When physical examination of the newborn shows signs of a vertically transmitted infection, the examiner may test blood, urine, and spinal fluid for evidence of the infections listed above. Diagnosis can be confirmed by culture of one of the specific pathogens or by increased levels of IgM against the pathogen.

Some vertically transmitted infections, such as toxoplasmosis and syphilis, can be effectively treated with antibiotics if the mother is diagnosed early in her pregnancy. Many viral vertically transmitted infections have no effective treatment, but some, notably rubella and varicella-zoster, can be prevented by vaccinating the mother prior to pregnancy.

If the mother has active herpes simplex (as may be suggested by a pap test), delivery by Caesarean section can prevent the newborn from contact, and consequent infection, with this virus.

IgG antibody may play crucial role in prevention of intrauterine infections and extensive research is going on for developing IgG-based therapies for treatment and vaccination.

Typically, diagnosis involves several preliminary tests of immune function, including basic evaluation of the humoral immune system and the cell-mediated immune system. A WBC differential will reveal extremely elevated levels of neutrophils (on the order of 6-10x normal) because they are unable to leave the blood vessels.

In the case of LAD-I, specific diagnosis is done by flow cytometry. This technique will reveal absent or reduced CD18 expression in the leukocyte membrane. Recently, prenatal diagnosis systems has been established, allowing an early detection of the disease.

LAD-II diagnosis includes the study of different glycosilated forms of the transferrin protein. In LAD-III, as platelet function is also affected, this could be used to differentiate it from the other types.

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.

Any age may be affected although it is most common in children aged five to fifteen years. By the time adulthood is reached about half the population will have become immune following infection at some time in their past. Outbreaks can arise especially in nursery schools, preschools, and elementary schools. Infection is an occupational risk for school and day-care personnel. There is no vaccine available for human parvovirus B19, though attempts have been made to develop one.

Diagnosis is achieved most commonly by serologic testing of the blood for the presence of antibodies against the ehrlichia organism. Many veterinarians routinely test for the disease, especially in enzootic areas. During the acute phase of infection, the test can be falsely negative because the body will not have had time to make antibodies to the infection. As such, the test should be repeated. A PCR (polymerase chain reaction) test can be performed during this stage to detect genetic material of the bacteria. The PCR test is more likely to yield a negative result during the subclinical and chronic disease phases. In addition, blood tests may show abnormalities in the numbers of red blood cells, white blood cells, and most commonly platelets, if the disease is present. Uncommonly, a diagnosis can be made by looking under a microscope at a blood smear for the presence of the "ehrlichia" morulae, which sometimes can be seen as intracytoplasmic inclusion bodies within a white blood cell.

Treatment is supportive as the infection is frequently self-limiting. Antipyretics (i.e., fever reducers) are commonly used. The rash usually does not itch but can be mildly painful. There is no specific therapy.

The prognosis is good for dogs with acute ehrlichiosis. For dogs that have reached the chronic stage of the disease, the prognosis is guarded. When bone marrow suppression occurs and there are low levels of blood cells, the animal may not respond to treatment.

A 2009 study reported results from 36 children who had received a stem cell transplant. At the time of follow-up (median time 62 months), 75% of the children were still alive.

There is currently no known treatment for Aleutian virus. When evidence of ADV shows in a ferret, it is strongly recommended that a CEP (counterimmunoelectrophoresis) blood test or an IFA (immunoflourescent antibody) test be done. The CEP test is usually faster and less expensive than the IFA test, but the IFA test is more sensitive and can detect the disease in borderline cases.

Additionally modern methods such as Real-Time PCR allow for rapid and accurate detection as well as determination of the amount of viron present.

Prevention is best accomplished by stopping the spread of ADV. Any new ferret, or those who have been confirmed as serum positive for the virus should be perpetually isolated from other ferrets. All items that may have come into contact with the infected ferret should be cleaned with a 10% bleach solution.

This is a growing concern within mink producers as it is the most crucial infectious disease which affects farmed mink worldwide.

Doxycycline and minocycline are the medications of choice. For people allergic to antibiotics of the tetracycline class, rifampin is an alternative. Early clinical experience suggested that chloramphenicol may also be effective, however, in vitro susceptibility testing revealed resistance.

