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"Campylobacter" organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR.
For the detection of "Staphylococcus aureus" food poisoning which can lead to staphylococcal enteritis a stool culture may be required. A stool culture is used to detect the presence of disease-causing bacteria (pathogenic) and help diagnose an infection of the digestive tract. In the case of staphylococcal enteritis, it is conducted to see if the stool is positive for a pathogenic bacterium.
The World Health Organization recommends the following:
- Food should be properly cooked and hot when served.
- Consume only pasteurized or boiled milk and milk products, never raw milk products.
- Make sure that ice is from safe water.
- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.
- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.
- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.
- Food handlers, professionals and at home, should observe hygienic rules during food preparation.
- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.
Diagnosis may be simple in cases where the patient's signs and symptoms are idiopathic to a specific cause. However this is generally not the case, considering that many pathogens which cause enteritis may exhibit the similar symptoms, especially early in the disease. In particular, "campylobacter, shigella, salmonella" and many other bacteria induce acute self-limited colitis, an inflammation of the lining of the colon which appears similar under the microscope.
A medical history, physical examination and tests such as blood counts, stool cultures, CT scans, MRIs, PCRs, colonoscopies and upper endoscopies may be used in order to perform a differential diagnosis. A biopsy may be required to obtain a sample for histopathology.
Treatment for colitis-X usually does not save the horse. The prognosis is average to poor, and mortality is 90% to 100%. However, treatments are available, and one famous horse that survived colitis-X was U.S. Triple Crown winner Seattle Slew, that survived colitis-X in 1978 and went on to race as a four-year-old.
Large amounts of intravenous fluids are needed to counter the severe dehydration, and electrolyte replacement is often necessary. Flunixin meglumine (Banamine) may help block the effects of toxemia. Mortality rate has been theorized to fall to 75% if treatment is prompt and aggressive, including administration of not only fluids and electrolytes, but also blood plasma, anti-inflammatory and analgesic drugs, and antibiotics. Preventing dehydration is extremely important. Nutrition is also important. Either parenteral or normal feeding can be used to support the stressed metabolism of the sick horse. Finally, the use of probiotics is considered beneficial in the restoration of the normal intestinal flora. The probiotics most often used for this purpose contain "Lactobacillus" and "Bifidobacterium".
Staphylococcal enteritis may be avoided by using proper hygiene and sanitation with food preparation. This includes thoroughly cooking all meats. If food is to be stored longer than two hours, keep hot foods hot (over 140 °F) and cold foods cold (40 °F or under). Ensure to refrigerate leftovers promptly and store cooked food in a wide, shallow container and refrigerate as soon as possible. Sanitation is very important. Keep kitchens and food-serving areas clean and sanitized. Finally, as most staphylococcal food poisoning are the result of food handling, hand washing is critical. Food handlers should use hand sanitizers with alcohol or thorough hand washing with soap and water.
Tips for hand washing:
1. Wash hands with warm, soapy water before and after handling raw foods.
2. Always wash your hands after using the bathroom, after changing a baby's diaper, after touching pets or other animals, and after sneezing or coughing
3. Properly dress or glove.
Mild cases usually do not require treatment and will go away after a few days in healthy people. In cases where symptoms persist or when it is more severe, specific treatments based on the initial cause may be required.
In cases where diarrhoea is present, replenishing fluids lost is recommended, and in cases with prolonged or severe diarrhoea which persists, intravenous rehydration therapy or antibiotics may be required. A simple oral rehydration therapy (ORS) can be made by dissolving one teaspoon of salt, eight teaspoons of sugar and the juice of an orange into one litre of clean water. Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis.
At necropsy, edema and hemorrhage in the wall of the large colon and cecum are pronounced, and the intestinal contents are fluid and often blood-stained. Macroscopic and microscopic findings include signs of disseminated intravascular coagulation, necrosis of colonic mucosa and presence of large numbers of bacteria in the devitalized parts of the intestine. Typically, the PCV is >65% even shortly after the onset of clinical signs. The leukogram ranges from normal to neutropenia with a degenerative left shift. Metabolic acidosis and electrolyte disorders are also present. There is leucopenia, initially characterized by neutropenia, which might evolve in neutrophilia. Moreover, haemoconcentration is noted with an increase in the packed cell volume; total proteins are initially increased, but changes into a lower than normal value. The most significant laboratory finding in colitis X is the increase of total cortisol concentration in blood plasma. Histopathologically, the mucosa of the large colon is hemorrhagic, necrotic and covered with fibrohemorrhagic exudate, while the submucosa, the muscular tunic and the local lymphonodes are edematous.
Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.
Among the causal agents of acute enterocolitis are:
- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;
- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;
- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;
- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).
Specific types of enterocolitis include:
- necrotizing enterocolitis (most common in premature infants)
- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")
All the factors collectively causing CNE are generally only present in the hinterlands of New Guinea and parts of Africa, Latin America, and Asia. These factors include protein deprivation (causing inadequate synthesis of trypsin protease (an enzyme), to which the toxin is very sensitive), poor food hygiene, episodic meat feasting, staple diets containing trypsin inhibitors (sweet potatoes), and infection by "Ascaris" parasites which secrete a trypsin inhibitor. In New Guinea (origin of the term "pigbel"), the disease is usually spread through contaminated meat (especially pork) and perhaps by peanuts. (CNE was also diagnosed in post World War II Germany, where it was known as "Darmbrand" or "fire bowels").
CNE is a necrotizing inflammation of the small bowel (especially the jejunum but also the ileum). Clinical results may vary from mild diarrhea to a life-threatening sequence of severe abdominal pain, vomiting, bloody stool, ulceration of the small intestine with leakage (perforation) into the peritoneal cavity and possible death within a single day due to peritonitis. Many patients exhibit meteorism. Treatment involves suppressing the toxin-producing organisms with antibiotics such as penicillin G or metronidazole. About half of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to the antibiotics. An investigational toxoid vaccine has been used successfully in some developing countries but is not available outside of research.
Under most situations, infection is hard to recognize because the symptoms are mild or even absent. In humans and wild animals, infection is not easily identified. Especially the adult flukes, even if in large number, generally do not cause complications. There is not yet a standard diagnostic test. Therefore, manual diagnosis is done at many levels. Diagnosis basically relies on a combination of postmortem analyses, clinical signs displayed by the animals, and response to drenching. In heavy infection, symptoms are easily observed in sheep and cattle as they become severely anorexic or inefficiently digest food, and become unthrifty. Copious fetid diarrhea is an obvious indication, as the soiling of hind legs and tails with fluid feces are readily noticeable. Even though it not always the case, immature flukes can be identified from the fluid excrement. On rare occasions, eggs can be identified from stools of suspected animals. In developing countries diagnosis and prognosis is often hindered by multiple infections with other trematodes, such as "Fasciola hepatica" and schistosomes, because these flukes are given primary importance due to their pervasive nature.
It is important to differentiate DPI from small intestinal obstruction, since obstruction may require surgical intervention, but this can at times be difficult. Horses suffering from DPI usually have a higher protein concentration in their peritoneal fluid compared to horses with small intestinal obstruction, often without a concurrent increase in nucleated cell count. They usually have some relief and decrease in pain after gastric decompression, while horses with an obstruction often still act colicky after nasogastric intubation. Distention of the small intestine may be less than what is felt on rectal examination of horses with obstruction, especially after gastric decompression. Horses with DPJ usually produce larger volumes of reflux (usually greater than 48 liters in the first 24 hours) than those with obstruction, and are often pyretic (temperatures of 101.5–102.5) and have alterations in white blood cell levels, while those with obstructions usually have a normal or lower than normal temperature and normal leukocyte levels.
Ultrasound can also be helpful to distinguish DPJ from obstruction. Horses with small intestinal obstruction will usually have an intestinal diameter of −10 cm with a wall thickness of 3–5mm. Horses with proximal enteritis usually have an intestinal diameter that is narrower, but wall thickness is often greater than 6mm, containing a hyperechoic or anechoic fluid, with normal, increased, or decreased peristalsis. However, obstructions that have been present for some time may present with thickened walls and distention of the intestine.
DPJ can only be definitively diagnosed during surgery or at necropsy, when its gross appearance of the small intestine may be evaluated.
