Rare cause of acute abdomen: group A streptococcus peritonitis

Summary

This report describes a previously healthy woman who presented with sepsis. Initial evaluation suggested an intra-abdominal or genitourinary source. An exploratory laparotomy was performed, revealing significant purulence in the lower right quadrant and pelvis without an obvious source of infection. Peripheral and peritoneal cultures revealed group A streptococcus (GAS), a rare cause of primary peritonitis. The patient had no acute history of upper respiratory infections. The pathogenesis and portal of entry for GAS peritonitis remain unclear, but recent research has identified oral sex practices as a conduit for infection. Prompt recognition and treatment are paramount to avoid mortality. This case report adds to the growing body of knowledge on unusual, life-threatening causes of acute abdominal pain.

Background

Over the last few decades, the incidence and severity of group A streptococcus (GAS) infections have increased, most likely due to the emergence of more virulent strains.¹ Primary GAS peritonitis is a rare but life-threatening infection that has been reported primarily in young, otherwise healthy individuals.

GAS infections are typically characterised by pharyngitis, integumentary infections and immune-mediated sequelae.² Systemic complications of GAS infection are most commonly seen in children up to the age of 5 years and in adults over the age of 60 years. The common risk factors include skin lesions or traumatic wounds.³ However, GAS peritonitis occurs in only 2% of invasive GAS infections.⁴ It has an unknown aetiology but can rapidly progress to shock and severe multiorgan dysfunction without appropriate treatment.¹ Given the typical location of GAS colonisation, the occasional isolation of GAS in vaginal cultures, and the higher proportion of GAS peritonitis cases in women compared with men, sexual transmission has been proposed as a route of infection. There are only two other reported cases of sexually transmitted GAS that used bacterial isolate typing to support this method of inoculation.⁵

Reported cases of GAS peritonitis are unique in that several occur in asymptomatic patients.^6–11 Progression to GAS peritonitis does not have established risk factors or aetiology, which makes diagnosis difficult. Recent research has associated GAS peritonitis with vaginal deliveries, gynaecological interventions and the insertion of contraceptive devices.⁵ This added evidence can inform appropriate history-taking and support timely diagnosis. Previous cases, as well as this one, demonstrate successful treatment of infection with antibiotics.

The symptoms of primary peritonitis mimic several other common gastrointestinal and genitourinary afflictions. A few reported cases describe a common presentation of acute-onset abdominal pain, fever, nausea and vomiting. Surgical intervention may be difficult to avoid, but a strong index of suspicion for GAS peritonitis when other obvious sources of infection have not been confirmed can potentially expedite non-invasive antibiotic therapy and replace unnecessary exploratory surgery.² Although GAS peritonitis is a rare manifestation of GAS sepsis, the increasing global incidence and severity of such infections suggest that such presentations may become more common, and vigilance in diagnosis will be necessary to avoid mortality.¹

Case presentation

A previously healthy female in her 30s, presented to the emergency department with a 1-day history of sudden-onset severe abdominal pain with nausea, vomiting and non-bloody diarrhoea.

On presentation, the patient had a temperature of 37.2°C, a blood pressure of 89/58 mm Hg, a heart rate of 112 beats per minute and a respiratory rate of 16 bpm. On physical examination, the patient had diffuse lower abdominal pain and tenderness with severe rebound tenderness in the right lower quadrant.

Basic blood work was conducted (see table 1) revealing an elevated white cell count, lactic acid and procalcitonin. Urinalysis was notable for elevated white cell count and red cell count, with moderate leucocytes. Initial bedside ultrasound revealed questionable fat stranding around the right kidney compared with the left kidney, but no evidence of hydronephrosis. Transvaginal ultrasound and Doppler studies showed mild uterine inflammation consistent with the menstrual cycle and a normal uterus, fallopian tubes and ovaries. CT with intravenous contrast revealed fluid collection in the pelvis with an indistinct uterine border. The appendix cannot be visualised. These findings led to the presumptive diagnosis of pelvic inflammatory disease (PID) and sepsis.

Table 1.

Laboratory evaluation

Blood, plasma and serum chemistry	Results
White cell count (4.0–10×109/L)	19.95
Haemoglobin (120–160 g/L)	93
Haematocrit (female 36–47%)	28.7
Platelets (150–350×109/L)	157
International normalised ratio (0.9–1.2)	1.3
Fibrinogen (150–350 mg/dL)	177
Creatinine (0.7–1.3 mg/dL)	1.12
Blood urea nitrogen (8–20 mg/dL)	16
Alanine aminotransferase (<35 U/L)	7
Aspartate aminotransferase (<35 U/L)	18
Total bilirubin (0.3–1.2 mg/dL)	0.3
Sodium (136–145 mmol/L)	138
Potassium (3.5–5.0 mmol/L)	3.8
Phosphorus (3–4.5 mg/dL)	2.9
Magnesium (1.5–2.5 mg/dL)	1.8
Total calcium (9–10.5 mg/dL)	8.9
Glucose (70–100 mg/dL)	101
Lactic acid (0.67–1.8 mmol/L)	2.3
Procalcitonin (<0.25 ng/mL)	1.51
Peripheral blood culture (GAS)	GAS+
Urinalysis
Total beta human chorionic gonadotropin	Negative
Leucocytes	Moderate
White blood cell (0–5/HPF)	64
Red blood cell (0–3/HPF)	24
Leucocyte esterase	Negative
Nitrites	Negative
Urine culture	Negative

HPF, high power field.