In the United States, certain breed clubs are strongly recommending screening for "Leishmania", especially in imported breeding stock from endemic locations. For reasons yet unidentified The Foxhound and Neapolitan Mastiff seem to be predisposed or at higher risk for disease. The Italian Spinone Club of America is also requesting all breeders and owners to submit samples for testing; the club reported 150 Spinone Italiano dogs have tested positive in the United States.

In the United States, the following veterinary colleges and government bodies assist with testing and treatment of "Leishmania"-positive dogs:

- Centers for Disease Control and Prevention on Leishmaniasis in dogs

- Iowa State University Department of Pathology

- North Carolina State University College of Veterinary Medicine

Diagnostic testing includes molecular biology and genetic techniques which provide high accuracy and high sensitivity/specificity. The most commonly employed methods in medical laboratories include Enzyme-Linked Immunosorbent Assays, aka ELISA (among other serological assays) and DNA amplification via Polymerase Chain Reaction (PCR).

The Polymerase Chain Reaction(PCR) method for detecting "Leishmania" DNA is a highly sensitive and specific test, producing accurate results in a relatively short amount of time.

A study completed in which Foxhounds were tested using PCR showed that approximately 20% of the tested dogs were positive for leishmaniasis; the same population tested with serological/antibody assays showed only 5% positive.

Diagnosis can be complicated by false positives caused by the leptospirosis vaccine and false negatives caused by testing methods lacking sufficient sensitivity.

The above signs, especially fever, respiratory signs, neurological signs, and thickened footpads occurring in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the signs of the disease and only recently has distinguishing between canine hepatitis, herpes virus, parainfluenza and leptospirosis been possible. Thus, finding the virus by various methods in the dog's conjunctival cells or foot pads gives a definitive diagnosis. In older dogs that develop distemper encephalomyelitis, diagnosis may be more difficult, since many of these dogs have an adequate vaccination history.

An additional test to confirm distemper is a brush border slide of the bladder transitional epithelium of the inside lining from the bladder, stained with Dif-Quick. These infected cells have inclusions which stain a carmine red color, found in the paranuclear cytoplasm readability. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper.

A number of vaccines against canine distemper exist for dogs (ATCvet code: and combinations) and domestic ferrets (), which in many jurisdictions are mandatory for pets. Infected animals should be quarantined from other dogs for several months owing to the length of time the animal may shed the virus. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris.

Despite extensive vaccination in many regions, it remains a major disease of dogs.

To prevent canine distemper, puppies should begin vaccination at six to eight weeks of age and then continue getting the “booster shot” every two to four weeks until they are 16 weeks of age. Without the full series of shots, the vaccination will not provide protection against the virus. Since puppies are typically sold at the age of eight to ten weeks, they typically receive the first shot while still with their breeder, but the new owner often does not finish the series. These dogs are not protected against the virus and so are susceptible to canine distemper infection, continuing the downward spiral that leads to outbreaks throughout the country.

Most patients recover completely within 1–2 months.

However many reported cases have lasted 18–24 months and longer.

This form usually lessens in severity within two years of diagnosis.

The use of prophylactic antibiotics has been proposed.

See article at BioMed Central site:

In areas where the known vector is a sandfly, deltamethrin collars worn by the dogs has been proven to be 86% effective. The sandfly is most active at dusk and dawn; keeping dogs indoors during those peak times will help minimize exposure.

Unfortunately, there is no one answer for leishmaniasis prevention, nor will one vaccine cover multiple species. "Different virulence factors have been identified for distinct "Leishmania" species, and there are profound differences in the immune mechanisms that mediate susceptibility/resistance to infection and in the pathology associated with disease."

In 2003, Fort Dodge Wyeth released the Leshmune vaccine in Brazil for "L. donovani" (also referred to as "kala-azar" in Brazil). Studies indicated up to 87% protection. Most common side effects from the vaccine have been noted as anorexia and local swelling.

