Severe acute intra-abdominal clostridial disease in two cats

Abstract

Case series summary

This case series describes two cats that developed intra-abdominal infections attributable to clostridial species. Case 1 describes a 3-year-old Oriental Shorthair that presented after acutely vomiting and rapidly declined, culminating in septic shock and death within hours of presentation. Imaging and post mortem revealed severe necrotising inflammation involving the right kidney and septic peritonitis. Histopathology revealed Gram-positive bacilli, consistent with a clostridial infection. Case 2, a 6-year-old Siamese, presented with acute lethargy, anorexia and abdominal pain. An enlarged, cavitated ileocaecal lymph node was identified on ultrasound. Cytology demonstrated abundant bacilli, and anaerobic culture and histopathology confirmed Clostridium septicum. The cat showed rapid clinical recovery after surgical excision of the affected lymph node and surrounding tissue.

Relevance and novel information

These cases highlight the potential for Clostridium species to cause fulminant intra-abdominal disease in previously healthy cats. Case 1 represents an unusual presentation of a septic abdomen due to Clostridium species and subsequent acute decline, while case 2 represents the first reported instance of spontaneous mesenteric lymphadenitis with abscessation due to C septicum in a previously healthy cat. Both cases demonstrate the severity of this bacterium in causing disease and the importance of early recognition. The findings highlight the aggressive nature of clostridial disease and the limitations of aerobic culture alone in diagnosis. This report expands the known host range and clinical manifestations of Clostridium species, supporting its inclusion in the differential diagnosis of necrotising intra-abdominal disease in cats, even in the absence of predisposing factors.

Introduction

Clostridium species are anaerobic, spore-forming bacilli that can act as opportunistic pathogens in both humans and animals. Although clostridial infections in animals are more commonly reported in dogs and large animals, such as horses and ruminants, feline cases remain under-reported in the literature. Previous reports have described mesenteric lymphadenitis and abscessation caused by other pathogens such as Escherichia coli and Listeria monocytogenes in cats;^1,2 however, the documentation of clostridial infections causing extensive intra-abdominal pathology remains limited.

Case series description

Case 1

A 3-year-old male castrated Oriental Shorthair with no prior medical concerns presented with acute vomiting, anorexia and abdominal pain with a duration of less than 3 h. The cat had undergone routine blood work 1 week prior for a prophylactic dental procedure that was unremarkable. On presentation, the patient was 8–10% dehydrated, mildly tachycardic (210 bpm), had a temperature of 39°C and marked abdominal pain. Initial biochemistry revealed mild alanine transaminase (ALT) elevation (136 U/l, reference interval [RI] 20–100), mild hyperglycaemia (12.7 mmol/l, RI 3.9–8.3) and a total protein of 80 g/l with packed cell volume of 40%. Haematology showed a mild leukopenia (white blood cells 2.52 × 10⁹/l, RI 3.5–20.7) with mild lymphopenia (0.34 × 10⁹/l, RI 0.83–9.1), while other parameters were within the normal RI. The cat was given methadone hydrochloride (0.3 mg/kg IM, Ilium; Troy Laboratories) and started on isotonic crystalloid intravenous (IV) fluid therapy (Compound Sodium Lactate Intravenous Infusion Hartmann’s Solution; Baxter) on presentation.

Abdominal ultrasound revealed reduced bilateral renal corticomedullary distinction, left-sided hydronephrosis (4.1 mm) with pelvic mineralisation and significantly enlarged ileocolic lymph node (12.7 mm). The small intestine was corrugated with non-obstructive fluid content; the caecum appeared dilated with mixed contents. Scant free peritoneal fluid was noted but abdominocentesis was not achievable.

Despite aggressive IV fluid resuscitation and active warming, the cat deteriorated rapidly, developing hypotension (systolic blood pressure 80 mmHg) and hypothermia (35°C). A repeat ultrasound showed increased peritoneal fluid. Abdominocentesis yielded a turbid sample, revealing bacilli-shaped bacteria, red blood cells and neutrophils on in-house cytology; total protein and urine specific gravity were not recorded. Urinalysis revealed bacilli-shaped bacteria; however, subsequent aerobic culture was negative for both fluid samples. The cat experienced cardiopulmonary arrest within 30 mins of repeat ultrasound. Resuscitation was unsuccessful.

