Botulism is generally treated with botulism antitoxin and supportive care.

Supportive care for botulism includes monitoring of respiratory function. Respiratory failure due to paralysis may require mechanical ventilation for 2 to 8 weeks, plus intensive medical and nursing care. After this time, paralysis generally improves as new neuromuscular connections are formed.

In some abnormal cases, physicians may try to remove contaminated food still in the digestive tract by inducing vomiting or using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria.

In adults, botulism can be treated by passive immunization with a horse-derived antitoxin, which blocks the action of the toxin circulating in the blood. A trivalent antitoxin containing antibodies raised against botulinum toxin types A, B, and E is used most commonly, however a heptavalent botulism antitoxin has also been developed and was approved by the U.S. FDA in 2013. In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins. To avoid this, a human-derived antitoxin has been developed and approved by the U.S. FDA in 2003 for the treatment of infant botulism. This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. However, the danger of equine-derived antitoxin to infants has not been clearly established, and one study showed the equine-derived antitoxin to be both safe and effective for the treatment of infant botulism.

Trivalent (A,B,E) botulinum antitoxin is derived from equine sources utilizing whole antibodies (Fab and Fc portions). In the United States, this antitoxin is available from the local health department via the CDC. The second antitoxin, heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated.

The presence of avian botulism is extremely hard to detect before an outbreak. Frequent surveillance of sites at risk is needed for early detection of the disease in order to take action and remove carcasses. Vaccines are also developed, but they are expected to have limited effectiveness in stemming outbreaks in wild waterbird populations. However may be effective in reducing mortality for endangered island waterfowl and small non-migratory wild populations. Field tests are needed.

Avian Botulism is a strain of botulism that affects wild and captive bird populations, most notably waterfowl. This is a paralytic disease brought on by the Botulinum neurotoxin (BoNt) of the bacterium "Clostridium botulinum". "C. botulinum" can fall into one of 7 different types which are strains A through G. Type C BoNt is most frequently associated with waterfowl mortality. The Type E strain is also commonly associated with avian outbreaks and is frequently found in fish species which is why most outbreaks occur in piscivorous birds.

Avian Botulism occurs all over the world and its understanding is important for wildlife managers, hunters, bird watchers, and anyone who owns wetland property as this disease can account for over 1,000,000 waterbird deaths in a year.

Prevention is mainly the role of the state, through the definition of strict rules of hygiene and a public services of veterinary surveying of animal products in the food chain, from farming to the transformation industry and delivery (shops and restaurants). This regulation includes:

- traceability: in a final product, it must be possible to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed; the origin of the illness can thus be tracked and solved (and possibly penalized), and the final products can be removed from the sale if a problem is detected;

- enforcement of hygiene procedures such as HACCP and the "cold chain";

- power of control and of law enforcement of veterinarians.

In August 2006, the United States Food and Drug Administration approved Phage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns, because without mandatory labelling consumers would not be aware that meat and poultry products have been treated with the spray.

At home, prevention mainly consists of good food safety practices. Many forms of bacterial poisoning can be prevented by cooking it sufficiently, and either eating it quickly or refrigerating it effectively. Many toxins, however, are not destroyed by heat treatment.

Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between , called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers

for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of or until hot or steaming to kill bacteria.

When infection attacks the body, "anti-infective" drugs can suppress the infection. Several broad types of anti-infective drugs exist, depending on the type of organism targeted; they include antibacterial (antibiotic; including antitubercular), antiviral, antifungal and antiparasitic (including antiprotozoal and antihelminthic) agents. Depending on the severity and the type of infection, the antibiotic may be given by mouth or by injection, or may be applied topically. Severe infections of the brain are usually treated with intravenous antibiotics. Sometimes, multiple antibiotics are used in case there is resistance to one antibiotic. Antibiotics only work for bacteria and do not affect viruses. Antibiotics work by slowing down the multiplication of bacteria or killing the bacteria. The most common classes of antibiotics used in medicine include penicillin, cephalosporins, aminoglycosides, macrolides, quinolones and tetracyclines.

