Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the placenta. Congenital toxoplasmosis is associated with fetal death and abortion, and in infants, it is associated with neurologic deficits, neurocognitive deficits, and chorioretinitis. A positive antibody titer indicates previous exposure and immunity, and largely ensures the unborn fetus' safety. A simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to "T. gondii" while pregnant, the fetus is at particular risk.

Not much evidence exists around the effect of education before pregnancy to prevent congenital toxoplasmosis. However educating parents before the baby is born has been suggested to be effective because it may improve food, personal and pet hygiene. More research is needed to find whether antenatal education can reduce congenital toxoplasmosis.

For pregnant women with negative antibody titers, indicating no previous exposure to "T. gondii", serology testing as frequent as monthly is advisable as treatment during pregnancy for those women exposed to "T. gondii" for the first time dramatically decreases the risk of passing the parasite to the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young.

Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries, for reasons of cost-effectiveness and the high number of false positives generated; Portugal, France, Austria, Uruguay, and Italy are notable exceptions, and some regional screening programmes operate in Germany, Switzerland and Belgium. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented), postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.

Pregnant women should avoid handling raw meat, drinking raw milk (especially goat milk) and be advised to not eat raw or undercooked meat regardless of type. Because of the obvious relationship between "Toxoplasma" and cats it is also often advised to avoid exposure to cat feces, and refrain from gardening (cat feces are common in garden soil) or at least wear gloves when so engaged. Most cats are not actively shedding oocysts, since they get infected in the first six months of their life, when they shed oocysts for a short period of time (1–2 weeks.) However, these oocysts get buried in the soil, sporulate and remain infectious for periods ranging from several months to more than a year. Numerous studies have shown living in a household with a cat is not a significant risk factor for "T. gondii" infection, though living with several kittens has some significance.

In 2006, a Czech research team discovered women with high levels of toxoplasmosis antibodies were significantly more likely to have baby boys than baby girls. In most populations, the birth rate is around 51% boys, but women infected with "T. gondii" had up to a 72% chance of a boy. In mice, the sex ratio was higher in early latent toxoplasmosis and lower in later latent toxoplasmosis.

When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine whether the fetus has been infected or not. When a pregnant woman develops acute toxoplasmosis, the tachyzoites have approximately a 30% chance of entering the placental tissue, and from there entering and infecting the fetus. As gestational age at the time of infection increases, the chance of fetal infection also increases.

If the parasite has not yet reached the fetus, spiramycin can help to prevent placental transmission. If the fetus has been infected, the pregnant woman can be treated with pyrimethamine and sulfadiazine, with folinic acid, after the first trimester. They are treated after the first trimester because pyrimethamine has an antifolate effect, and lack of folic acid can interfere with fetal brain formation and cause thrombocytopaenia. Infection in earlier gestational stages correlates with poorer fetal and neonatal outcomes, particularly when the infection is untreated.

Babies can also become infected by their mothers during birth. Some infectious agents may be transmitted to the embryo or fetus in the uterus, while passing through the birth canal, or even shortly after birth. The distinction is important because when transmission is primarily during or after birth, medical intervention can help prevent infections in the infant.

During birth, babies are exposed to maternal blood, body fluids, and to the maternal genital tract without the placental barrier intervening. Because of this, blood-borne microorganisms (hepatitis B, HIV), organisms associated with sexually transmitted disease (e.g., "Neisseria gonorrhoeae" and "Chlamydia trachomatis"), and normal fauna of the genitourinary tract (e.g., "Candida albicans") are among those commonly seen in infection of newborns.

The embryo and fetus have little or no immune function. They depend on the immune function of their mother. Several pathogens can cross the placenta and cause (perinatal) infection. Often, microorganisms that produce minor illness in the mother are very dangerous for the developing embryo or fetus. This can result in spontaneous abortion or major developmental disorders. For many infections, the baby is more at risk at particular stages of pregnancy. Problems related to perinatal infection are not always directly noticeable.