An in-house post mortem revealed free peritoneal fluid and a small volume of retroperitoneal fluid surrounding the left kidney. The peritoneal fluid creatinine (394 µmol/l) and potassium (>12 mmol/l) values were markedly elevated when compared with blood values (creatinine 134 µmol/l, RI 88–195; potassium 3.6 mmol/l, RI 2.9–4.2) before the cat’s death, which supported the finding of a uroabdomen. There was no evidence of gastrointestinal perforation, and the right caecal lymph node was darkly discoloured and enlarged. Full thickness biopsies of the gastrointestinal tract, including en bloc samples of the duodenum, pancreas, ileocaecal junction, caecal lymph node, and left ureter and kidney were submitted for histopathology (Figure 1). The kidney demonstrated severe acute segmental necrotising pyelitis, focal mineralisation and minor medullary nephritis, and fibrosing pyelonephritis with tubular atrophy and loss (Figure 1a). The caecal lymph node showed necrotising and haemorrhagic lymphadenitis and fibrinous peritonitis (Figure 1b). The caecal mucosa was unremarkable as was the rest of the gastrointestinal tract. The surrounding mesentery demonstrated fibrinous peritonitis and steatitis extending into the outer layer of the tunica muscularis (Figure 1c). The kidney, caecal lymph node and mesentery all had myriad intralesional Gram-positive spore-forming bacilli.

Figure 1

Photomicrographs of histological sections of (a) renal pelvis at × 20, with the inset demonstrating bacilli within the section using haematoxylin and eosin (H&E) stain, (b) Gram-stained caecal lymph node viewed at × 40 demonstrating Gram-positive appearance of bacilli and (c) caecum with mesentery in H&E stain viewed at × 20, with inset depicting bacilli. All three figures demonstrate myriad intralesional bacilli with necrotic debris

The morphology and number of bacteria, combined with the intensely necrotising nature of the tissue reaction, were strongly suspicious of Clostridium species, with toxaemia being the cause of death. Because of the severity of the pyelitis and the concentration of bacteria visualised in this area, it was hypothesised that this was the source of peritonitis, likely predisposed by the reported nephrolithiasis. It was thought that the infection had spread from the renal pelvis via the retroperitoneal tissue with restricted spread in the peritoneal cavity and mesentery. Aerobic culture of the abdominal fluid and blood showed no growth; anaerobic culture was not performed.

Case 2

A 6-year-old female spayed Siamese cat presented after a 3-day history of anorexia and lethargy. The cat was quiet but responsive, 5% dehydrated, with severe pain on abdominal palpation. She had an inflammatory leukogram with neutrophilia, elevated ALT (146 U/l, RI 12–130), hyperglobulinaemia (54 g/l, RI 28–51), total bilirubin of 17 μmol/l (RI 0–15) and markedly increased creatine kinase (3002 U/l, RI 0–314). The cat tested negative for feline leukaemia virus/feline immunodeficiency virus (WITNESS FeLV-FIV Test kit; Zoetis).

Abdominal ultrasound revealed hyperechoic mesentery surrounding a mesenteric lymph node near the ileocaecal junction. The lymph node was heterogenous with anechoic areas and measured 14.4 mm (Figure 2). A small volume of free fluid was observed surrounding this area. Fine-needle aspiration of the lymph node, spleen and liver was performed to investigate for infiltrative disease, which revealed degenerate neutrophils and abundant extracellular bacilli (Figure 3). Cytology of the liver demonstrated neutrophilic inflammation, while the spleen was unremarkable.

Figure 2

Ultrasonographic image of the mesenteric lymph node near the ileocecal junction depicting the hypoechoic centre measuring 14.4 mm, with hyperechoic mesentery surrounding

Figure 3

Photomicrograph of aspirated material from the lymph node demonstrating abundance of highly degenerate neutrophils, accompanied by high numbers of extracellular bacterial bacilli. Modified Wright’s stain, × 500 magnification

The patient was commenced on amoxicillin-clavulanate acid (30 mg/kg IV q8h, Amoxyclav Juno 500/100; Juno), metronidazole (10 mg/kg IV q12h; Baxter), maropitant (1 mg/kg IV q24h, Prevomax; Dechra) and fentanyl (Fentanyl GH; Ceva). An oesophagostomy tube (18 Fr × 75 cm; MILA) was placed to support nutrition. The patient was hospitalised for 3 days, where repeat biochemistry and haematology returned to normal range, patient demeanour and pain score improved, and discharge was elected with medication of amoxicillin-clavulanate (20 mg/kg PO q12h, Clavulox; Zoetis), metronidazole (10 mg/kg PO q12h, Flagyl; Sanofi-aventis), mirtazapine (2 mg PO q24h; BOVA Compounding), gabapentin (50 mg PO q12h; BOVA Compounding) and sublingual buprenorphine (0.015 mg/kg q8h, Vetergesic; Ceva). Two days later, the patient was only eating small amounts voluntarily, had moderate abdominal pain and no improvement was observed via ultrasonography of the mesenteric lymph node. As a result, exploratory laparotomy was elected.

