

Twenty milliliters of ascitic fluid were dialyzed against 0.005 M Tris-HCI buffer, pH 8.0, 

and then layered over a column (Pharmacia; K 26/30) of diethylaminoethyl Sephadex A-50 

balanced by the same buffer. The proteins eluted in this step form a first fraction. Asecond 

fraction results from the elution by a 0.04 M Tris-HCI buffer, pH 8.0; and a third one from 

the elution by a 0.04 M Tris-HCI buffer, pH 8.0, containing 1 M NaCI. The three fractions 

were concentrated before electrophoretic and immunoelectrophoretic analysis in agarose 

gel. 

The eluates were concentrated through ultrafiltration Millipore cells, with Pellicon 

PSAC membranes, under a pressure of 4 kg/cm2. 

Antiserum against cat IgG was prepared by intradermic inoculations of the rabbit 

with the second fraction obtained by ion exchange chromatography, emulsified in the 

complete Freund’s adjuvant. The y-globulins thus obtained were purified by 40% ammo- 

nium sulfate precipitation, then absorbed on the first elution fraction on Sephadex G-200 

of the ascitic fluid. 

Results 

Experimental Disease 

Two of the four inoculated cats (exp. 10 and 11) had a typical experimen- 

tal disease (table I). The clinical evolution, hematological findings, body 

temperature, macroscopic and microscopic lesions corresponded to those 

previously described [6,12,14,25]. The duration of the experimental disease 

ranged from 2 to 3 weeks. The most important clinical findings were anorexia, 

weakness, and wasting; the first sign was a rise in body temperature on the 

second day; after a short remission, there was hyperthermia and, before 

death, strong hypothermia. The leukocyte count was usually elevated shortly 

after the onset of the fever. There was marked neutrophilia up to 90%. The 

red blood cell count showed no significant modification. Each infected cat 

had less than 100 ml of fluid in the peritoneal cavity and had diffuse fibrinous 

peritonitis. Discrete, white foci were obvious all over the liver and kidneys. 

Many foci of necrosis and neutrophilic infiltration of fibrinous exudate were 

found on the serosae, and within the parenchyma of the liver and kidneys. 

Germinative follicles of the spleen and abdominal lymph nodes were hyper- 

trophied by accumulation of cellular debris, histiocytes, and neutrophils [ 151. 

One cat (exp. 12) showed clinical, hematological and electrophoretic 

signs of an experimental disease until the 10th day, then everything returned 



338 GOUFFAUX er al. 

Origin 

Table It. Agarose gel electrophoreses; 

values for normal plasma and plasma and ascitic fluid 20 days after inoculation 

Plasma exp. 10 

before inoculation 

Plasma exp. I0 

20 days 

after inoculation 

Ascitic fluid exp. 10 

20 days 

after inoculation 

Units A1 buniin a, u, P? y Total 

protein 

45.00 

3.06 

29.23 

3.10 

35.19 

2.01 

~ 

8.50 10.00 13.50 8.00 1.50 100 

0.58 0.68 0.92 0.55 1.02 6.88 

12.31 18.46 13.85 18.46 7.69 100 

1.30 1.96 1.47 1.96 0.82 10.60 

9.26 20.37 11.11 7.41 16.67 100 

0.53 1.16 0.63 0.42 0.95 5.70 

to normal. Clinical and hematological recovery coincided with an increase 

of the serum y-globulins, but a decrease of hyperalpha-2 globulinemia 

occurred. One cat (exp. 13) showed no signs of the disease. 

Total protein values of plasma and sera of cats (exp. 10, 11) showed no 

modifications that could be significantly related to the disease since there are 

important variations of these values in sera of cats without disease [4,5, 141. 

The ascitic fluid contained fewer proteins than plasma and serum. The al- 

bumin/globulin ratio was decreased in relation to hypergammaglobul- 

inemia. 

Serum transaminases determinations showed no significant variations in 

the course of the experimental disease, except for a high increase of the 

SGOT at the last stage of the disease in one cat (exp. 10) [ 1,201. Electrophoreses 

of serum and plasma of animals with typical experimental disease showed 

important modifications in albumin and a- and P-globulins (table 11; fig. 1,2). 

Fibrinogen increased as early as the 8th day after inoculation (fig. 1). 