Coccidiosis is a significant disease for chickens, especially affecting the young chicks. It can be fatal or leave the bird with compromised digestion. There are chick feed mixes that contain a coccidiostat to manage exposure levels and control disease. In an outbreak, coccidiocidal medications are given. Examples are toltrazuril (Baycox) or amprolium. After multiple infections, surviving chickens become resistant to the coccidia.

They are treated with antiprotozoal agents. Recent papers have also proposed the use of viruses to treat infections caused by protozoa.

Cryptococcosis is a defining opportunistic infection for AIDS, and is the second-most-common AIDS-defining illness in Africa. Other conditions that pose an increased risk include certain lymphomas (e.g., Hodgkin's lymphoma), sarcoidosis, liver cirrhosis, and patients on long-term corticosteroid therapy.

Distribution is worldwide in soil. The prevalence of cryptococcosis has been increasing over the past 20 years for many reasons, including the increase in incidence of AIDS and the expanded use of immunosuppressive drugs.

In humans, "C. neoformans" causes three types of infections:

- Wound or cutaneous cryptococcosis

- Pulmonary cryptococcosis

- Cryptococcal meningitis.

Cryptococcal meningitis (infection of the meninges, the tissue covering the brain) is believed to result from dissemination of the fungus from either an observed or unappreciated pulmonary infection. Often there is also silent dissemination throughout the brain when meningitis is present. "Cryptococcus gattii" causes infections in immunocompetent people (fully functioning immune system), but "C. neoformans v. grubii", and "v. neoformans" usually only cause clinically evident infections in persons with some form of defect in their immune systems (immunocompromised persons). People with defects in their cell-mediated immunity, for example, people with AIDS, are especially susceptible to disseminated cryptococcosis. Cryptococcosis is often fatal, even if treated. It is estimated that the three-month case-fatality rate is 9% in high-income regions, 55% in low/middle-income regions, and 70% in sub-Saharan Africa. As of 2009 there were globally approximately 958,000 annual cases and 625,000 deaths within three months after infection.

Although the most common presentation of cryptococcosis is of "C. neoformans" infection in an immunocompromised person (such as persons living with AIDS), the "C. gattii" is being increasingly recognised as a pathogen in what is presumed to be immunocompetent hosts, especially in Canada and Australia. This may be due to rare exposure and high pathogenicity, or to unrecognised isolated defects in immunity, specific for this organism.

The most common medications used to treat coccidian infections are in the sulfonamide antibiotic family.

Depending on the pathogen and the condition of the animal, untreated coccidiosis may clear of its own accord, or become severe and damaging, and sometimes cause death.

Developing countries are more severely affected by TORCH syndrome.

Outbreaks of zoonoses have been traced to human interaction with and exposure to animals at fairs, petting zoos, and other settings. In 2005, the Centers for Disease Control and Prevention (CDC) issued an updated list of recommendations for preventing zoonosis transmission in public settings. The recommendations, developed in conjunction with the National Association of State Public Health Veterinarians, include educational responsibilities of venue operators, limiting public and animal contact, and animal care and management.

Pregnant women are more severely affected by influenza, hepatitis E, herpes simplex and malaria. The evidence is more limited for coccidioidomycosis, measles, smallpox, and varicella. Pregnancy may also increase susceptibility for toxoplasmosis.

During the 2009 H1N1 pandemic, as well as during interpandemic periods, women in the third trimester of pregnancy were at increased risk for severe

disease, such as disease requiring admission to an intensive care unit or resulting in death, as compared with women in an earlier stage of pregnancy.

For hepatitis E, the case fatality rate among pregnant women has been estimated to be between 15% and 25%, as compared with a range of 0.5 to 4% in the population overall, with the highest susceptibility in the third trimester.

