Though caused by different infections, the signs and symptoms of TORCH syndrome are consistent. They include hepatosplenomegaly (enlargement of the liver and spleen), fever, lethargy, difficulty feeding, anemia, petechiae, purpurae, jaundice, and chorioretinitis. The specific infection may cause additional symptoms.

TORCH syndrome may develop before birth, causing stillbirth, in the neonatal period, or later in life.

TORCH syndrome is caused by in utero infection with one of the TORCH agents, disrupting fetal development.

Fifth disease starts with a low-grade fever, headache, rash, and cold-like symptoms, such as a runny or stuffy nose. These symptoms pass, then a few days later the rash appears. The bright red rash most commonly appears in the face, particularly the cheeks. This is a defining symptom of the infection in children (hence the name "slapped cheek disease"). Occasionally the rash will extend over the bridge of the nose or around the mouth. In addition to red cheeks, children often develop a red, lacy rash on the rest of the body, with the upper arms, torso, and legs being the most common locations. The rash typically lasts a couple of days and may itch; some cases have been known to last for several weeks. Patients are usually no longer infectious once the rash has appeared.

Teenagers and adults may present with a self-limited arthritis. It manifests in painful swelling of the joints that feels similar to arthritis. Older children and adults with fifth disease may have difficulty in walking and in bending joints such as wrists, knees, ankles, fingers, and shoulders.

The disease is usually mild, but in certain risk groups it can have serious consequences:

- In pregnant women, infection in the first trimester has been linked to hydrops fetalis, causing spontaneous miscarriage.

- In people with sickle-cell disease or other forms of chronic hemolytic anemia such as hereditary spherocytosis, infection can precipitate an aplastic crisis.

- Those who are immuno-compromised (HIV/AIDS, chemotherapy) may be at risk for complications if exposed.

The signs and symptoms of a vertically transmitted infection depend on the individual pathogen. It may cause subtle signs such as a influenza-like illness and may not even be noticed by the mother during the pregnancy. In such cases, the effects may be seen first at birth.

Symptoms of a vertically transmitted infection may include fever and flu like symptoms. The newborn is often small for gestational age. A petechial rash on the skin may be present, with small reddish or purplish spots due to bleeding from capillaries under the skin. An enlarged liver and spleen (hepatosplenomegaly) is common, as is jaundice. However, jaundice is less common in hepatitis B because a newborn's immune system is not developed well enough to mount a response against liver cells, as would normally be the cause of jaundice in an older child or adult. Hearing impairment, eye problems, mental retardation, autism, and death can be caused by vertically transmitted infections. The mother often has a mild infection with few or no symptoms.

The genetic conditions of Aicardi-Goutieres syndrome are possibly present in a similar manner.

Erythema infectiosum or fifth disease is one of several possible manifestations of infection by parvovirus B19.

The name "fifth disease" comes from its place on the standard list of rash-causing childhood diseases, which also includes measles (1st), scarlet fever (2nd), rubella (3rd), Dukes' disease (4th, however is no longer widely accepted as distinct) and roseola (6th).

LAD was first recognized as a distinct clinical entity in the 1970s. The classic descriptions of LAD included recurrent bacterial infections, defects in neutrophil adhesion, and a delay in umbilical cord sloughing. The adhesion defects result in poor leukocyte chemotaxis, particularly neutrophil, inability to form pus and neutrophilia.

Individuals with LAD suffer from bacterial infections beginning in the neonatal period. Infections such as omphalitis, pneumonia, gingivitis, and peritonitis are common and often life-threatening due to the infant's inability to properly destroy the invading pathogens. These individuals do not form abscesses because granulocytes cannot migrate to the sites of infection.

The severe combined immunodeficiency (SCID) is a severe immunodeficiency genetic disorder that is characterized by the complete inability of the adaptive immune system to mount, coordinate, and sustain an appropriate immune response, usually due to absent or atypical T and B lymphocytes. In humans, SCID is colloquially known as "bubble boy" disease, as victims may require complete clinical isolation to prevent lethal infection from environmental microbes.