From the 4th day, a net and progressive increase of a narrow band of an 

a,-protein occurred (fig. 2). This protein has a slightly lighter molecular 

weight than the 7s immunoglobulins, as its presence in the 4th fraction of 

elution on Sephadex (3-200 suggests (fig. 3). Its glycoprotein nature appears 

after using PAS to analyze the electrophoreses of the same sera. We showed 

by electrophoresis of the serum after addition of hemoglobin that this a,- 

band corresponded to the haptoglobin. The increase of haptoglobulinemia 

was demonstrated by electrophoresis of serum sampled at different stages of 

the disease, after addition of hemoglobin in an amount slightly above that 

needed for the saturation of haptoglobin of the richest serum, taken before 



1 


2 3 4 5 6 

Fig. 1. Agarose gel electrophoresis. Cat exp. 10. Anode upwards. I = Plasma before 

inoculation; 2-6 = plasma from 4th to 20th day after inoculation. 

1 2 3 4 5 . 6 7 

Fig. 2. Agarose gel electrophoresis. Cat exp. 10. Anode upwards. 1 = Serum before 

inoculation; 2-6 = sera from 4th to 20th day after inoculation; 7 = ascitic fluid at the 

20th day. 



340 GOUFFAUX ei at. 

A F 1 2 3 4 5 

Fig. 3. Agarose gel electrophoresis. Eluted fractions one through five on Sephadex 

G-200 of ascitic fluid compared to whole ascitic fluid (AF). Anode upwards. 

death. The decrease of the free hemoglobin band and the progressive develop- 

ment of the haptoglobin-hemoglobin complex band proved the evolutive 

character of the increasing serum value in haptoglobin (fig. 4). At the last stage 

of the disease, the saturation capacity of the serum in hemoglobin amounts 

to 10 mg/ml, whereas the control serum is already saturated by 1.5 mg/ml. 

Electrophoreses of sera taken during the disease and stained by PAS or 

by amido-black (fig. 2) showed a steady increase of an a,-glycoprotein. 

A steady increase of a band with P,-mobility can be followed until the 

20th day in serum and plasma (fig. 1,2); it was also found in the fifth eluted 

fraction of the ascitic fluid on Sephadex G-200; its molecular weight is there- 

fore close to that of albumin. The rabbit serum against dog transferrine [23] 

showed in the serum of affected cats and in the fifth eluted fraction of the 

ascitic fluid on Sephadex G-200 a protein arc resulting from a cross-reaction 

between cat and dog transferrine. 

The y-globulins’ electrophoretic pattern showed no change in the course 

of the experimental disease (fig. 2). The proteins of the ascitic fluid were 

similar in quantity to those of the serum (table 11; fig. 2); the ascitic fluid did 




1 2 3 4 5 6 7 8 

Fig. 4. Agarose gel electrophoresis. Cat exp. 10. Anode upwards. 1 = Pure human 

hemoglobin (7.5 mglml); 2-7 = serum before inoculation and sera from 4th to 20th day 

added with 10 mg/mI of pure hemoglobin and stained for hemoglobin; 8 = serum at the 

20th day added with 10 mg/ml of pure hemoglobin and stained with amido-black. 

not contain increased fibrinogen. Comparison between immunoelectropho- 

resis of serum and plasma taken at the beginning and at the end of the dis- 

ease gave no further information. 

Natural Disease 

Clinical, hematological and anatomopathological aspects of the natural 

disease have been reported [12, 15, 17,25,29, 301. Its evolution ranges from 

a few weeks to several months. The main clinical findings are anorexia, 

weakness, often hyperthermia, and progressive abdominal distension. Other 

symptoms such as diarrhea and icterus exudative uveitis may be seen. Hema- 

tological examination shows a mild anemia and leukocytosis, with neutro- 

philia, lymphopenia and eosinopenia. The abdominal cavity is filled by an 

abundant and characteristic ascitic fluid containing fibrin tags; layers or 

small plaques of fibrinous material can be seen on the serosae, mainly at the 

surface of parenchyma. Pleural exudate is less frequently encountered. Prin- 

cipal microscopic lesions are fibrinous peritonitis. Fibrinous deposits are 

seen on the serosae of abdominal organs and contain many plasma cells, 

lymphocytes, histiocytes, neutrophils and cellular debris. Inflammatory reac- 

tion frequently involves underlying parenchyma of the liver and kidneys. 

