Could be they were already on the upswing when you dosed them with Sulmet, but I'm glad that worked for you. There seems to be some disagreement in the literature, but I did see that they often use something like ethopabate along with Amprolium in feeds to "round out" the protection. Seems that some coccidia are becoming resistant to Amprolium now, so that may be what you encountered, depending on the type that is in your soil. Whatever type is in mine was resistant to Sulmet. Whatever works, that is what you should use, no matter what the literature says, because cocci can kill quickly if not treated.
Eimeria necatrix & Eimeria tenella are two types of cocci that are the most pathogenic and cause the most extensive hemorrhage of the small intestine. Found this article:
Along with controlling the environment we raise our fowl in, the administration of antibacterial or antiprotozoal drugs may need to be administered. The ideal compound along with proper administration inhibits and acts against the bacterial cells. In general most of the drugs used to treat act by altering and
inhibiting the way the microbe functions typically by protein synthesis. Thus effecting reproduction and shedding of infective oocysts. Sulfur drugs inhibit cocci protozoan. Sulfadimethoxine (Albon/ corid) and Sodium sulfamethazine (Sulmet) have been proven effective in inhibiting Protista. Yet improperly administered for prolonged periods, or at improper doses the use of sulfur drugs can be detrimental to other organs and systems for the animals body. Sulfur drugs can have an adverse effect on kidneys and the deposits of uric acid. Some also inhibit and deplete Thiamin and Niacin absorption. Compound this with the deficiency that the Protista create and you will see underdeveloped chicks. After any treatment for Coccidiosis or during the use of medicated feed, vitamins should be given. Sulmet is only effective at high concentrations thus posing another potential health problem.
Antiprotozoal drugs are aimed at inhibiting protozoan and allowing the fowl to develop its immunities and tolerance of protistas at safe levels. If the lining and cells of the intestines have been damaged the result may be evident in survivors by stunted growth. Prolonged use of antibiotics administered incorrectly allows for microbes to reproduce generations that become resistant and adapt to the stress of antibiotics. Their ability to reproduce asexually and very quickly, about an hour, enables them to reproduce generations of resistant microbes each passing on that resistance to the next generation. This brings into focus the use of medicated feed and its efficiency.
Understanding that protozoan that produce the clinical illness coccidiosis, are living creatures able to feed and reproduce, producing offspring that are resistant aided by means of environmental conditions may enable us to effectively control the damaging effects these microbes have upon our livestock.
A good reference website of veterinary manual for domestic animal health and infectious diseases including Coccidiosis is
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/205700.htm
Etiology:
Coccidiosis is caused by protozoa of the phylum Apicomplexa, family Eimeriidae. In poultry, most species belong to the genus Eimeria and infect various sites in the intestine. The infectious process is rapid (4-7 days) and is characterized by parasite replication in host cells with extensive damage to the intestinal mucosa.
Poultry coccidia are strictly host-specific, and the different species parasitize specific parts of the intestine.
Coccidia are distributed worldwide in poultry and wild birds. (See also CRYPTOSPORIDIOSIS, Cryptosporidiosis.)
Coccidia are almost universally present in poultry-raising operations, but clinical disease occurs only after ingestion of relatively large numbers of sporulated oocysts by susceptible birds. Both clinically infected and recovered birds shed oocysts in their droppings, which contaminate feed, dust, water, litter, and soil. Oocysts may be transmitted by mechanical carriers (eg, equipment, clothing, insects, and other animals). Fresh oocysts are not infective until they sporulate; under optimal conditions (70-90°F [21-32°C] with adequate moisture and oxygen), this requires 1-2 days. The prepatent period is 4-7 days. Sporulated oocysts may survive for long periods, depending on environmental factors. Oocysts are resistant to some disinfectants commonly used around livestock but are killed by freezing or high environmental temperatures. (See also
COCCIDIOSIS IN MAMMALS).
Pathogenicity is influenced by host genetics, nutritional factors, concurrent diseases, and species of the coccidium. Eimeria necatrix and E tenella are the most pathogenic in chickens because schizogony occurs in the lamina propria and crypts of Lieberkühn of the small intestine and ceca, respectively, and causes extensive hemorrhage. Most species develop in epithelial cells lining the villi. Protective immunity usually develops in response to moderate and continuing infection. True age-immunity does not occur, but older birds are usually more resistant than young birds because of earlier exposure to infection.