The president of the Brazil Regional Council of Veterinary Medicine, Marcia Villa, warned since vaccinated dogs develop antibodies, they can be difficult to distinguish from asymptomatic, infected dogs.

Studies also indicate the Leshmune vaccine may be reliable in treating "L. chagasi", and a possible treatment for dogs already infected with "L. donovani".

No human vaccine is available for ehrlichiosis. Tick control is the main preventive measure against the disease. However, in late 2012 a breakthrough in the prevention of CME (canine monocytic ehrlichiosis) was announced when a vaccine was accidentally discovered by Prof. Shimon Harrus, Dean of the Hebrew University of Jerusalem's Koret School of Veterinary Medicine.

The cause of TEC is unknown, but it thought to be triggered by a viral infection. While rare cases have been attributed to infection with Parvovirus B19, the majority of cases are not related to Parvovirus infection. This is in contrast to transient aplastic crisis, seen in patients with hemoglobinopathies such as sickle cell disease, which is usually caused by Parvovirus infection.

SMEDI (an acronym of stillbirth, mummification, embryonic death, and infertility) is a reproductive disease of swine caused by "Porcine parvovirus" ("PPV") and "Porcine enterovirus". The term SMEDI usually indicates "Porcine enterovirus", but it also can indicate "Porcine parvovirus", which is a more important cause of the syndrome. SMEDI also causes abortion, neonatal death, and decreased male fertility.

From an economic standpoint SMEDI is an important disease because of the loss of productivity from fetal death in affected herds. Initial infection of a herd causes the greatest effect, but losses slow over time. The disease is spread most commonly by ingestion of food and water contaminated with infected feces and occasionally through sexual contact and contact with aborted tissue. A vaccine is available (ATCvet code: ).

SCID mice are routinely used as model organisms for research into the basic biology of the immune system, cell transplantation strategies, and the effects of disease on mammalian systems. They have been extensively used as hosts for normal and malignant tissue transplants. In addition, they are useful for testing the safety of new vaccines or therapeutic agents in immunocompromised individuals.

The condition is due to a rare recessive mutation on Chromosome 16 responsible for deficient activity of an enzyme involved in DNA repair (Prkdc or "protein kinase, DNA activated, catalytic polypeptide"). Because V(D)J recombination does not occur, the humoral and cellular immune systems fail to mature. SCID mice, therefore, present with impaired ability to make T or B lymphocytes, or activate some components of the complement system, and cannot efficiently fight infections, nor reject tumors and transplants.

By crossing SCID mice with mice carrying mutations in related genes, such as interleukin-2Rgamma, more efficient immunocompromised strains can be created to further aid research. The degree to which the various components of the immune system are compromised varies according to what other mutations the mice carry along with the SCID mutation.

Equine SCID is an autosomal recessive disorder that affects the Arabian horse. Similar to the "bubble boy" condition in humans, an affected foal is born with no immune system, and thus generally dies of an opportunistic infection, usually within the first four to six months of life. There is a DNA test that can detect healthy horses who are carriers of the gene causing SCID, thus testing and careful, planned matings can now eliminate the possibility of an affected foal ever being born.

SCID is one of six genetic diseases known to affect horses of Arabian bloodlines, and the only one of the six for which there is a DNA test to determine if a given horse is a carrier of the allele. There are other genetic diseases that affect other horse breeds, and horses of part-Arabian bloodlines can be carriers of SCID.

Unlike SCID in humans, which can be treated, for horses, to date, the condition remains a fatal disease. When a horse is heterozygous for the gene, it is a carrier, but perfectly healthy and has no symptoms at all. If two carriers are bred together, however, classic Mendelian genetics indicate that there is a 50% chance of any given mating producing a foal that is a carrier heterozygous for the gene, and a 25% risk of producing a foal affected by the disease. If a horse is found to carry the gene, the breeder can choose to geld a male or spay a female horse so that they cannot reproduce, or they can choose to breed the known carrier only to horses that have been tested and found to be "clear" of the gene. In either case, careful breeding practices can avoid ever producing an SCID-affected foal.

Autoimmune neutropenia is a form of neutropenia which is most common in infants and young children where the body identifies the neutrophils as enemies and makes antibody to destroy them.

