"Toxoplasma" infection can be prevented in large part by:

- cooking meat to a safe temperature (i.e., one sufficient to kill "Toxoplasma")

- peeling or thoroughly washing fruits and vegetables before eating

- cleaning cooking surfaces and utensils after they have contacted raw meat, poultry, seafood, or unwashed fruits or vegetables

- pregnant women avoiding changing cat litter or, if no one else is available to change the cat litter, using gloves, then washing hands thoroughly

- not feeding raw or undercooked meat to cats to prevent acquisition of "Toxoplasma"

Prolonged and intense rainfall periods are significantly associated with the reactivation of toxoplasmic retinochoroiditis. Changes promoted by this climatic condition concern both the parasite survival in the soil as well as a putative effect on the host immune response due to other comorbidities.

Small extramacular lesions (lesions not threatening vision) may be observed without treatment. Sight-threatening lesions are treated for 4–6 weeks with triple therapy consisting of pyrimethamine, sulfadiazine, and folinic acid. During treatment with pyrimethamine, leukocyte and platelet counts should be monitored weekly. Folinic acid protects against the decrease in platelets and white blood cells induced by pyrimethamine.

Prednisone may be used for 3–6 weeks to reduce macular or optic nerve inflammation and can be started on day 3 of antibiotic therapy. Corticosteroids should not be used without concurrent antibiotic treatment or in immunocompromised patients due to the risk of exacerbation of the disease. Currently, there is no published evidence from randomized controlled trials demonstrating that corticosteroids would be an effective adjunct for treating ocular toxoplasmosis.

Trimethoprim-Sulfamethoxazole has been shown to be equivalent to triple therapy in the treatment of ocular toxoplasmosis and may be better tolerated. Clindamycin and azithromycin can also be considered as alternative therapies. Spiramycin may be used safely without undue risk of teratogenicity and may reduce the rate of transmission to the fetus.

AIDS patients require chronic maintenance treatment.

TORCH syndrome can be prevented by treating an infected pregnant person, thereby preventing the infection from affecting the fetus.

The treatment of TORCH syndrome is mainly supportive and depends on the symptoms present; medication is an option for herpes and cytomegalovirus infections.

Chorioretinitis is usually treated with a combination of corticosteroids and antibiotics. However, if there is an underlying cause such as HIV, specific therapy can be started as well.

A 2012 Cochrane Review found weak evidence suggesting that ivermectin could result in reduced chorioretinal lesions in patients with onchocercal eye disease. More research is needed to support this finding.

Reductions in morbidity and mortality are due to the use of antiviral treatments such as vidarabine and acyclovir. However, morbidity and mortality still remain high due to diagnosis of DIS and CNS herpes coming too late for effective antiviral administration; early diagnosis is difficult in the 20-40% of infected neonates that have no visible lesions. A recent large scale retrospective study found disseminated NHSV patients least likely to get timely treatment, contributing to the high morbidity/mortality in that group.

Harrison's Principles of Internal Medicine, recommends that pregnant women with active genital herpes lesions at the time of labor be delivered by caesarean section. Women whose herpes is not active can be managed with acyclovir. The current practice is to deliver women with primary or first episode non primary infection via caesarean section, and those with recurrent infection vaginally, even in the presence of lesions because of the low risk (1-3%) of vertical transmission associated with recurrent herpes.

It can be treated with systemic antiviral drugs, such as aciclovir or valganciclovir. Foscarnet may also be used for immunocompromised host with Herpes simplex and acyclovir-resistant Herpes simplex.

Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.

The majority of cases (85%) occur during birth when the baby comes in contact with infected genital secretions in the birth canal, most common with mothers that have newly been exposed to the virus (mothers that had the virus before pregnancy have a lower risk of transmission), an estimated 5% are infected in utero, and approximately 10% of cases are acquired postnatally. Detection and prevention is difficult because transmission is asymptomatic in 60% - 98% of cases.

Progressive disseminated histoplasmosis is an infection caused by Histoplasma capsulatum, and most people who develop this severe form of histoplasmosis are immunocompromised or taking systemic corticosteroids. Skin lesions are present in approximately 6% of patients with dissemination.

Fungal meningitis is treated with long courses of high dose antifungal medications. The duration of treatment is dependent upon the causal pathogen and the patient's ability to stave off the infection; for patients with a weaker immune system or diabetes, treatment will often take longer.

In the US, neuroborreliosis is typically treated with intravenous antibiotics which cross the blood–brain barrier, such as penicillins, ceftriaxone, or cefotaxime. One relatively small randomized controlled trial suggested ceftriaxone was more effective than penicillin in the treatment of neuroborreliosis. Small observational studies suggest ceftriaxone is also effective in children. The recommended duration of treatment is 14 to 28 days.

Several studies from Europe have suggested oral doxycycline is equally as effective as intravenous ceftriaxone in treating neuroborreliosis. Doxycycline has not been widely studied as a treatment in the US, but antibiotic sensitivities of prevailing European and US isolates of "Borrelia burgdorferi" tend to be identical. However, doxycycline is generally not prescribed to children due to the risk of bone and tooth damage.

Discreditied or doubtful treatments for neuroborreliosis include:

- Malariotherapy

- Hyperbaric oxygen therapy

- Colloidal silver

- Injections of hydrogen peroxide and bismacine

Nocardiosis requires at least 6 months of treatment, preferably with trimethoprim/sulfamethoxazole or high doses of sulfonamides. In patients who do not respond to sulfonamide treatment, other drugs, such as ampicillin, erythromycin, or minocycline, may be added.