Similar lesions may be seen on the thoracic serosae, meninges and in the 



342 GOUFFAUX ei al. 

Table III. Agarose gel electrophoreses; values for normal plasma and plasma and ascitic 

fluid taken from cat with a natural case, at end of evolution 

Origin Units Albumin a, a? p, p2 y Total 

protein 

~~ 

Plasma exp. 10 Yo 45.00 8.50 10.00 13.50 8.00 15.00 100 

before inoculation g/dl 3.06 0.58 0.68 0.92 0.55 1.02 6.88 

Plasma NOC 08 at YO 18.20 7.90 17.00 7.90 29.60 19.40 100 

end of evolution g/dl 1.47 0.64 1.38 0.64 2.40 1.57 8.10 

Ascitic fluid NOC 08 % 19.10 7.35 17.65 7.36 20.59 27.95 100 

at end of evolution g/dl 1.24 0.48 1.15 0.48 1.34 1.82 6.50 

ocular tissues. Germinative follicles of the spleen and mesenteric lymph nodes 

show an hyperplasia resulting from antigenic stimulation [ 151. 

In five of our nine cases, the total protein in the ascitic fluid, taken a little 

before death, was more than 6 g/dl. In four cases, we have also been able to 

measure it in the serum; it was always richer than the ascitic fluid. 

The electrophoreses performed with sera and ascitic fluids taken just 

before death show important modifications of the relative protein concentra- 

tions (table 111; fig. 5). The albumin/globulin ratio was notably decreased in 

relation to both albumin decrease and globulin increase (table Ill). 

Haptoglobin is found in large quantity, as in the experimental disease. 

The amount of y-globulin is largely increased. The immunoelectrophoreses 

done with antisera against cat IgA, IgG and IgM show that most of these 

immunoglobulins are of the IgG class [18, 231. There is no change in the 

IgM or IgA classes. It may be inferred from the electrophoreses of ascitic 

fluids that the amount of IgG can reach up to 2 g/dl. The IgG of ascitic fluid 

is purifiable by ion-exchange chromatography; the second fraction of the 

step-wise separation contains pure IgG (fig. 6). The antiserum obtained by 

inoculation of this fraction into the rabbit appears to be specific of the cat 

IgG, and IgG2, after absorption on the first fraction of elution of the ascitic 

fluid on Sephadex G-200, rich in IgM. 

The following were seen after examination of the ascitic fluid stored at 

different temperatures: fluids frozen at -20 "C were completely coagulated; 

those stored at 4°C contained a clot that filled up a quarter of the volume; 

those at 20°C contained a small clot; the two tubes at 37°C had only very 

small clots, whereas those raised to 56°C were made cloudy, without coag- 

ulation. At -20, 4 and 56"C, there was no difference between the fluids of 

the same pair. After fluids were stored at 20 and 37 "C, a small clot appeared 




Fig. 5. Agarose gel electrophoresis. Ascitic fluid (I), plasma (2) and serum (3) from a 

cat with a naturally occurring case, at the end of evolution. 

at the bottom of nonheparinized tubes but not in the heparinized ones. After 

clarification of the turbid fluids, further storage of all tubes at -20°C for 16 h 

showed, after the fluids were reheated at 20"C, that all were completely co- 

agulated except those that had stayed previously at 56°C. This stay at 56°C 

prevented further coagulation of the ascitic fluid. There was no difference 

between heparinized and nonheparinized tubes. After removing clots, elec- 

trophoresis showed no difference between the clotted fluids stored at -20,4, 

20 and 37°C; on the other hand, the fluids (heparinized or not) previously 

raised to 56 "C had their electrophoretic pattern deeply modified (fig. 7). 

Discussion 

Feline infectious peritonitis seems to be of viral origin; the agent is prob- 

ably a coronavirus not yet isolated [26,27,3 I]. Viral particles can be detected 



344 GOUFFAUX EI ai. 

2 

Fig. 6. Agarose gel electrophoresis. Fractions 1-3 of DEAE-cellulose chromatography 

of ascitic fluid taken from a cat with a naturally occurring case. Anode upwards. 

by electron microscopy in mesothelial cells. Local and general inflammatory 

reactions induce the clinical pattern of the disease and accompany the cellular 

lesions. The intensity of these reactions is remarkable, and as soon as 

they have reached a clinically perceptible stage they are usually irreversible. 