Primary autoimmune neutropenia (AIN) is an autoimmune disease first reported in 1975 that primarily occurs in infancy. In autoimmune neutropenia, the immune system produces autoantibodies directed against the neutrophilic protein antigens in white blood cells known as granulocytic neutrophils (granulocytes, segmented neutrophils, segs, polysegmented neutrophils, polys). These antibodies destroy granulocytic neutrophils. Consequently, patients with autoimmune neutropenia have low levels of granulocytic neutrophilic white blood cells causing a condition of neutropenia. Neutropenia causes an increased risk of infection from organisms that the body could normally fight easily.

Who is Affected?

Primary autoimmune neutropenia has been reported as early as the second month of life although most cases are diagnosed in children between 5 and 15 months of age. Girls have a slightly higher risk of developing AIN than boys. In neutropenia discovered at birth or shortly after birth, a diagnosis of allo-immune neutropenia (from maternal white blood cell antibodies passively transferred to the infant) is more likely.

Neutropenia

In infants neutropenia is defined by absolute neutrophil counts less than 1000/uL. After the first year of life neutropenia is defined by absolute counts less than 1500/uL. Neutropenia may be primary in which it is the only blood abnormality seen. In secondary neutropenia, other primary conditions occur, including other autoimmune diseases, infections, and malignancies. Neutropenia is considered chronic when it persists for more than 6 months.

Symptoms and Disease Course

Neutropenia, which may be discovered on routine blood tests, typically causes benign infections even when the condition is severe. Ear infections (otitis media) are the most common infection seen in autoimmune neutropenia and typically infection responds to antibiotic treatment alone. Infections associated with primary AIN are usually mild and limited, including skin infections such as impetigo, gastroenteritis, upper respiratory tract infections, and ear infections. Rarely, cellulitis and abscesses may occur.

Studies of children studied for up to six years showed that most cases of autoimmune neutropenia resolved spontaneously after a median of 17 months. In 80 percent of patients, neutropenia persisted for 7 to 24 months.

Diagnosis

Patients with autoimmune neutropenia are diagnosed on the basis of blood tests showing neutropenia and the presence of granulocyte-specific antibodies. In some cases, tests for granulocyte-specific antibodies need to be repeated several times before a positive result is seen. Bone marrow aspiration, if performed, is typically normal or it can show increased cell production with a variably diminished number of segmented granulocytes.

s association with prior parvovirus B19 has been made, but this hasn’t been confirmed. Similar to the platelet deficiency idiopathic thrombocytopenic purpura, vaccines are suspected of triggering this disorder.

Treatment

Treatment consists of corticosteroids to reduce autoantibody production, antibiotics to prevent infection and granulocyte colony-stimulating factor (G-CSF) to temporarily increase neutrophil counts. In cases of severe infection or the need for surgery, intravenous immunoglobulin therapy may be used.

This depends on the age of the animal affected and the efficiency of its immune system.

Colostral protection lasts up to 5 months of age, after which it decreases to an all-time low to increase yet again at about 12 months of age.

- Prenatal infection: virus travels from infected mother to fetus via the placenta. In this case, the time of gestation determines the result of the infection.

- If the fetus is infected in the first 30 days of fetal life, death and absorption of all, or some of the fetuses may occur. In this case, some immunotolerant healthy piglets may be born.

- If the infection happens at 40 days, death and mummification may occur. Also in this case, some or all the fetuses are involved, i.e. some of the fetuses can be born healthy and immunotolerant, or else carriers of the disease.

- If the viruses crosses the placenta in the last trimester, neonatal death may occur, or the birth of healthy piglets with a protective pre-colostral immunity.

- Postnatal infection (pigs up to 1 year of age): Infection occurs oro-nasally, followed by a viremic period associated with transitory leucopenia.

- Infection in adults (over 1 year of age): These subject would have an active, protective immune system which protects them from future exposures (e.g. mating with an infected male).

Therefore, it is important to note that the virus is particularly dangerous for the sow in her first gestation, which would be at 7–8 months of age, as she would have a particularly low antibody count at this age and could easily contract the virus via copulation.