Not all infections require treatment, and for many self-limiting infections the treatment may cause more side-effects than benefits. Antimicrobial stewardship is the concept that healthcare providers should treat an infection with an antimicrobial that specifically works well for the target pathogen for the shortest amount of time and to only treat when there is a known or highly suspected pathogen that will respond to the medication.

Antiemetic medications may be helpful for treating vomiting in children. Ondansetron has some utility, with a single dose being associated with less need for intravenous fluids, fewer hospitalizations, and decreased vomiting. Metoclopramide might also be helpful. However, the use of ondansetron might possibly be linked to an increased rate of return to hospital in children. The intravenous preparation of ondansetron may be given orally if clinical judgment warrants. Dimenhydrinate, while reducing vomiting, does not appear to have a significant clinical benefit.

Antibiotics are not usually used for gastroenteritis, although they are sometimes recommended if symptoms are particularly severe or if a susceptible bacterial cause is isolated or suspected. If antibiotics are to be employed, a macrolide (such as azithromycin) is preferred over a fluoroquinolone due to higher rates of resistance to the latter. Pseudomembranous colitis, usually caused by antibiotic use, is managed by discontinuing the causative agent and treating it with either metronidazole or vancomycin. Bacteria and protozoans that are amenable to treatment include "Shigella" "Salmonella typhi", and "Giardia" species. In those with "Giardia" species or "Entamoeba histolytica", tinidazole treatment is recommended and superior to metronidazole. The World Health Organization (WHO) recommends the use of antibiotics in young children who have both bloody diarrhea and fever.

Bacteria are a common cause of foodborne illness. In the United Kingdom during 2000, the individual bacteria involved were the following: "Campylobacter jejuni" 77.3%, "Salmonella" 20.9%, 1.4%, and all others less than 0.56%. In the past, bacterial infections were thought to be more prevalent because few places had the capability to test for norovirus and no active surveillance was being done for this particular agent. Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12–72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food.

Most common bacterial foodborne pathogens are:

- "Campylobacter jejuni" which can lead to secondary Guillain–Barré syndrome and periodontitis

- "Clostridium perfringens", the "cafeteria germ"

- "Salmonella" spp. – its "S. typhimurium" infection is caused by consumption of eggs or poultry that are not adequately cooked or by other interactive human-animal pathogens

- "" enterohemorrhagic (EHEC) which can cause hemolytic-uremic syndrome

Other common bacterial foodborne pathogens are:

- "Bacillus cereus"

- "Escherichia coli", other virulence properties, such as enteroinvasive (EIEC), enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroaggregative (EAEC or EAgEC)

- "Listeria monocytogenes"

- "Shigella" spp.

- "Staphylococcus aureus"

- "Staphylococcal enteritis"

- "Streptococcus"

- "Vibrio cholerae", including O1 and non-O1

- "Vibrio parahaemolyticus"

- "Vibrio vulnificus"

- "Yersinia enterocolitica" and "Yersinia pseudotuberculosis"

Less common bacterial agents:

- "Brucella" spp.

- "Corynebacterium ulcerans"

- "Coxiella burnetii" or Q fever

- "Plesiomonas shigelloides"

Recovery from an anaerobic infection depends on adequate and rapid management. The main principles of managing anaerobic infections are neutralizing the toxins produced by anaerobic bacteria, preventing the local proliferation of these organisms by altering the environment and preventing their dissemination and spread to healthy tissues.

Toxin can be neutralized by specific antitoxins, mainly in infections caused by Clostridia (tetanus and botulism). Controlling the environment can be attained by draining the pus, surgical debriding of necrotic tissue, improving blood circulation, alleviating any obstruction and by improving tissue oxygenation. Therapy with hyperbaric oxygen (HBO) may also be useful. The main goal of antimicrobials is in restricting the local and systemic spread of the microorganisms.