Experimental disease is characterized by rapid evolution and largely nonspecific 

clinical signs. Death ensues in about 15-20 days. The most significant 

lesions are necrosis of mesothelial cells and of subjacent parenchyma. The 

disease has a feature relevant to nonspecific and general reactions of inflammation: 

neutrophilia, hyperthermia and modifications of the plasmatic level 

of the so-called inflammatory proteins [2,7,8, 10, 13,271. We have been able 

to characterize fibrinogen and haptoglobin on the basis of their biochemical 

properties. The work of OKOSHI et al. [ 141, the electrophoretic mobility, and 

the glycoprotein nature of the increased a,-protein suggest that it can be 

orosomucoid. The electrophoretic mobility of P,-protein, its molecular 

weight, and the cross-reaction between this protein and dog transferrine 


vet.sagepub.com by guest on January 23, 2013 

3


1 2 3 4 5 

Fig. 7. Agarose gel electrophoresis. Ascitic fluid from a cat with a naturally occurring 

case after 16 h at -20°C (l), 4°C (2), 20°C (3), 37°C (4) and 56°C (5). 

indicate, in agreement with OKOSHI et al. [14], that it is a transferrine. The 

mechanism of the modifications in level of plasma proteins still remains unexplained. 

It is known that the hepatic synthesis is influenced by various 

factors; some of them have been extracted from neutrophilic leukocytes and 

hepatic cells [13]. The accumulation of necrotic material in the central part 

of germinative follicles in lymphoid tissue, towards the end of experimental 

disease [15, 271, can be interpreted as a sign of antigenic stimulation; however, 

the rapid evolution of experimental disease explains the unincreased 

content of immunoglobulins. 

In the natural disease, the evolution takes longer. Clinical signs are progressive 

wasting, ascites and sometimes thoracic, ocular or neurological 

manifestations. There is leukocytosis with neutrophilia, and a mild anemia. 

Serosae are overlayed with a fibrinous exudate infiltrated by numerous 

plasma cells, lymphocytes, and histiocytes relevant to a chronic inflammatory 

process. Histologic examination shows also antigenic stimulation in 

lymphoid tissue [ 151; this lesion and plasma cell accumulation on the serosae 

are proof of the outcome of an immunological process. As in the experimental 

disease, some of the so-called inflammatory proteins are modified : fibri- 



346 GOUFFAUX er a/. 

nogen, haptoglobin, orosomucoid and transferrine are strongly increased; 

whereas the concentration of albumin decreases, probably because of its des- 

truction in inflamed tissues and of disturbance in its hepatic synthesis [ 131. 

At the last stage of the disease, many immunoglobulins of the IgG class are 

found in the serum and ascitic fluid. The great amount of ascitic fluid and 

its very high immunoglobulin content suggest that it is a source of cat poly- 

clonal IgG. 

The immunological processes in this disease will have to be studied further 

when the antigen becomes available. 

Researchers have described the coagulability of the ascitic fluid when 

exposed to air. We ascertained that this coagulability occurs with plasma 

taken in natural as well in experimental cases on the 8th day of illness, 

whatever the anticoagulant used. The same observation applies to heparinized 

ascitic and pleural fluid. 

Our preliminary observations on the coagulation of sera, plasma and 

pleural and ascitic fluid indicate that it operates in two stages. The first is 

precocious and quantitatively not important and concerns the transforma- 

tion of fibrinogen into fibrin; the second, quantitatively much more impor- 

tant, is slower, independent of the action of usual anticoagulants, and in- 

fluenced by temperature; it depends on factors destroyed after a period of 

16 h at 56°C. 

The authors thank Dr. J. P. VAERMAN for advice and for supplying antisera. 

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Dr M. GOUFFAUX, Department of Pathology, Faculty of Veterinary Medicine, 45, rue des 

VCtCrinaires, B-1070 Briixelles (Belgium)

Feline Infectious Peritonitis - Veterinary Pathology

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