Primary herpes simplex infection, when occurring in pregnant women, has an increased risk of dissemination and hepatitis, an otherwise rare complication in immunocompetent adults, particularly during the third trimester. Also, recurrences of herpes genitalis increase in

frequency during pregnancy.

The risk of severe malaria by "Plasmodium falciparum" is three times as high in pregnant women, with a median maternal mortality of 40% reported in studies in the Asia–Pacific region. In women where the pregnancy is not the first, malaria infection is more often asymptomatic, even at high parasite loads, compared to women having their first pregnancy. There is a decreasing susceptibility to malaria with increasing parity, probably due to immunity to pregnancy-specific antigens. Young maternal age and increases the risk. Studies differ whether the risk is different in different . Limited data suggest that malaria caused by "Plasmodium vivax" is also more severe during pregnancy.

Severe and disseminated coccidioidomycosis has been reported the occur in increased frequency in pregnant women in several reports and case series, but subsequent large surveys, with the overall risk being rather low.

Varicella occurs at an increased rate during pregnancy, but mortality is not higher than that among men and non-pregnant women.

Listeriosis mostly occurs during the third trimester, with Hispanic women appearing to be at particular risk. Listeriosis is a vertically transmitted infection that may cause miscarriage, stillbirth, preterm birth, or serious neonatal disease.

Some infections are vertically transmissible, meaning that they can affect the child as well.

The immune reconstitution inflammatory syndrome (IRIS) has been described in those with normal immune function with meningitis caused by "C. gattii" and "C. grubii". Several weeks or even months into appropriate treatment, there can be deterioration with worsening meningitis symptoms and progression or development of new neurological symptoms. IRIS is however much more common in those with poor immune function (≈25% vs. ≈8%).

Magnetic resonance imaging shows increase in the size of brain lesions, and CSF abnormalities (white cell count, protein, glucose) increase. Radiographic appearance of cryptococcal IRIS brain lesions can mimic that of toxoplasmosis with ring enhancing lesions on head computed tomography (CT). CSF culture is sterile, and there is no increase in CSF cryptococcal antigen titre.

The increasing inflammation can cause brain injury or be fatal.

The mechanism behind IRIS in cryptococcal meningitis is primarily immunologic. With reversal of immunosuppression, there is paradoxical increased inflammation as the recovering immune system recognises the fungus. In severe IRIS cases, treatment with systemic corticosteroids has been utilized - although evidence-based data are lacking.

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

Congenital disease occurs due to the acquisition of the organism by a pregnant woman exposed to tissue cysts or oocytes in uncooked meat or substances contaminated with cat feces. Spontaneous abortion may result if the disease is acquired during the first trimester.

Congenital toxoplasmosis may lead to hydrocephalus, seizures, lymphadenopathy, hepatosplenomegaly, rash, and fever. However, retinochoroiditis is the most common manifestation, occurring in 3/4 of cases.

In congenital toxoplasmosis, the disease is bilateral in 65–85% of cases and involves the macula in 58%.

Chronic or recurrent maternal infection during pregnancy is not thought to confer a risk of congenital toxoplasmosis because maternal immunity protects against fetal transmission. In contrast, pregnant women without serologic evidence of prior exposure to Toxoplasma should take sanitary precautions when cleaning up after cats and avoid undercooked meats.

"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.

Contact with farm animals can lead to disease in farmers or others that come into contact with infected animals. Glanders primarily affects those who work closely with horses and donkeys. Close contact with cattle can lead to cutaneous anthrax infection, whereas inhalation anthrax infection is more common for workers in slaughterhouses, tanneries and wool mills. Close contact with sheep who have recently given birth can lead to clamydiosis, or enzootic abortion, in pregnant women, as well as an increased risk of Q fever, toxoplasmosis, and listeriosis in pregnant or the otherwise immunocompromised. Echinococcosis is caused by a tapeworm which can be spread from infected sheep by food or water contaminated with feces or wool. Bird flu is common in chickens. While rare in humans, the main public health worry is that a strain of bird flu will recombine with a human flu virus and cause a pandemic like the 1918 Spanish flu. In 2017, free range chickens in the UK were temporarily ordered to remain inside due to the threat of bird flu. Cattle are an important reservoir of cryptosporidiosis and mainly affects the immunocompromised.

