Acute bloody diarrhoea with fever: Etiology

This is the picture of a bacillary dysentery. Pathogens are Shigella, Salmonella, Campylobacter and some Escherichia coli. Some bacteria are very aggressive, while others give rise to milder infections, for example Shigella dysenteriae , S. flexneri, S. boydii , S. sonnei. Complications can occur: toxic megacolon, recta, prolapse, septicaemia, haemolytic-uraemic syndrome (TTP-HUS, often triggered by Shiga toxin produced by Escherichia coli O157:H7 or other verotoxin producing bacteria (VTEC), reactive arthritis, Reiter’s syndrome [urethritis, arthritis, conjunctivitis, uveitis, hyperkeratosis of the palms of the hand (keratoderma blennorrhagicum) and painless ulcers in the mouth and on the glans (balanitis circinata)]. If HUS occurs, antibiotics are contraindicated because otherwise still more toxins are released from the bacteria that have been killed, which aggravate the clinical status. After using antibiotics an overgrowth of Clostridium difficile can occur in the intestine. The toxins that are produced by this bacterium can cause a severe inflammation of the colon (pseudomembranous colitis).

A very serious complication after Campylobacter enteritis is the Guillain-Barré syndrome, which is characterised by ascending paralysis caused by a demyelinating process of the spinal roots. Similarly there is Fischer's syndrome in which the cranial nerves are affected. The protein content of the cerebrospinal fluid is very high, but the fluid contains few cells. There are usually prodromata of headache, nausea, back pain and pain in the limbs. It can start very quickly with a progressively reducing strength in the legs and later in the arms. If the paralysis ascends to C3 (level of the phrenic nerve), paralysis of the diaphragm ensues. The seventh cranial nerve can also be affected. There are also sensory symptoms, but these are not prominent. Initially, treatment in an intensive care unit is necessary. The vital respiratory capacity must be monitored. Plasmapheresis and IV immunoglobulins (400 mg/kg/day x 5 days) are required. Steroids are no longer recommended. Most people make a full recovery, but this can take several months. In 10-20% of cases there are permanent neurological sequelae.

Guillain-Barré syndrome is due to an immunological process of molecular mimicry that is not fully understood. There is a connection with anti-GM₁ IgG antibodies following Campylobacter jejuni enteritis. Infection by C. jejuni carrying GM₁-like LPS induces a high production of anti-GM₁ IgG antibodies. The autoantibodies bind GM₁ that is present on the nodal axolemma of the motor nerve and block electrophysiological conduction. After this, macrophages, guided by the anti-GM₁ IgG, enter the periaxonal space and degeneration of the motor axon follows.

In case of bacillary dysentery, examination of the faeces under the microscope shows numerous white blood cells (pus) and red blood cells. Bacillary dysentery is associated with a marked disappearance of the normal bacterial intestinal flora. It is not possible to distinguish between the different bacteria by microscopy alone (culture is needed for this). As always, fluid and electrolytes form the basis for treatment. With bacillary dysentery, antibiotics are an important part of therapy. The resistance of the various bacteria varies. Multi-resistant bacteria are becoming more common. Depending on the local conditions, cotrimoxazole, ampicillin or a quinolone (such as ofloxacin [Tarivid®]) should be used. The use of diarrhoea-inhibitors (loperamide) is not recommended.

Category: Medical Subject Notes , Medicine Notes