In most instances, the diagnosis of toxoplasmic retinochoroiditis is made clinically on the basis of the appearance of the characteristic lesion on eye examination.

Seropositivity (positive blood test result) for Toxoplasma is very common and therefore not useful in diagnosis; however, a negative result i.e. absence of antibodies is often used to rule out disease. Others believe that serology is useful to confirm active toxoplasmic retinochoroiditis, not only by showing positivity but by also showing a significant elevation of titers: The mean IgG values were 147.7 ± 25.9 IU/ml for patients with active disease versus 18.3 ± 20.8 IU/ml for normal individuals.

Antibodies against Toxoplasma:

- IgG : appear within the first 2 weeks after infection, typically remain detectable for life, albeit at low levels;and may cross the placenta.

- IgM : rise early during the acute phase of the infection, typically remain detectable for less than 1 year, and do not cross the placenta.

- IgA : Measurement of IgA antibody titers may also be useful in a diagnosis of congenital toxoplasmosis in a fetus or newborn because IgM production is often weak during this period and the presence of IgG antibodies may indicate passive transfer of maternal antibodies in utero. IgA antibodies however usually disappear by 7 months.

In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine intraocular production of specific antibody may be helpful for establishing etiology.

Neuroimaging is warranted in AIDS patients presenting with these findings because intracranial toxoplasmic lesions have been reported in up to 29% of these patients who have toxoplasmic chorioretinitis.

"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.

Neonatal sepsis of the newborn is an infection that has spread through the entire body. The inflammatory response to this systematic infection can be as serious as the infection itself. In infants that weigh under 1500 g, sepsis is the most common cause of death. Three to four percent of infants per 1000 births contract sepsis. The mortality rate from sepsis is near 25%. Infected sepsis in an infant can be identified by culturing the blood and spinal fluid and if suspected, intravenous antibiotics are usually started. Lumbar puncture is controversial because in some cases it has found not to be necessary while concurrently, without it estimates of missing up to one third of infants with meningitis is predicted.

If suspected, fungal meningitis is diagnosed by testing blood and CSF samples for pathogens. Identifying the specific pathogen is necessary to determine the proper course of treatment and the prognosis. Measurement of opening pressure, cell count with differential, glucose and protein concentrations, Gram's stain, India ink, and culture tests should be preformed on CSF samples when fungal meningitis is suspected.

Diagnosis of nocardiosis can be done by a doctor using various techniques. These techniques include, but are not limited to: a chest x-rays of the lung, a bronchoscopy, a brain/lung/skin biopsy, or a sputum culture.

However, diagnosis may be difficult. Nocardiae are gram positive weakly acid-fast branching rod-shaped bacteria and can be visualized by a modified Ziehl–Neelsen stain like Fite-Faraco method. In the clinical laboratory, routine cultures may be held for insufficient time to grow nocardiae, and referral to a reference laboratory may be needed for species identification. Infiltration and pleural effusion are usually seen via x-ray.

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.

Clinically, there is a wide spectrum of disease manifestation, making diagnosis somewhat difficult. More severe forms include: (1) the chronic pulmonary form, often occurring in the presence of underlying pulmonary disease; and (2) a disseminated form, which is characterized by the progressive spread of infection to extra-pulmonary sites. Oral manifestations have been reported as the main complaint of the disseminated forms, leading the patient to seek treatment, whereas pulmonary symptoms in disseminated disease may be mild or even misinterpreted as flu. Histoplasmosis can be diagnosed by samples containing the fungus taken from sputum (via bronchoalveolar lavage), blood, or infected organs. It can also be diagnosed by detection of antigens in blood or urine samples by ELISA or PCR. Antigens can cross-react with antigens of African histoplasmosis (caused by Histoplasma duboisii), blastomycosis, coccidioidomycosis, paracoccidioidomycosis, and Penicillium marneffei infection. Histoplasmosis can also be diagnosed by a test for antibodies against "Histoplasma" in the blood. "Histoplasma" skin tests indicate whether a person has been exposed, but do not indicate whether they have the disease. Formal histoplasmosis diagnoses are often confirmed only by culturing the fungus directly. Sabouraud agar is one type of agar growth media on which the fungus can be cultured. Cutaneous manifestations of disseminated disease are diverse and often present as a nondescript rash with systemic complaints. Diagnosis is best established by urine antigen testing, as blood cultures may take up to 6 weeks for diagnostic growth to occur and serum antigen testing often comes back with a false negative before 4 weeks of disseminated infection.

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.

Symptoms and the isolation of the virus pathogen the upper respiratory tract is diagnostic. Virus identification is specific immunologic methods and PCR. The presence of the virus can be rapidly confirmed by the detection of the virus antigen. The methods and materials used for identifying the RSV virus has a specificity and sensitivity approaching 85% to 95%. Not all studies confirm this sensitivity. Antigen detection has comparatively lower sensitivity rates that approach 65% to 75%.

Developing countries are more severely affected by TORCH syndrome.

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

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 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.

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.

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.

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.

The diagnosis relies on the findings outlined above. In addition, other specific markers of macrophage activation (e.g. soluble CD163), and lymphocyte activation (e.g. soluble IL-2 receptor) can be helpful. NK cell function analysis may show depressed NK function, or, flow cytometry may show a depressed NK cell population.

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.

The diagnostic workup is directed by the presenting signs and symptoms, and can involve:

- blood counts, clotting studies, and other laboratory testing

- imaging tests (ultrasound, CT scan, MRI, sometimes angiography, and rarely nuclear medicine scans)

- biopsy of the tumor.

Patients uniformly show severe thrombocytopenia, low fibrinogen levels, high fibrin degradation products (due to fibrinolysis), and microangiopathic hemolysis.

The retinal lesion can mimic retinoblastoma in appearance, and mistaken diagnosis of the latter condition can lead to unnecessary "enucleation".

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.

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

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

Routine vaccination against meningococcus is recommended by the Centers for Disease Control and Prevention for all 11- to 18-year-olds and people who have poor splenic function (who, for example, have had their spleen removed or who have sickle-cell disease which damages the spleen), or who have certain immune disorders, such as a complement deficiency.

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.