Vancomycin and piperacillin-tazobactam were administered. The patient was also administered intravenous fluids. This initially improved her condition enough to allow for further evaluation and transfer to the intensive care unit (ICU). Laparoscopy was scheduled to evaluate gastrointestinal versus gynaecological complications. In the ICU, she again became haemodynamically unstable and, on repeat examination, was found to have severe pain on palpation of all four abdominal quadrants and a diffusely rigid abdomen. She was immediately taken to the operating room, where she underwent an exploratory laparotomy. This revealed a small amount of blood in the pelvis and a large amount of thick, yellow purulence and sticky mucoid plaques adherent to the bowel, bilateral fallopian tubes and falciform ligaments. No evidence of bowel abnormalities or inflammatory changes was found in the appendix. No obvious sources of infection were observed. Cultures were collected, and the abdomen was suctioned.

The previously obtained blood cultures, vaginal swabs and peritoneal fluid analysis revealed GAS colonisation. Specific typing of GAS isolates from the samples was not completed.

Differential diagnosis

The clinical presentation of acute-onset lower abdominal pain, nausea, vomiting and fever with leucocytosis was associated with perforated appendicitis. The appendix could not be visualised well on a CT scan. Direct visualisation in the operating room during the diagnostic laparotomy revealed a normal appendix without signs of inflammation or perforation.

Given the patient’s age and symptoms, gynaecological pathologies were also considered. The patient admitted that her husband had several partners before her but was unsure about the risk of contracting sexually transmitted infections. She had a remote history of several episodes of uncomplicated cystitis, which all resolved with antibiotics. She reported no recent episodes. The pregnancy test results were negative. Pelvic examination revealed no cervical motion tenderness but moderate right-sided adnexal tenderness. The patient had two prior caesarean sections with a well-healed scar and no complications after delivery.

Treatment

Following the culture results, the patient was placed on a continuous penicillin infusion while hospitalised. Her condition improved, and she was transferred to the ICU. She was discharged on hospital day 4 with amoxicillin (1 g three times a day orally) to complete a total course of 14 days.

Outcome and follow-up

Postoperatively, she reported no worsening of her acute abdomen, nausea or vomiting. The patient’s appetite and diarrhoea improved. Alternative sources of infection were not identified. The patient was discharged on postoperative day 4. At her follow-up visit with her primary care physician, 2 weeks after discharge, the patient reported resolution of symptoms and no additional concerns.

Discussion

GAS infections are typically characterised by upper respiratory and cutaneous infections. It is a rare cause of primary peritonitis.¹² GAS is not part of the normal bowel flora but can occasionally colonise the female genital tract. A majority of reported systemic GAS infections are associated with gynaecological procedures such as intrauterine device (IUD) insertion and caesarean delivery. This patient did not have an IUD but was making use of a menstrual cup. Menstrual cups are reusable alternatives to tampons or sanitary napkins. They have gained popularity and are associated with minimal risks if used appropriately. Few cases have reported complications, including improper placement leading to hydronephrosis, external urogenital abrasions and recurrent urinary tract infections.⁷ Menstrual cups are typically made of silicone, which does not promote bacterial growth; however, the collection of blood within the cup may serve as a growth medium, facilitating the proliferation of skin and urogenital flora.¹³ If the menstrual cup was the primary source of infection, this would be the first reported case.

Another proposed mechanism of infection is orogenital transmission.¹⁴ Oral sex is a well-known path of transmission for various infections, but only a few cases have associated oral sex as a potential contributor to GAS peritonitis. Prior cases have confirmed this route of transmission by comparing the strain of GAS in patient peritoneal fluid and blood cultures with their partner’s throat cultures. Without this data, it is impossible to confirm this proposition in this particular case. However, the narrative of a spontaneous systemic infection in a patient with a partner who has chronic streptococcal infections adds to the growing body of literature that systemic GAS may be transmitted orogenitally. As there remains no specific recommendation for prevention or prophylaxis, this case aids in informing providers to consider this mode of transmission during patient counselling.¹⁵

Prior cases have been reported with IUD; however, the use of a menstrual cup in this patient suggests that temporary insertion of devices can also contribute to an ascending infection. There are cases of GAS ascending infection leading to toxic shock-like syndrome, requiring surgical debridement of necrotic tissues and extended hospital stays with other systemic complications such as disseminated intravascular coagulation, drain placement and acute respiratory distress syndrome. Although these complications are rare, they indicate the potential for mortality in such infections.¹⁴