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Oral agents adequate for polymicrobial oral infections include the combinations of amoxicillin plus clavulanate, clindamycin and metronidazole plus a macrolide. Penicillin can be added to metronidazole in the treating dental and intracranial infections to cover "Actinomyces" spp., microaerophilic streptococci, and "Arachnia" spp. A macrolide can be added to metronidazole in treating upper respiratory infections to cover "S. aureus" and aerobic streptococci. Penicillin can be added to clindamycin to supplement its coverage against "Peptostreptococcus" spp. and other Gram-positive anaerobic organisms.

Doxycycline is added to most regimens in the treatment of pelvic infections to cover chlamydia and mycoplasma. Penicillin is effective for bacteremia caused by non-beta lactamase producing bacteria. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producing bacteria.

Because the length of therapy for anaerobic infections is generally longer than for infections due to aerobic and facultative anaerobic bacteria, oral therapy is often substituted for parenteral treatment. The agents available for oral therapy are limited and include amoxacillin plus clavulanate, clindamycin, chloramphenicol and metronidazole.

In 2010 the American Surgical Society and American Society of Infectious Diseases have updated their guidelines for the treatment of abdominal infections.

The recommendations suggest the following:

For mild-to-moderate community-acquired infections in adults, the agents recommended for empiric regimens are: ticarcillin- clavulanate, cefoxitin, ertapenem, moxifloxacin, or tigecycline as single-agent therapy or combinations of metronidazole with cefazolin, cefuroxime, ceftriaxone, cefotaxime, levofloxacin, or ciprofloxacin. Agents no longer recommended are: cefotetan and clindamycin ( Bacteroides fragilis group resistance) and ampicillin-sulbactam (E. coli resistance) and ainoglycosides (toxicity).

For high risk community-acquired infections in adults, the agents recommended for empiric regimens are: meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, ciprofloxacin or levofloxacin in combination with metronidazole, or ceftazidime or cefepime in combination with metronidazole. Quinolones should not be used unless hospital surveys indicate >90% susceptibility of "E. coli" to quinolones.

Aztreonam plus metronidazole is an alternative, but addition of an agent effective against gram-positive cocci is recommended. The routine use of an aminoglycoside or another second agent effective against gram-negative facultative and aerobic bacilli is not recommended in the absence of evidence that the infection is caused by resistant organisms that require such therapy.

Empiric use of agents effective against enterococci is recommended and agents effective against methicillin-resistant "S. aureus" (MRSA) or yeast is not recommended in the absence of evidence of infection due to such organisms.

Empiric antibiotic therapy for health care-associated intra-abdominal should be driven by local microbiologic results. Empiric coverage of likely pathogens may require multidrug regimens that include agents with expanded spectra of activity against gram-negative aerobic and facultative bacilli. These include meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Aminoglycosides or colistin may be required.

Antimicrobial regimens for children include an aminoglycoside-based regimen, a carbapenem (imipenem, meropenem, or ertapenem), a beta-lactam/beta-lactamase-inhibitor combination (piperacillin-tazobactam or ticarcillin-clavulanate), or an advanced-generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime, or cefepime) with metronidazole.

Clinical judgment, personal experience, safety and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. The length of therapy generally ranges between 2 and 4 weeks, but should be individualized depending on the response. In some instances treatment may be required for as long as 6–8 weeks, but can often be shortened with proper surgical drainage.

Sleeping on the back has been found to reduce the risk of SIDS. It is thus recommended by the American Academy of Pediatrics and promoted as a best practice by the US National Institute of Child Health and Human Development (NICHD) "Safe to Sleep" campaign. The incidence of SIDS has fallen in a number of countries in which this recommendation has been widely adopted. Sleeping on the back does not appear to increase the risk of choking even in those with gastroesophageal reflux disease. While infants in this position may sleep more lightly this is not harmful. Sharing the same room as one's parents but in a different bed may decrease the risk by half.