Diagnosis is by a swab of the affected area for laboratory testing. A Gram stain is performed to show Gram-positive cocci in chains. Then, the organism is cultured on blood agar with an added bacitracin antibiotic disk to show beta-hemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Culture on agar not containing blood, and then performing the catalase test should show a negative reaction for all streptococci. "S. pyogenes" is CAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group-A-specific polysaccharide in the bacterium's cell wall using the Phadebact test.
The rapid pyrrolidonyl arylamidase (PYR) test is used for the presumptive identification of group A beta-hemolytic streptococci. GBS gives a negative finding on this test.
Proximal enteritis usually is managed medically. This includes nasogastric intubation every 1–2 hours to relieve gastric pressure secondary to reflux, which often produces to 2–10 L, as well as aggressive fluid support to maintain hydration and correct electrolyte imbalances. Maintaining hydration in these patients can be very challenging. In some cases, fluid support may actually increase reflux production, due to the decreased intravascular oncotic pressure from low total protein and albumin levels, leading to loss of much of these IV fluids into the intestinal lumen. These horses will often display dependent edema (edema that collects in locations based on gravity). Colloids such as plasma or Hetastarch may be needed to improve intravascular oncotic pressure, although they can be cost prohibitive for many owners. Reflux levels are monitored closely to help evaluate fluid losses, and horses recovering from DPJ show improved hydration with decreased reflux production and improved attitude.
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain relief, reduction of inflammation, and for their anti-endotoxin effects, but care must be taken since they may produce gastrointestinal ulceration and damage the kidneys. Due to a suspected link to "Clostridial" infection, anti-microbials are often administered, usually penicillin or metronidazole. Aminoglycosides should be used with extreme caution due to the risk of nephrotoxicosis (damage to the kidney). The mucosa of the intestines is damaged with DPJ, often resulting in absorption of endotoxin and risking laminitis, so therapy to combat and treat endotoxemia is often employed. This includes treatment with drugs that counteract endotoxin such as Polymyxin B and Bio-Sponge, fluid support, and laminitis prevention such as icing of the feet. Prokinetic drugs such as lidocaine, erythromycin, metoclopramide, and bethanechol are often used to treat the ileus associated with the disease.
Horses are withheld food until reflux returns to less than 1–2 L of production every 4 hours, and gut sounds return, often requiring 3–7 days of therapy. Parenteral nutrition is often provided to horses that are withheld feed for greater than 3–4 days. It is suspected to improve healing and shorten the duration of the illness, since horses often become cachexic due to the protein losing enteropathy associated with this disease.
Surgery may need to be performed to rule out colic with similar presenting signs such as obstruction or strangulation, and in cases that are long-standing (> 7 days) to perform a resection and anastomosis of the diseased bowel. However, some horses have recovered with long-term medical support (up to 20 days).
The use of a seven-way clostridial vaccination is the most common, cheapest, and efficacious preventative measure taken against blackleg. Burning the upper layer of soil to eradicate left-over spores is the best way to stop the spread of blackleg from diseased cattle. Diseased cattle should be isolated. Treatment is generally unrewarding due to the rapid progression of the disease, but penicillin is the drug of choice for treatment. Treatment is only effective in the early stages and as a control measure.
Dr. Oliver Morris (O.M.) Franklin made a significant contribution to the welfare of cattle and the livestock industry with his development of the blackleg vaccine. Franklin developed the original method of giving the vaccine while at Kansas State Agriculture College using live cattle. Franklin and another graduate veterinarian founded the original Kansas Blackleg Serum Co. in Wichita in 1916.
Yersiniosis is usually self-limiting and does not require treatment. For severe infections (sepsis, focal infection) especially if associated with immunosuppression, the recommended regimen includes doxycycline in combination with an aminoglycoside. Other antibiotics active against "Y. enterocolitica" include trimethoprim-sulfamethoxasole, fluoroquinolones, ceftriaxone, and chloramphenicol. "Y. enterocolitica" is usually resistant to penicillin G, ampicillin, and cephalotin due to beta-lactamase production.
Gastroscopy, or endoscopic evaluation of the stomach, is useful in chronic cases of colic suspected to be caused by gastric ulcers, gastric impactions, and gastric masses. A 3-meter scope is required to visualize the stomach of most horses, and the horse must be fasted prior to scoping.
