People with herpes esophagitis experience pain with eating and trouble swallowing. Other symptoms can include food impaction, hiccups, weight loss, fever, and on rare occasions upper gastrointestinal bleeding as noted in the image above and tracheoesophageal fistula. Frequently one can see herpetiform lesions in the mouth and lips.

Fungal meningitis refers to meningitis caused by a fungal infection.

Symptoms of fungal meningitis are generally similar to those of other types of meningitis, and include: a fever, stiff neck, severe headache, photophobia (sensitivity to light), nausea and vomiting, and altered mental status (drowsiness or confusion).

Pulmonary infection

- Produces a virulent form of pneumonia (progressive)

- Night sweats, fever, cough, chest pain

- Pulmonary nocardiosis is subacute in onset and refractory to standard antibiotherapy

- Symptoms are more severe in immunocompromised individuals

- Radiologic studies show multiple pulmonary infiltrates with tendency to central necrosis

Neurological infection

- Headache, lethargy, confusion, seizures, sudden onset of neurological deficit

- CT scan shows cerebral abscess

- Nocardial meningitis is difficult to diagnose

Cardiac conditions

- Nocardia has been highly linked to endocarditis as a main manifestation

- In recorded cases, it has caused damage to heart valves whether natural or prosthetic

Lymphocutaneous disease

- Nocardial cellulitis is akin to erysipelas but is less acute

- Nodular lymphangeitis mimics sporotrichosis with multiple nodules alongside a lymphatic pathway

- Chronic subcutaneous infection is a rare complication and osteitis may ensue

- May be misidentified and treated for as a staph infection, specifically superficial skin infections

- Cultures must sit more than 48 hours to guarantee an accurate test

Ocular disease

- Very rarely nocardiae cause keratitis

- Generally there is a history of ocular trauma

Disseminated nocardiosis

- Dissemination occurs through the spreading enzymes possessed by the bacteria

- Disseminated infection can occur in very immunocompromised patients

- It generally involves both lungs and brain

- Fever, moderate or very high can be seen

- Multiple cavitating pulmonary infiltrates develop

- Cerebral abscesses arise later

- Cutaneous lesions are very rarely seen

- If untreated, the prognosis is poor for this form of disease

Neonatal herpes manifests itself in three forms: skin, eyes, and mouth herpes (SEM) sometimes referred to as "localized", disseminated herpes (DIS), and central nervous system herpes(CNS).

- SEM herpes is characterized by external lesions but no internal organ involvement. Lesions are likely to appear on trauma sites such as the attachment site of fetal scalp electrodes, forceps or vacuum extractors that are used during delivery, in the margin of the eyes, the nasopharynx, and in areas associated with trauma or surgery (including circumcision).

- DIS herpes affects internal organs, particularly the liver.

- CNS herpes is an infection of the nervous system and the brain that can lead to encephalitis. Infants with CNS herpes present with seizures, tremors, lethargy, and irritability, they feed poorly, have unstable temperatures, and their fontanelle (soft spot of the skull) may bulge.

CNS herpes is associated with highest morbidity, and DIS herpes has a higher mortality rate. These categories are not mutually exclusive and there is often overlap of two or more types. SEM herpes has the best prognosis of the three, however, if left untreated it may progress to disseminated or CNS herpes with its attendant increases in mortality and morbidity.

Death from neonatal HSV disease in the U.S. is currently decreasing; The current death rate is about 25%, down from as high as 85% in untreated cases just a few decades ago. Other complications from neonatal herpes include prematurity with approximately 50% of cases having a gestation of 38 weeks or less, and a concurrent sepsis in approximately one quarter of cases that further clouds speedy diagnosis.

Upper Endoscopy often reveals ulcers throughout the esophagus with intervening normal-appearing mucosa. In severe cases the ulcers can coalesce and on rare occasions have a black appearance known as black esophagus. While the diagnosis of herpes esophagitis can be inferred clinically it can only be accurately diagnosed through endoscopically obtained biopsies with microscopic evaluation by a pathologist finding the appropriate inclusion bodies and diagnostic immunochemical staining. False negative findings may occur if biopsies are taken from the ulcer rather than from the margin of the ulcer as the inclusion particles are to be found in viable epithelial cells. Viral tissue culture represents the most accurate means of diagnosing the precise cause.

Nocardiosis is an infectious disease affecting either the lungs ("pulmonary nocardiosis") or the whole body ("systemic nocardiosis"). It is due to infection by bacterium of the genus Nocardia, most commonly "Nocardia asteroides" or "Nocardia brasiliensis".

It is most common in men, especially those with a weakened immune system. In patients with brain infection, mortality exceeds 80%; in other forms, mortality is 50%, even with appropriate therapy.

It is one of several conditions that have been called the great imitator. Cutaneous nocardiosis commonly occurs in immunocompetent hosts.

If symptoms of histoplasmosis infection occur, they will start within 3 to 17 days after exposure; the average is 12–14 days. Most affected individuals have clinically silent manifestations and show no apparent ill effects. The acute phase of histoplasmosis is characterized by non-specific respiratory symptoms, often cough or flu-like. Chest X-ray findings are normal in 40–70% of cases. Chronic histoplasmosis cases can resemble tuberculosis; disseminated histoplasmosis affects multiple organ systems and is fatal unless treated.

While histoplasmosis is the most common cause of mediastinitis, this remains a relatively rare disease. Severe infections can cause hepatosplenomegaly, lymphadenopathy, and adrenal enlargement. Lesions have a tendency to calcify as they heal.

Presumed ocular histoplasmosis syndrome (POHS) causes chorioretinitis, where the choroid and retina of the eyes are scarred, resulting in a loss of vision not unlike macular degeneration. Despite its name, the relationship to "Histoplasma" is controversial. Distinct from POHS, acute ocular histoplasmosis may rarely occur in immunodeficiency.

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.

In absence of proper treatment and especially in immunocompromised individuals, complications can arise. These include recurrent pneumonia, respiratory failure, fibrosing mediastinitis, superior vena cava syndrome, pulmonary vessel obstruction, progressive fibrosis of lymph nodes. Fibrosing mediastinitis is a serious complication and can be fatal. Smokers with structural lung disease have higher probability of developing chronic cavitary histoplasmosis.

After healing of lesions, hard calcified lymph nodes can erode the walls of airway causing hemoptysis.

Cytomegalovirus colitis, also known as CMV colitis, is an inflammation of the colon

Causes

The infection is spread by saliva, urine, respiratory droplets, sexual contact, and blood transfusions. Most people are exposed to the virus in their lifetime, but it usually produces mild or no symptoms in healthy people.

However, serious CMV infections can occur in people with weakened immune systems. This includes patients receiving chemotherapy for cancer and patients on immune-suppressing medicines following an organ transplant.

In rare instances, more severe CMV infection involving the GI tract has been reported in people with a healthy immune system.

Neonatal infections are infections of the neonate (newborn) during the neonatal period or first four weeks after birth. Neonatal infections may be contracted by transplacental transfer in utero, in the birth canal during delivery (perinatal), or by other means after birth. Some neonatal infections are apparent soon after delivery, while others may develop postpartum within the first week or month. Some infections acquired in the neonatal period do not become apparent until much later such as HIV, hepatitis B and malaria.

There is a higher risk of infection for preterm or low birth weight neonates. Respiratory tract infections contracted by preterm neonates may continue into childhood or possibly adulthood with long-term effects that limit one's ability to engage in normal physical activities, decreasing one's quality of life and increasing health care costs. In some instances, neonatal respiratory tract infections may increase one's susceptibility to future respiratory infections and inflammatory responses related to lung disease.

Antibiotics can be effective treatments for neonatal infections, especially when the pathogen is quickly identified. Instead of relying solely on culturing techniques, pathogen identification has improved substantially with advancing technology; however, neonate mortality has not kept pace and remains 20% to 50%. While preterm neonates are at a particularly high risk, full term and post-term infants can also develop infection. Neonatal infection may also be associated with premature rupture of membranes (breakage of the amniotic sac) which substantially increases the risk of neonatal sepsis by allowing passage for bacteria to enter the womb prior to the birth of the infant. Neonatal infection can be distressing to the family and it initiates concentrated effort to treat it by clinicians.Research to improve treatment of infections and prophylactic treatment of the mother to avoid infections of the infant is ongoing.