Several forms of SCID occur in animal species. Not all forms of SCID have the same cause; different genes and modes of inheritance have been implicated in different species.

Transient erythroblastopenia of childhood (TEC) is a slowly developing anemia of early childhood characterized by gradual onset of pallor.

A vertically transmitted infection is an infection caused by pathogens (such as bacteria and viruses) that uses mother-to-child transmission, that is, transmission directly from the mother to an embryo, fetus, or baby during pregnancy or childbirth. It can occur when the mother gets an infection as an intercurrent disease in pregnancy. Nutritional deficiencies may exacerbate the risks of perinatal 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: ).

Cat flu is the common name for a feline upper respiratory tract disease. While feline upper respiratory disease can be caused by several different pathogens, there are few symptoms that they have in common.

While Avian Flu can also infect cats, Cat flu is generally a misnomer, since it usually does not refer to an infection by an influenza virus. Instead, it is a syndrome, a term referring to the fact that patients display a number of symptoms that can be caused by one or more of the following infectious agents (pathogens):

1. Feline herpes virus causing feline viral rhinotracheitis (cat common cold, this is the disease that is closely similar to cat flu)

2. Feline calicivirus—(cat respiratory disease)

3. "Bordetella bronchiseptica"—(cat kennel cough)

4. "Chlamydophila felis"—(chlamydia)

In South Africa the term cat flu is also used to refer to Canine Parvo Virus. This is misleading, as transmission of the Canine Parvo Virus rarely involves cats.

Individuals with TEC have a median age of presentation of 18–26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years.

Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels.

Leukocyte adhesion deficiency (LAD), is a rare autosomal recessive disorder characterized by immunodeficiency resulting in recurrent infections. LAD is currently divided into three subtypes: LAD1, LAD2, and the recently described LAD3, also known as LAD-1/variant. In LAD3, the immune defects are supplemented by a Glanzmann thrombasthenia-like bleeding tendency.

In dogs, signs of distemper vary widely from no signs, to mild respiratory signs indistinguishable from kennel cough, to severe pneumonia with vomiting, bloody diarrhea and death.

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue. Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time, this tic will usually diminish somewhat in its severity.

A dog that survives distemper will continue to have both nonlife-threatening and life-threatening signs throughout its lifespan. The most prevalent nonlife-threatening symptom is hard pad disease. This occurs when a dog experiences the thickening of the skin on the pads of its paws as well as on the end of its nose. Another lasting symptom commonly is enamel hypoplasia. Puppies, especially, will have damage to the enamel of teeth that are not completely formed or those that have not yet grown through the gums. This is a result of the virus's killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.

Life-threatening signs usually include those due to the degeneration of the nervous system. Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can acquire more severe seizures, paralysis, reduction in sight and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.

The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, vasculitis, lymphadenopathy, discharge from the nose and eyes, and edema of the legs and scrotum. There are no outward signs of the subclinical phase. Clinical signs of the chronic phase include weight loss, pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease. Dogs that are severely affected can die from this disease.

Although people can get ehrlichiosis, dogs do not transmit the bacteria to humans; rather, ticks pass on the "ehrlichia" organism. Clinical signs of human ehrlichiosis include fever, headache, eye pain, and gastrointestinal upset. It is quite similar to Rocky Mountain spotted fever, but rash is not seen in patients.

Histologically, the pregnant sow suffers lesions in the myometrium due to the infiltration of monocytes.

The fetus presents: retarded growth, congestion of superficial vessels which may be associated with hemorrhage and dehydration which results in mummification of the fetus.

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.

Porcine circoviral disease (PCVD) and Porcine circovirus associated disease (PCVAD), is a disease seen in domestic pigs. This disease causes illness in piglets, with clinical signs including progressive loss of body condition, visibly enlarged lymph nodes, difficulty in breathing, and sometimes diarrhea, pale skin, and jaundice. PCVD is very damaging to the pig-producing industry and has been reported worldwide. PCVD is caused by porcine circovirus type 2 (PCV-2).

The North American industry endorses "PCVAD" and European use "PCVD" to describe this disease.

The most common symptoms include headache, muscle aches, and fatigue. A rash may occur, but is uncommon. Ehrlichiosis can also blunt the immune system by suppressing production of TNF-alpha, which may lead to opportunistic infections such as candidiasis.

Most of the signs and symptoms of ehrlichiosis can likely be ascribed to the immune dysregulation that it causes. A "toxic shock-like" syndrome is seen in some severe cases of ehrlichiosis. Some cases can present with purpura and in one such case the organisms were present in such overwhelming numbers that in 1991 Dr. Aileen Marty of the AFIP was able to demonstrate the bacteria in human tissues using standard stains, and later proved that the organisms were indeed Ehrlichia using immunoperoxidase stains.

Experiments in mouse models further supports this hypothesis, as mice lacking TNF-alpha I/II receptors are resistant to liver injury caused by ehrlichia infection.

3% of human monocytic ehrlichiosis cases result in death; however, these deaths occur "most commonly in immunosuppressed individuals who develop respiratory distress syndrome, hepatitis, or opportunistic nosocomial infections."

The domestic ferret is known to be affected by several distinct ferret health problems. Among the most common are cancers affecting the adrenal glands, pancreas, and lymphatic system. Viral diseases include canine distemper and influenza. Certain health problems have also been linked to ferrets being neutered before sexual maturity was reached. Certain colors of ferret may also carry a genetic defect known as Waardenburg syndrome. Similar to domestic cats, ferrets may also be affected by hairballs, or dental problems.

Aleutian disease, also known as mink plasmacytosis, is a disease which causes spontaneous abortion and death in minks and ferrets. It is caused by "Carnivore amdoparvovirus 1" (also known as "Aleution diease virus", ADV), a highly contagious parvovirus in the genus "Amdoparvovirus".

The virus has been found as a natural infection in the "Mustelidae" family within mink, ferrets, otters, polecats, stone and pine martens and within other varying carnivores such as skunks, genets, foxes and raccoons. This is most commonly explained as because they all share resources and habitats.

Adrenal disease, a growth of the adrenal glands that can be either hyperplasia or cancer, is most often diagnosed by signs like unusual hair loss, increased aggression, constant grooming of owner or other ferrets as well as themselves, difficulty urinating (caused by an enlarged prostate) or defecating, or agitation when urinating, and (in the case of females) an enlarged vulva. Signs of an enlarged prostate should be considered an emergency; even if the growth is benign, it can still cause a hormonal imbalance which can have devastating effects on the ferret's health.

Treatment options include surgery or cryosurgery to excise the affected glands, melatonin or deslorelin implants, which treat the symptoms but not the disease itself, and/or hormone therapy. The causes of adrenal disease are as yet uncertain, but speculated triggers include unnatural light cycles, diets based around processed ferret foods, and prepubescent neutering. It has also been suggested that there may be a hereditary component to adrenal disease.

Adrenal disease is usually detected during the spring or fall, as it affects the hormones that make the fur grow. When affected ferrets shed their winter coat, the fur does not grow back. The hair loss pattern is usually very specific for adrenal disease. It begins at the base of the tail and then continues up the back. Ferrets treated for adrenal disease may temporarily have severe hair loss as their bodies recover.

A lethal infection in mink, the Aleutian disease virus lies dormant in ferrets until stress or injury allows it to surface. While the parvovirus itself causes little or no harm to the ferret host, the large number of antibodies produced in response to the presence of the virus results in a systemic vasculitis, resulting in eventual renal failure, bone marrow suppression and death.

The symptoms are chronic, progressive weight loss, lethargy, splenomegaly (enlarged spleen), anemia, rear leg weakness, seizures and black tarry stool. Additional symptoms include poor reproduction and/or oral bleeding/gastrointestinal bleeding. Lesions can also be found within the pelt depending on the severity of the disease. This virus can unfortunately reduce fitness of wild mink especially, by disturbing both the productivity within adult females and the overall survivor rates of both juveniles and adults. Likewise, in the mink kits that survive, it infects the alveolar cells and ultimately causes respiratory distress, possibly leading to death.

Once symptoms show themselves, the disease progresses rapidly, usually to death within a few months.

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.