When infection begins, the animal may develop a fever, and the affected limb can feel hot to the touch. The limb usually swells significantly, and the animal can develop lameness on the affected leg. Crepitation (the sensation of air under the skin) can be noticed in many infections, as the area seems to crackle under pressure.
Once clinical signs develop, the animal may only live a short while, sometimes as few as 12 hours. Occasionally, cattle succumb to the disease without showing any symptoms, and only a necropsy reveals the cause. During a necropsy, a diagnosis is usually made very quickly, as the affected muscle is usually mottled with black patches, which are dead tissue, killed by the toxins the bacteria release when they infect live tissue. If viewed under a microscope, small rod-like bacteria can be seen to confirm the diagnosis.
Radiographs (x-rays) are sometimes used to look for sand and enteroliths. Due to the size of the adult horse's abdomen, it requires a powerful machine that is not available to all practitioners. Additionally, the quality of these images is sometimes poor.
Reoviruses vaccines are advocated (in dams or in broilers) do not entirely solve the problem.
General hygiene and correct breeding conditions (especially correct brooding temperatures) may be efficient, but the disease often disappears as it had appeared, which makes it difficult to appreciate the effectiveness of control measures.
Early diagnosis is difficult as the disease often looks early on like a simple superficial skin infection. While a number of laboratory and imaging modalities can raise the suspicion for necrotizing fasciitis, the gold standard for diagnosis is a surgical exploration in the setting of high suspicion. When in doubt, a small "keyhole" incision can be made into the affected tissue, and if a finger easily separates the tissue along the fascial plane, the diagnosis is confirmed and an extensive debridement should be performed.
Computed tomography (CT scan) is able to detect approximately 80% of cases while MRI may pick up slightly more.
Amphistomiasis is considered a neglected tropical disease, with no prescription drug for treatment and control. Therefore, management of infestation is based mainly on control of the snail population, which transmit the infective larvae of the flukes. However, there are now drugs shown to be effective including resorantel, oxyclozanide, clorsulon, ivermectin, niclosamide, bithional and levamisole. An in vitro demonstration shows that plumbagin exhibits high efficacy on adult flukes. Since the juvenile flukes are the causative individuals of the disease, effective treatment means control of the immature fluke population. Prophylaxis is therefore based on disruption of the environment (such as proper drainage) where the carrier snails inhabit, or more drastic action of using molluscicides to eradicate the entire population. For treatment of the infection, drugs effective against the immature flukes are recommended for drenching. For this reason oxyclozanide is advocated as the drug of choice. It effectively kills the flukes within a few hours and it effective against the flukes resistant to other drugs. The commercially prescribed dosage is 5 mg/kg body weight or 18.7 mg/kg body weight in two divided dose within 72 hours. Niclosamide is also extensively used in mass drenching of sheep. Successfully treated sheep regain appetite within a week, diarrhoea stops in about three days, and physiological indicators (such as plasma protein and albumin levels) return to normal in a month.
The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score can be utilized to risk stratify people having signs of cellulitis to determine the likelihood of necrotizing fasciitis being present. It uses six serologic measures: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine and glucose. A score greater than or equal to 6 indicates that necrotizing fasciitis should be seriously considered. The scoring criteria are as follows:
- CRP (mg/L) ≥150: 4 points
- WBC count (×10/mm)
- <15: 0 points
- 15–25: 1 point
- >25: 2 points
- Hemoglobin (g/dL)
- >13.5: 0 points
- 11–13.5: 1 point
- <11: 2 points
- Sodium (mmol/L) <135: 2 points
- Creatinine (umol/L) >141: 2 points
- Glucose (mmol/L) >10: 1 point
As per the derivation study of the LRINEC score, a score of ≥6 is a reasonable cut-off to rule in necrotizing fasciitis, but a LRINEC <6 does not completely rule out the diagnosis. Diagnoses of severe cellulitis or abscess should also be considered due to similar presentations. 10% of patients with necrotizing fasciitis in the original study still had a LRINEC score <6. But a validation study showed that patients with a LRINEC score ≥6 have a higher rate of both mortality and amputation.