Treatment also includes surgical drainage of abscesses and excision of necrotic tissue. The acute phase requires complete bed rest; as the patient improves, activity can increase.

A new combination drug therapy (sulfonamide, ceftriaxone, and amikacin) has also shown promise.

Chorioretinitis is often caused by toxoplasmosis and cytomegalovirus infections (mostly seen in immunodeficient subjects such as people with HIV or on immunosuppressant drugs). Congenital toxoplasmosis via transplacental transmission can also lead to sequelae such as chorioretinitis along with hydrocephalus and cerebral calcifications. Other possible causes of chorioretinitis are syphilis, sarcoidosis, tuberculosis, Behcet's disease, onchocerciasis, or West Nile virus. Chorioretinitis may also occur in presumed ocular histoplasmosis syndrome (POHS); despite its name, the relationship of POHS to "Histoplasma" is controversial.

In the majority of immunocompetent individuals, histoplasmosis resolves without any treatment. Antifungal medications are used to treat severe cases of acute histoplasmosis and all cases of chronic and disseminated disease. Typical treatment of severe disease first involves treatment with amphotericin B, followed by oral itraconazole.

Liposomal preparations of amphotericin B are more effective than deoxycholate preparations. The liposomal preparation is preferred in patients that might be at risk of nephrotoxicity, although all preparations of amphotericin B have risk of nephrotoxicity. Individuals taking amphotericin B are monitored for renal function.

Treatment with itraconazole will need to continue for at least a year in severe cases, while in acute pulmonary histoplasmosis, 6 to 12 weeks treatment is sufficient. Alternatives to itraconazole are posaconazole, voriconazole, and fluconazole. Individuals taking itraconazole are monitored for hepatic function.

Mendelian susceptibility to mycobacterial disease, also called familial disseminated atypical mycobacterial infection, is a rare genetic disease characterized by susceptibility to mycobacteria and Salmonella infection outside of the intestinal tract.

This infection affects multiple organs, including the eyes, brain, lung, and liver, and can be fatal.

The prognosis of nocardiosis is highly variable. The state of the host's health, site, duration, and severity of the infection all play parts in determining the prognosis. As of now, skin and soft tissue infections have a 100% cure rate, and pleuropulmonary infections have a 90% cure rate with appropriate therapy. The cure rate falls to 63% with those infected with dissemented nocardiosis, with only half of those surviving infections that cause brain abscess. Additionally, 44% of people who are infected in the spinal cord/brain die, increasing to 85% if that person has an already weakened immune system. Unfortunately, there is not a preventative to nocardiosis. The only recommendation is to protect open wounds to limit access.

It is not practical to test or decontaminate most sites that may be contaminated with "H. capsulatum", but the following sources list environments where histoplasmosis is common, and precautions to reduce a person's risk of exposure, in the three parts of the world where the disease is prevalent. Precautions common to all geographical locations would be to avoid accumulations of bird or bat droppings.

The US National Institute for Occupational Safety and Health (NIOSH) provides information on work practices and personal protective equipment that may reduce the risk of infection. This document is available in English and Spanish.

Authors at the University of Nigeria have published a review which includes information on locations in which histoplasmosis has been found in Africa (in chicken runs, bats and the caves bats infest, and in soil), and a thorough reference list including English, French, and Spanish language references.

To reduce neonatal infection, routine screening of pregnant women for HIV, hepatitis B, syphilis, and rubella susceptibility is required in the UK.

Treatment with an vaginal antibiotic wash prior to birth does not prevent infection with group B streptococcus bacteria. Breast milk protects against necrotizing enterocolitis.

Because GBS bacteria can colonize the lower reproductive tract of 30% of women, typically pregnant women are tested for this pathogen from 35 to 37 weeks of pregnancy. Before delivery treatment of the mother with antibiotics reduces the rate of neonatal infection. Prevention of the infection of the baby is done by treating the mother with penicillin. Since the adoption of this prophylatic treatment, infant mortality from GBS infection has decreased by 80%.

Mothers with symptomatic HSV and who are treated with antiviral prophylaxis are less prone to have an active, symptomatic case at the time of birth and it may be able to reduce the risk of passing on HSV during birth. Cesarean delivery reduces the risk of infection of the infant.

The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.

Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.

Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis.

Disseminated disease refers to a diffuse disease-process, generally either infectious or neoplastic. The term may sometimes also characterize connective tissue disease.

A disseminated infection, for example, has extended beyond its origin or nidus and involved the bloodstream to "seed" other areas of the body. Similarly, one can view metastatic cancer as a disseminated infection in that it has extended into the bloodstream or into the lymphatic system and thus "seeded" distant sites (a process known as metastasis).

Disseminated disease often contrasts localized disease.

In contrast to visceral larva migrans, ocular toxocariasis usually develops in older children or young adults with no history of pica. These patients seldom have eosinophilia or visceral manifestations.

For people who have severe congenital protein C deficiency, protein C replacement therapies are available, which is indicated and approved for use in the United States and Europe for the prevention of purpura fulminans. Protein C replacement is often in combination with anticoagulation therapy of injectable low molecular weight heparin or oral warfarin. Before initiating warfarin therapy, a few days of therapeutic heparin may be administered to prevent warfarin skin necrosis and other progressive or recurrent thrombotic complications.

The best treatment for MAS has not been firmly established. Most commonly used treatments include high-dose glucocorticoids, and cyclosporine. In refractory cases treatment regimens are used similar to that in HLH.