Clinical Findings:
Signs range from decreased growth rate to a high percentage of visibly sick birds, severe diarrhea, and high mortality. Feed and water consumption are depressed. Weight loss, development of culls, decreased egg production, and increased mortality may accompany outbreaks. Mild infections of intestinal species, which would otherwise be classed as subclinical, may cause depigmentation. Survivors of severe infections recover in 10-14 days but may never recover lost performance.
Chickens:
E tenella infections are found only in the ceca and can be recognized by accumulation of blood in
the ceca and by bloody droppings. Cecal cores, which are accumulations of clotted blood, tissue
debris, and oocysts, may be found in birds surviving the acute stage.
E necatrix produces major lesions in the anterior and middle portions of the small intestine. Small white spots, usually intermingled with rounded, bright- or dull-red spots of various sizes, can be seen on the serosal surface. The white spots are diagnostic for E necatrix if clumps of large schizonts can be demonstrated microscopically. In severe cases, the intestinal wall is thickened, and the infected area dilated to 2-2.5 times the normal diameter. The lumen may be filled with blood, mucus, and fluid. Fluid loss may result in marked dehydration. Although the damage is in the small intestine, the sexual phase of the life cycle is completed in the ceca. Oocysts of E necatrix are found only in the ceca. Due to concurrent infections, oocysts of other species may be found in the area of major lesions, misleading the diagnostician.
E acervulina , the most common infection, is characterized by numerous, whitish, oval or transverse patches in the upper half of the small intestine and may be easily distinguished on gross examination. The clinical course in a flock is usually protracted and results in poor growth, an increase in culls, and slightly increased mortality.
E brunetti is found in the lower small intestine, rectum, ceca, and cloaca. In moderate infections, the mucosa is pale and disrupted but lacking in discrete foci, and may be thickened. In severe infections, extensive coagulative necrosis and sloughing of the mucosa occurs throughout most of the small intestine.
E maxima develops in the small intestine, where it causes dilatation and thickening of the wall; petechial hemorrhage; and a reddish, orange, or pink viscous mucous exudate and fluid. The oocysts and gametocytes (particularly macrogametocytes), which are present in the lesions, are distinctly large.
E mitis is recognized as pathogenic in the lower small intestine. Lesions resemble moderate infections of E brunetti but can be distinguished by finding small, round oocysts associated with the lesion. E praecox , which infects the upper small intestine, does not cause distinct lesions but may decrease rate of growth. It is considered to be of less economic importance than the other species.
E hagani and E mivati are of dubious status but are thought to develop in the anterior part of the small intestine.
Control:
Practical methods of management cannot prevent infection. Poultry that are maintained at all times on wire floors to separate birds from droppings have fewer infections; clinical coccidiosis is seen only rarely under such circumstances. Other methods of control are vaccination or prevention with anticoccidial drugs.
Vaccination:
A species-specific immunity develops after natural infection, the degree of which largely depends on the extent of infection and the number of reinfections. Protective immunity is primarily a T-cell response.....
Continuous use of anticoccidial drugs promotes the emergence of drug-resistant strains of coccidia. Various programs are used in attempts to slow or stop selection of resistance. For instance, producers may use one anticoccidial continuously through succeeding flocks, rotate anticoccidials every 4-6 mo, or change anticoccidials during a single growout (ie, a shuttle program). While there is little cross-resistance to anticoccidials with different modes of action, there is widespread resistance to most drugs. Change of drug may be beneficial when resistance has been established. Shuttle programs, in which 1 group of chickens is treated sequentially with different drugs (usually a change between the starter and grower rations), are common practice in many countries, and offer some benefit in reducing emergence of resistance. In the USA, the FDA considers shuttle programs as extra-label usage, but producers may use such programs on the
recommendation of a veterinarian.
The effects of anticoccidial drugs may be coccidiostatic, in which growth of intracellular coccidia is arrested but development may continue after drug withdrawal, or coccidiocidal, in which coccidia are killed during their development. Some anticoccidial drugs may be coccidiostatic when given short-term but coccidiocidal when given longterm. Most anticoccidials currently used in poultry production are coccidiocidal.
The natural development of immunity to coccidiosis can be slowed by use of some highly effective
anticoccidials. In the production of broilers during a short growout of 37-44 days, this may be of little
consequence. However, natural immunity is important in replacement layers because they are likely to be exposed to coccidial infections for extended periods after terminating anticoccidial drugs....