Other possibilities include direct transluminal spread from the colon and haematogenous spread from a distant site, such as the upper respiratory tract.¹⁶ The greatest challenge with GAS peritonitis is diagnosis. The majority of cases of peritonitis stem from a secondary source, such as complicated appendicitis, PID, ruptured ovaries or bowel perforation. The established and effective treatment for these conditions is surgical exploration with source control or removal/repair of the primary anatomical source. Even without obvious evidence of a source of infection, exploratory laparoscopy can lead to the diagnosis and treatment of the majority of complicated acute abdominal cases. It is not clear whether surgical exploration actively harms patients with GAS peritonitis, as it does in patients with peritonitis due to significant liver or kidney disease. However, unnecessary surgery always poses a risk to the patient and should be avoided when possible.²

With a high index of suspicion, a rapid antigen detection test can be conducted, particularly in young female patients without an identifiable source of sepsis.⁶ Consideration of GAS peritonitis in an otherwise healthy demographic will expedite the diagnosis and antibiotic treatment. Further research is required to identify the risk factors and mechanisms of infection in GAS peritonitis, but this case adds to the growing differential and describes key features of the clinical presentation of a rare and treatable cause of acute abdomen.

Patient perspective.

I woke up feeling pretty normal. Around 9:00 AM I began having some lower right abdominal pain. The pain worsened over the next hour so I took Ibuprofen thinking they were weird period cramps even though I was on day five of my period so cramping would have been unusual. The pain continued to worsen so I went to lay down in bed but couldn't find a position that would provide any relief. I began to moan because the pain was intensifying and I became very, very cold. I was nauseas but could barely walk to the bathroom because I was doubled over from the pain and weak. I vomited but there was no relief from the pain. My partner called my doctor who said to go to the emergency room. I had a hard time being convinced that was necessary, which is ridiculous given the severity of the pain. My partner then called my mother who is public health nurse. My mother said that severe abdominal pain with no diarrhea is concerning. We decided to go to the emergency room. My partner dropped me off at the door to the ER and went to park the car. I wheeled in a wheelchair to wait in line. I vomited repeatedly and couldn't stop moaning from the pain. Eventually I made it through intake and was asked to give urine sample which was excruciating. I waited in the waiting room briefly, still in severe pain but was seen by ER doctors relatively quickly. The ER doctors were kind and wonderful but my pain was awful. I was also terribly thirsty, really being driven crazy by how thirsty I was but couldn't drink any water because of potential surgery. As I went through ultrasounds, a pelvic exam, CAT scan and several blood draws my pain increased as did my maddening thirst. Eventually I was brought to surgery but I only remember being wheeled in and talking to the doctor. The next thing I remember was waking up in recovery, asking for water and then nearly vomiting again. My recovery nurse wasn't very kind. I think doctors came to speak with me but I don't really remember. I was moved to the ICU where I felt terrible but I wasn't in the same kinds of pain as before the surgery. I received excellent care in the ICU but recovery was very hard. I remember everyone being worried about how long my blood pressure remained and feeling miserable. One doctor informed me that if my blood pressure didn't increase l would have to undergo another surgery to try to understand what was happening. I think after I was switched to penicillin things started to get better. I was told as I child I was allergic to penicillin but it turned out to be fine. I still felt miserable and really struggled to drink any fluid or eat crackers without throwing up. I also started to have diarrhea which was very unpleasant since I had to be assisted to the toilet and could barely clean myself. I must have gotten better because eventually they moved me to the regular hospital where l was still uncomfortable and unable to eat without being extremely nauseas but was no longer close to death. Eventually I was approved to leave the hospital and when I was leaving they weighed me and found l was thirty pounds heavier than when I was admitted because of all of the fluids that had been pumped into my body. I looked like I just had a baby. But instead I had an infection. Upon returning home I had a lot of anxiety about the infection coming back. could barely walk and was extremely sore. Over the next few weeks I struggled with diarrhea and abdominal pain but nothing so bad that I went into the ER. In the following weeks and month I had frequent and terrible UTI symptoms. I would go to the doctor to get tested and the in-office test would come back as positive but the lab test would be negative. I continue to struggle with more frequent UTI symptoms than before my illness. I received amazing lifesaving care and I will be forever grateful to the team of doctors who worked to diagnose and treat my illness.

LEARNING POINTS.

• Group A streptococcus (GAS) infection is typically characterised by upper respiratory and cutaneous infections. It is a rare cause of primary peritonitis and may be sexually transmitted.

• GAS peritonitis is a rare cause of acute abdomen that should be suspected in otherwise healthy young women presenting with sudden-onset abdominal pain without another obvious source of infection. Sexual history and partner history may aid in diagnosis.

• GAS is not part of the normal bowel flora but can occasionally colonise the female genital tract. With a high index of suspicion, a rapid antigen detection test can be conducted, particularly in young female patients.

• The diagnosis of primary GAS peritonitis is challenging and may require surgical exploration in haemodynamically unstable patients to evaluate for other causes of sepsis.

• This condition is life-threatening, but if assessed early, it can be adequately treated with antibiotics.

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