Surgical findings included a necrotic, abscessed caecal lymph node with extensive adjacent mesenteric fat necrosis. The rest of the abdomen appeared grossly normal, and surgical excision of the abscessed lymph node and surrounding adipose tissue was performed. Histopathology revealed pyogranulomatous lymphadenitis and mesenteric cellulitis with fibrosis, consistent with chronic inflammation. Culture of abscessed fluid confirmed the presence of Clostridium septicum despite previously being on antibiotics. The cat recovered well postoperatively, resumed voluntary feeding within 24 h and completed a 2-week course of oral amoxicillin-clavulanate with full resolution of clinical signs. On follow-up examination 1 month postoperatively, the cat was doing well, maintaining weight and back to normal activity.

Discussion

These two cases demonstrate the unique and significant abdominal pathology that can result from clostridial infections in cats, which, to the authors’ knowledge, has not been reported in the veterinary literature. Both cases involved previously healthy domestic cats that developed rapidly progressive intra-abdominal infections. Although clostridial myonecrosis and gangrene have been reported in other species, ³ these cases highlight the organism’s capacity to cause severe necrotising and septic disease in the absence of immunosuppression or overt trauma.

The first case deteriorated acutely within hours of admission. Despite aggressive supportive care, the cat succumbed to suspected clostridial toxaemia. Post-mortem histopathology revealed myriad Gram-positive, spore-forming bacilli. Although aerobic culture was negative and anaerobic culture was not performed (preventing definitive microbial identification), the morphology of the organisms, rapid clinical decline and pattern of necrosis are all characteristic of Clostridium species infection.^3,4

At the time of clinical examination, the bacilli on urinalysis were not directly correlated to the cat’s rapid deterioration and septic shock, as pyelitis is a rare cause of secondary septic peritonitis. Clostridium species urinary tract infections are rarely reported, and to the authors’ knowledge, have not been reported to cause septic peritonitis in cats.^5,6 A human case report detailing bacteraemia of urinary origin linked to Clostridium perfringens infection associated with a ureteral stone and hydronephrosis has been described. ⁷ In humans, anaerobes are isolated in only 1% of urine samples, with Gram-positive bacilli considered rare and usually not resulting in clinical disease. ⁷ The prevalence rate has not been investigated in cats but is likely to be low. It is hypothesised that the origin of this infection was due to the enteric bacterium ascending the urinary tract, with the nephrolithiasis acting as a nidus of infection.

The second case, a 6-year-old Siamese cat, presented with acute abdominal pain. Cytology of the mesenteric lymph node revealed abundant necrotic inflammation with extracellular bacilli, and subsequent culture confirmed the presence of C septicum. This case is notable for the lack of predisposing comorbidities, unlike most documented cases in humans, which are often associated with gastrointestinal malignancy or immunosuppression. ⁸ This supports previous findings that C septicum can cause spontaneous severe infections in otherwise healthy hosts; however, disease usually results in myonecrosis and not lymphatic abscesses.^9,10 These cases often require immediate surgical intervention. ¹¹ Case 2 had no underlying cause, trauma or evidence of myonecrosis, with localisation of the bacterium within the caecal lymph node without evidence of an inciting cause, which has not previously been reported.

Comparing case 2 with other published feline intra-abdominal lymphadenopathies, such as Sakai et al, ¹ which described suppurative mesenteric lymphadenitis due to E coli, a distinct difference in clinical trajectory is apparent. In their case, the cat underwent prolonged medical management, including extended antimicrobial therapy before eventual resolution. In contrast, our patient with C septicum infection showed only mild clinical improvement with amoxicillin-clavulanate and metronidazole. This is likely attributable to the bacterium’s potent exotoxins, such as alpha toxin, that induce rapid tissue breakdown and create anaerobic microenvironments. These environments are favourable for continued bacterial proliferation and tissue destruction, which may render conservative antimicrobial treatment ineffective. Antimicrobial sensitivities are not routinely reported for anaerobes; however, clindamycin, metronidazole and penicillins are usually effective.^{12 –14} Definitive resolution was only achieved in our case after surgical excision of the necrotic lymph node and debridement of the surrounding devitalised tissue. Continued medical management may not have resulted in a successful outcome, especially as the lesion was culture positive after appropriate antimicrobial therapy. This case demonstrates the role surgical intervention may have in managing future intra-abdominal clostridial infections.

Conclusions

These cases both describe an unusual presentation of clostridial disease that has not previously been reported and highlight the rapid clinical deterioration that can occur. Clinicians should maintain a high index of suspicion for anaerobic infections in cats presenting with acute abdominal pain, particularly when imaging and cytology suggest necrosis and bacilli presence. Early culture under anaerobic conditions, surgical exploration and targeted antimicrobial therapy may be critical for successful outcomes.