Protozoan infections are parasitic diseases caused by organisms formerly classified in the Kingdom Protozoa. They include organisms classified in Amoebozoa, Excavata, and Chromalveolata.

Examples include "Entamoeba histolytica", "Plasmodium" (some of which cause malaria), and "Giardia lamblia". "Trypanosoma brucei", transmitted by the tsetse fly and the cause of African sleeping sickness, is another example.

The species traditionally collectively termed "protozoa" are not closely related to each other, and have only superficial similarities (eukaryotic, unicellular, motile, though with exceptions). The terms "protozoa" (and protist) are usually discouraged in the modern biosciences. However, this terminology is still encountered in medicine. This is partially because of the conservative character of medical classification, and partially due to the necessity of making identifications of organisms based upon appearances and not upon DNA.

Protozoan infections in animals may be caused by organisms in the sub-class Coccidia (disease: Coccidiosis) and species in the genus "Besnoitia" (disease: Besnoitiosis).

Several pathogenic protozoans appear to be capable of sexual processes involving meiosis (or at least a modified form of meiosis). Included among these protozoans are "Plasmodium falciparum" (malaria), "Toxoplasma gondii" (toxoplasmosis), "Leishmania" species (leishmaniases), "Trypanosoma brucei" (African sleeping sickness), "Trypanosoma cruzi" (Chagas disease) and "Giardia intestinalis" (giardiasis).

"Babesia" parasites reproduce in red blood cells, where they can be seen as cross-shaped inclusions (four merozoites asexually budding, but attached together forming a structure looking like a "Maltese cross") and cause hemolytic anemia, quite similar to malaria.

Unlike the "Plasmodium" parasites that cause malaria, "Babesia" species lack an exoerythrocytic phase, so the liver is usually not affected.

In nonhuman animals, "Babesia canis rossi", "Babesia bigemina", and "Babesia bovis" cause particularly severe forms of the disease, including a severe haemolytic anaemia, with positive erythrocyte-in-saline-agglutination test indicating an immune-mediated component to the haemolysis. Common sequelae include haemoglobinuria "red-water", disseminated intravascular coagulation, and "cerebral babesiosis" caused by sludging of erythrocytes in cerebral capillaries.

In bovine species, the organism causes hemolytic anemia, so an infected animal shows pale mucous membranes initially. As the levels of bilirubin (a byproduct of red blood cell lysis) continue to increase, the visible mucous membranes become yellow in color (icterus) due to the failure of the liver to metabolize the excess bilirubin. Hemoglobinuria is seen due to excretion of red-blood-cell lysis byproducts via the kidneys. Fever of 40.5 °C (105 °F) develops due to release of inflammatory byproducts.

Babesiosis is a malaria-like parasitic disease caused by infection with "Babesia", a genus of Apicomplexa. Human babesiosis is an uncommon but emerging disease in the Northeastern and Midwestern United States and parts of Europe, and sporadic throughout the rest of the world. It occurs in warm weather. Ticks transmit the human strain of babesiosis, so it often presents with other tick-borne illnesses such as Lyme disease. After trypanosomes, "Babesia" is thought to be the second-most common blood parasite of mammals, and they can have a major impact on health of domestic animals in areas without severe winters. In cattle, a major host, the disease is known as Texas cattle fever, redwater, or piroplasmosis.

Individuals with a weak immune system are most at risk. This includes individuals taking immunosuppressive medication, cancer patients, HIV patients, premature babies with very low birth weight, the elderly, etc.

People who are at an increased risk of acquiring particular fungal infections in general may also be at an increased risk of developing fungal meningitis, as the infection may in some cases spread to the CNS. People residing in the Midwestern United States, and Southwestern United States and Mexico are at an increased risk of infection with "Histoplasma" and "Coccidioides", respectively.