In colder environments where bedding is required to maintain a baby's body temperature, the use of a "baby sleep bag" or "sleep sack" is becoming more popular. This is a soft bag with holes for the baby's arms and head. A zipper allows the bag to be closed around the baby. A study published in the "European Journal of Pediatrics" in August 1998 has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study, "The use of a sleeping-sack should be particularly promoted for infants with a low birth weight." The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head.

There is usually an indication for a specific identification of an infectious agent only when such identification can aid in the treatment or prevention of the disease, or to advance knowledge of the course of an illness prior to the development of effective therapeutic or preventative measures. For example, in the early 1980s, prior to the appearance of AZT for the treatment of AIDS, the course of the disease was closely followed by monitoring the composition of patient blood samples, even though the outcome would not offer the patient any further treatment options. In part, these studies on the appearance of HIV in specific communities permitted the advancement of hypotheses as to the route of transmission of the virus. By understanding how the disease was transmitted, resources could be targeted to the communities at greatest risk in campaigns aimed at reducing the number of new infections. The specific serological diagnostic identification, and later genotypic or molecular identification, of HIV also enabled the development of hypotheses as to the temporal and geographical origins of the virus, as well as a myriad of other hypothesis. The development of molecular diagnostic tools have enabled physicians and researchers to monitor the efficacy of treatment with anti-retroviral drugs. Molecular diagnostics are now commonly used to identify HIV in healthy people long before the onset of illness and have been used to demonstrate the existence of people who are genetically resistant to HIV infection. Thus, while there still is no cure for AIDS, there is great therapeutic and predictive benefit to identifying the virus and monitoring the virus levels within the blood of infected individuals, both for the patient and for the community at large.

Intestinal infectious diseases include a large number of infections of the bowels including: cholera, typhoid fever, paratyphoid fever, other types of salmonella infections, shigellosis, botulism, gastroenteritis, and amoebiasis among others.

Typhoid and paratyphoid resulted in 221,000 deaths in 2013 down from 259,000 deaths in 1990. Other diseases which result in diarrhea caused another 1.3 million additional deaths in 2013 down from 2.6 million deaths in 1990.

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

In terms of treatment for neuromuscular diseases (NMD), "exercise" might be a way of managing them, as NMD individuals would gain muscle strength. In a study aimed at results of exercise, in muscular dystrophy and Charcot-Marie-Tooth disease, the later benefited while the former did not show benefit; therefore, it depends on the disease Other management routes for NMD should be based on medicinal and surgical procedures, again depending on the underlying cause.

Neurotoxin may act on the neuromuscular junction either post synaptically or presynaptically as there are several different forms of toxins that the NMJ is sensitive to.(reference 14) Common mechanisms of action include blockage of acetylcholine release at the synapse thus causing the NMJ to become abnormal in function.(reference 12)

Appropriate treatment for lameness depends on the condition diagnosed, but at a minimum it usually includes rest or decreased activity and anti-inflammatory medications. Other treatment options, such as corrective shoeing, joint injections, and regenerative therapies, are pursued based on the cause of lameness and the financial limits of the owner. Consultation with a veterinarian is generally recommended, even for mild cases, as some types of lameness may worsen if not properly diagnosed and treated.

Aponeurotic and congenital ptosis may require surgical correction if severe enough to interfere with vision or if cosmetics is a concern.

Treatment depends on the type of ptosis and is usually performed by an ophthalmic plastic and reconstructive surgeon, specializing in diseases and problems of the eyelid.

Surgical procedures include:

- Levator resection

- Müller muscle resection

- Frontalis sling operation (preferred option for oculopharyngeal muscular dystrophy)

Non-surgical modalities like the use of "crutch" glasses or Ptosis crutches or special scleral contact lenses to support the eyelid may also be used.

Ptosis that is caused by a disease may improve if the disease is treated successfully, although some related diseases, such as oculopharyngeal muscular dystrophy currently have no treatments or cures.

Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly.