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.

The earliest symptoms of shingles, which include headache, fever, and malaise, are nonspecific, and may result in an incorrect diagnosis. These symptoms are commonly followed by sensations of burning pain, itching, hyperesthesia (oversensitivity), or paresthesia ("pins and needles": tingling, pricking, or numbness). Pain can be mild to extreme in the affected dermatome, with sensations that are often described as stinging, tingling, aching, numbing or throbbing, and can be interspersed with quick stabs of agonizing pain.

Shingles in children is often painless, but people are more likely to get shingles as they age, and the disease tends to be more severe.

In most cases after one to two days, but sometimes as long as three weeks, the initial phase is followed by the appearance of the characteristic skin rash. The pain and rash most commonly occurs on the torso, but can appear on the face, eyes or other parts of the body. At first the rash appears similar to the first appearance of hives; however, unlike hives, shingles causes skin changes limited to a dermatome, normally resulting in a stripe or belt-like pattern that is limited to one side of the body and does not cross the midline. "Zoster sine herpete" ("zoster without herpes") describes a person who has all of the symptoms of shingles except this characteristic rash.

Later the rash becomes vesicular, forming small blisters filled with a serous exudate, as the fever and general malaise continue. The painful vesicles eventually become cloudy or darkened as they fill with blood, and crust over within seven to ten days; usually the crusts fall off and the skin heals, but sometimes, after severe blistering, scarring and discolored skin remain.

Anterior uveitis develops in 40–50% of cases with HZO within 2 weeks of onset of the skin rashes. Typical HZO keratitis at least mild iritis, especially if Hutchinson's sign is positive for the presence of vescicles upon the tip of the nose.

Features:

This non-granulomatous iridocyclitis is associated with:

- Small keratic precipitates

- Mild aqueous flare

- Occasionally haemorrhagic hypopion.

HZO uveitis is associated with complications such as iris atrophy and secondary glaucoma are not uncommon. Complicated cataract may develop in the late stages of the disease.

Shingles may have additional symptoms, depending on the dermatome involved. The trigeminal nerve is the most commonly involved nerve, of which the ophthalmic division is the most commonly involved branch. When the virus is reactivated in this nerve branch it is termed "zoster ophthalmicus". The skin of the forehead, upper eyelid and orbit of the eye may be involved. Zoster ophthalmicus occurs in approximately 10% to 25% of cases. In some people, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain.

"Shingles oticus", also known as Ramsay Hunt syndrome type II, involves the ear. It is thought to result from the virus spreading from the facial nerve to the vestibulocochlear nerve. Symptoms include hearing loss and vertigo (rotational dizziness).

Shingles may occur in the mouth if the maxillary or mandibular division of the trigeminal nerve is affected, in which the rash may appear on the mucous membrane of the upper jaw (usually the palate, sometimes the gums of the upper teeth) or the lower jaw (tongue or gums of the lower teeth) respectively. Oral involvement may occur alone or in combination with a rash on the skin over the cutaneous distribution of the same trigeminal branch. As with shingles of the skin, the lesions tend to only involve one side, distinguishing it from other oral blistering conditions. In the mouth, shingles appears initially as 1–4 mm opaque blisters (vesicles), which break down quickly to leave ulcers that heal within 10–14 days. The prodromal pain (before the rash) may be confused with toothache. Sometimes this leads to unnecessary dental treatment. Post herpetic neuralgia uncommonly is associated with shingles in the mouth. Unusual complications may occur with intra-oral shingles that are not seen elsewhere. Due to the close relationship of blood vessels to nerves, the virus can spread to involve the blood vessels and compromise the blood supply, sometimes causing ischemic necrosis. Therefore, oral involvement rarely causes complications such as osteonecrosis, tooth loss, periodontitis (gum disease), pulp calcification, pulp necrosis, periapical lesions and tooth developmental anomalies.

Mollaret's meningitis is characterized by chronic, recurrent episodes of headache, stiff neck, meningismus, and fever; cerebrospinal fluid (CSF) pleocytosis with large "endothelial" cells, neutrophil granulocytes, and lymphocytes; and attacks separated by symptom-free periods of weeks to years; and spontaneous remission of symptoms and signs. Many people have side effects between bouts that vary from chronic daily headaches to after-effects from meningitis such as hearing loss and visual impairment, nerve pain and twitches. Symptoms may be mild or severe. Some cases may be short, lasting only 3–7 days, while others last for weeks to months.

While herpes simplex and varicella can cause rash, Mollaret's patients may or may not have a rash. Herpes simplex virus is likely the most common cause of Mollaret's meningitis.

Progressive outer retinal necrosis, also known as Varicella zoster virus retinitis (VZVR), is an aggressive, necrotizing inflammation of the eye's retina caused by herpes varicella zoster virus. It is typically found in people with advanced AIDS, but has also been reported in those who are severely immunocompromised due to chemotherapy.

The majority of those with progressive outer retinal necrosis develop severe vision loss and blindness. Systemic antiviral drugs may improve the long-term visual outcome in those with the disease.

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

Mollaret's meningitis is a recurrent or chronic inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. Since Mollaret's meningitis is a recurrent, benign (non-cancerous), aseptic meningitis, it is now referred to as benign recurrent lymphocytic meningitis. It was named for Pierre Mollaret, the French neurologist who first described it in 1944.

Although chronic meningitis has been defined as "irritation and inflammation of the meninges persisting for more than 4 weeks being associated with pleocytosis in the cerebrospinal fluid", cerebrospinal fluid abnormalities may not be detectable for the entire time. Diagnosis can be elusive, as Helbok et al. note: "in reality, many more weeks, even months pass by until the diagnosis is established. In many cases the signs and symptoms of chronic meningitis not only persist for periods longer than 4 weeks, they even progress with continuing deterioration, i. e. headache, neck stiffness and even low grade fever. Impairment of consciousness, epileptic seizures, neurological signs and symptoms may evolve over time."

Erythema toxicum neonatorum (also known as erythema toxicum, urticaria neonatorum and toxic erythema of the newborn) is a common rash in neonates. It appears in up to half of newborns carried to term, usually between day 2–5 after birth; it does not occur outside the neonatal period.

Erythema toxicum is characterized by blotchy red spots on the skin with overlying white or yellow papules or pustules. These lesions may be few or numerous. The eruption typically resolves within first two weeks of life, and frequently individual lesions will appear and disappear within minutes or hours. It is a benign condition thought to cause no discomfort to the baby.

Acute cerebellar ataxia usually follows 2–3 weeks after an infection. Onset is abrupt. Vomiting may be present at the onset but fever and nuchal rigidity characterestically are absent. Horizontal nystagmus is present is approximately 50% of cases.

- Truncal ataxia with deterioration of gait

- Slurred speech and nystagmus

- Afebrile

The rash is composed of small papular lesions, each on a separate reddened base.

Symptoms:

- With resolution of the herpes zoster eruption, pain that continues for three months or more is defined as postherpetic neuralgia.

- Pain is variable, from discomfort to very severe, and may be described as burning, stabbing, or gnawing.

Signs:

- Area of previous herpes zoster may show evidence of cutaneous scarring.

- Sensation may be altered over the areas involved, in the form of either hypersensitivity or decreased sensation.

- In rare cases, the patient might also experience muscle weakness, tremor, or paralysis if the nerves involved also control muscle movement.

The signs and symptoms of DOCK8 deficiency are similar to the autosomal dominant form, STAT3 deficiency. However, in DOCK8 deficiency, there is no skeletal or connective tissue involvement, and affected individuals do not have the characteristic facial features of those with autosomal dominant hyper-IgE syndrome. DOCK8 deficient children often have eczema, respiratory and skin staphylococcus infections.

Beyond these, many other recurrent infections have been observed, including recurrent fungal infections and recurrent viral infections (including molluscum contagiosum, herpes simplex, and herpes zoster), recurrent upper respiratory infection (including "Streptococcus pneumoniae", "Haemophilus influenzae", respiratory syncytial virus, and adenovirus), recurrent sinusitis, recurrent otitis media, mastoiditis, pneumonia, bronchitis with bronchiectasis, osteomyelitis, candidiasis, meningitis (caused by cryptococcus or H. influenzae), pericarditis, salmonella enteritis, and giardiasis. Other dermatologic problems include squamous-cell carcinoma/dysplasia (vulvar, anal, and facial). Immune problems are also common, including autoimmune hemolytic anemia, severe allergies (both food and environmental), asthma, and reactive airway disease. The nervous system may also be affected; observed conditions in DOCK8 deficient people include hemiplegia, ischemic stroke, subarachnoid hemorrhage, and facial paralysis. Vascular complications are common, including aortic aneurysm, cerebral aneurysm, vessel occlusion and underperfusion, and leukocytoclastic vasculitis.

Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles. Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.

Herpetic keratoconjunctivitis, a primary infection, typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.

Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpetic whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS, are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder, and Alzheimer's disease, although this is often dependent on the genetics of the infected person.

In all cases, HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1-infected individuals, seroconversion after an oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.

Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days before recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus ceases.

The condition usually resolves by itself within a couple of weeks. The rash may, however, last for up to one month. Chickenpox is contagious starting from one to two days before the appearance of the rash and lasts until the lesions have crusted.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the "varicella zoster" virus decades after the initial, often childhood, chickenpox infection.

Patients with ARN typically present

- floaters

- redness of the eye

- flashes

- decreased sharpness of vision

- photophobia.

Though uncommon, some patients may experience pain. Most patients will only experience this in one eye (unilateral), though possible for the condition to be seen in both (bilateral, BARN). If the first eye is left without treatment, some cases have shown the disease progressing to the other eye in a month's time. Further progressed stages of the disease can cause blindness in the eye experiencing ARN. Though the disease may be present itself, the inflammation of the retina may not been visualized for decades after the initial signs.

Viral meningitis characteristically presents with fever, headache and neck stiffness. Fever is the result of cytokines released that affect the thermoregulatory neurons of the hypothalamus. Cytokines and increased intracranial pressure stimulate nociceptors in the brain that lead to headaches. Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine. In contrast to bacterial meningitis, symptoms are often less severe and do not progress as quickly. Nausea, vomiting and photophobia (light sensitivity) also commonly occur, as do general signs of a viral infection, such as muscle aches and malaise. Increased cranial pressure from viral meningitis stimulates the area postrema, which causes nausea and vomiting. Photophobia is due to meningeal irritation. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits.

Babies with viral meningitis may only appear irritable, sleepy or have trouble eating. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits. The pediatric population may show some additional signs and symptoms that include jaundice and bulging fontanelles.

Acute cerebellar ataxia of childhood is a childhood condition characterized by an unsteady gait, most likely secondary to an autoimmune of postinfectious cause, drug induced or paraneoplastic. Most common virus causing acute cerebellar ataxia are Chickenpox virus and Epstein Barr Virus. It is a diagnosis of exclusion.

Postherpetic neuralgia is a nerve pain due to damage caused by the varicella zoster virus. Typically, the neuralgia is confined to a dermatomic area of the skin, and follows an outbreak of herpes zoster (commonly known as shingles) in that same dermatomic area. The neuralgia typically begins when the herpes zoster vesicles have crusted over and begun to heal, but can begin in the absence of herpes zoster—a condition called "zoster sine herpete" (see Herpes zoster).

Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality. Increased numbers of white blood cells can be found in patient's cerebrospinal fluid, without the presence of pathogenic bacteria and fungi. Patients typically have a fever and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure). Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap) for presence of the virus. The testing takes several days to perform, and patients with suspected Herpes encephalitis should be treated with acyclovir immediately while waiting for test results.

Acantholysis is the loss of intercellular connections, such as desmosomes, resulting in loss of cohesion between keratinocytes, seen in diseases such as pemphigus vulgaris. It is absent in bullous pemphigoid, making it useful for differential diagnosis.

This histological feature is also seen in herpes simplex infections (HSV 1 and 2) and varicella zoster infections (chicken pox and shingles).

An exanthem or exanthema (from Greek ἐξάνθημα "exánthēma", "a breaking out") is a widespread rash usually occurring in children. An exanthem can be caused by toxins, drugs, or microorganisms, or can result from autoimmune disease.

It can be contrasted with an enanthem.

The symptoms and signs include acute facial nerve paralysis, pain in the ear, taste loss in the front two-thirds of the tongue, dry mouth and eyes, and an erythematous vesicular rash in the ear canal, the tongue, and/or hard palate.

Since the vestibulocochlear nerve is in proximity to the geniculate ganglion, it may also be affected, and patients may also suffer from tinnitus, hearing loss, and vertigo. Involvement of the trigeminal nerve can cause numbness of the face.