Carrión's disease, or Oroya fever, or Peruvian wart is a rare infectious disease found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru, is caused by infection with the bacterium "Bartonella bacilliformis", and transmitted by sandflies of genus "Lutzomyia".

Cat scratch disease occurs worldwide. Cats are the main reservoir of "Bartonella henselae", and the bacterium is transmitted to cats by the cat flea "Ctenocephalides felis". Infection in cats is very common with a prevalence estimated between 40-60%, younger cats being more commonly infective. Cats usually become immune to the infection, while dogs may be very symptomatic. Humans may also acquire it through flea or tick bites from infected dogs, cats, coyotes, and foxes.

Trench fever, produced by "Bartonella quintana" infection, is transmitted by the human body louse "Pediculus humanus corporis". Humans are the only known reservoir. Thorough washing of clothing may help to interrupt the transmission of infection.

A possible role for ticks in transmission of "Bartonella" species remains to be elucidated; in November 2011, "Bartonella rochalimae", "B. quintana", and "B. elizabethae" DNA was first reported in "Rhipicephalus sanguineus" and "Dermacentor nitens" ticks in Peru.

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.

Treatment of infections caused by "Bartonella" species include:

Some authorities recommend the use of azithromycin.

Neonatal HSV rates in the U.S. are estimated to be between 1 in 3,000 and 1 in 20,000 live births. Approximately 22% of pregnant women in the U.S. have had previous exposure to HSV-2, and an additional 2% acquire the virus during pregnancy, mirroring the HSV-2 infection rate in the general population. The risk of transmission to the newborn is 30-57% in cases where the mother acquired a primary infection in the third trimester of pregnancy. Risk of transmission by a mother with existing antibodies for both HSV-1 and HSV-2 has a much lower (1-3%) transmission rate. This in part is due to the transfer of significant titer of protective maternal antibodies to the fetus from about the seventh month of pregnancy. However, shedding of HSV-1 from both primary genital infection and reactivations is associated with higher transmission from mother to infant.

HSV-1 neonatal herpes is extremely rare in developing countries because development of HSV-1 specific antibodies usually occurs in childhood or adolescence, precluding a later genital HSV-1 infection. HSV-2 infections are much more common in these countries. In industrialized nations, the adolescent HSV-1 seroprevalance has been dropping steadily for the last 5 decades. The resulting increase in the number of young women becoming sexually active while HSV-1 seronegative has contributed to increased HSV-1 genital herpes rates, and as a result, increased HSV-1 neonatal herpes in developed nations. A recent three-year study in Canada (2000–2003) revealed a neonatal HSV incidence of 5.9 per 100,000 live births and a case fatality rate of 15.5%. HSV-1 was the cause of 62.5% of cases of neonatal herpes of known type, and 98.3% of transmission was asymptomatic. Asymptomatic genital HSV-1 has been shown to be more infectious to the neonate, and is more likely to produce neonatal herpes, than HSV-2, However, with prompt application of antiviral therapy, the prognosis of neonatal HSV-1 infection is better than that for HSV-2.

Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become immunosuppressed. It presents with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. The worms enter the bloodstream from the bowel wall, simultaneously allowing entry of bowel bacteria such as "Escherichia coli". This may cause symptoms such as sepsis (bloodstream infection), and the bacteria may spread to other organs where they may cause localized infection such as meningitis.

Dissemination can occur many decades after the initial infection and has been associated with high dose corticosteroids, organ transplant, HIV, lepromatous leprosy, tertiary syphilis, aplastic anemia, malnutrition, advanced tuberculosis and radiation poisoning. It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are often unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is very small, so screening is usually not cost-effective, except in endemic areas.

It is important to note that there is not necessarily any eosinophilia in the disseminated disease. Absence of eosinophilia may indicate poor prognosis.