Neonatal herpes simplex is a rare but serious condition, usually caused by vertical transmission of herpes simplex virus from mother to newborn. Around 1 in every 3,500 babies in the United States contract the infection.

In very low birth weight infants (VLBWI), systemic fungus infection is a hospital-acquired infection with serious consequences. The pathogens are usually "Candida albicans" and "Candida parapsilosis". A small percentage of fungal infections are caused by "Aspergillus", "Zygomycetes", "Malassezia", and "Trichosporon". Infection is usually late-onset. Up to 9% of VLBWI with birth weights of <1,000 g develop these fungus infections leading to sepsis or meningitis. As many as one-third of these infants can die. Candidiasis is associated with retinopathy, prematurity and negative neurodevelopmental consequences. Candida can colonize the gastrointestinal tract of low birthweight infants (LBI). This gastrointestinal colonization is often a precursor to a more serious invasive infection. The risk of serious candida infection increases when multiple factors are present. These are: thrombocytopenia, the presence of candidal dermatitis, the use of systemic steroids, birth weights of <1,000 g, presence of a central catheter, postponing enteral feeding, vaginal delivery, and the amount of time broad-spectrum antibiotics were given.

Systemic candidiasis is an infection of Candida albicans causing disseminated disease and sepsis, invariably when host defenses are compromised.

Fungal pneumonia is an infection of the lungs by fungi. It can be caused by either endemic or opportunistic fungi or a combination of both. Case mortality in fungal pneumonias can be as high as 90% in immunocompromised patients, though immunocompetent patients generally respond well to anti-fungal therapy.

Eczema herpeticum is a rare but severe disseminated infection that generally occurs at sites of skin damage produced by, for example, atopic dermatitis, burns, long term usage of topical steroids or eczema. It is also known as Kaposi varicelliform eruption, Pustulosis varioliformis acute and Kaposi-Juliusberg dermatitis.

Some sources reserve the term "eczema herpeticum" when the cause is due to human herpes simplex virus, and the term "Kaposi varicelliform eruption" to describe the general presentation without specifying the virus.

This condition is most commonly caused by herpes simplex virus type 1 or 2, but may also be caused by coxsackievirus A16, or vaccinia virus. It appears as numerous umbilicated vesicles superimposed on healing atopic dermatitis. it is often accompanied by fever and lymphadenopathy. Eczema herpeticum can be life-threatening in babies.

Congenital cytomegalovirus infection refers to a condition where cytomegalovirus is transmitted in the prenatal period.

Human cytomegalovirus is one of the vertically transmitted infections that lead to congenital abnormalities. (Others are: toxoplasmosis, rubella, and herpes simplex. )

Mendelian susceptibility to mycobacterial disease, also called familial disseminated atypical mycobacterial infection, is a rare genetic disease characterized by susceptibility to mycobacteria and Salmonella infection outside of the intestinal tract.

For infants who are infected by their mothers before birth, two potential adverse scenarios exist:

- Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice). Though severe cases can be fatal, with supportive treatment most infants with CMV disease will survive. However, from 80% to 90% will have complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of learning disability.

- Another 5% to 10% of infants who are infected but without symptoms at birth will subsequently have varying degrees of hearing and mental or coordination problems. The onset of hearing loss can occur at any point during childhood, although commonly within the first decade. It is progressive and can affect both ears.

These risks appear to be almost exclusively associated with women who previously have not been infected with CMV and who are having their first infection with the virus during pregnancy. There appears to be little risk of CMV-related complications for women who have been infected at least 6 months prior to conception. For this group, which makes up 50% to 80% of the women of child-bearing age, the rate of newborn CMV infection is 1%, and these infants appear to have no significant illness or abnormalities.

The virus can also be transmitted to the infant at delivery from contact with genital secretions or later in infancy through breast milk. However, these infections usually result in little or no clinical illness in the infant.

To summarise, during a pregnancy when a woman who has never had CMV infection becomes infected with CMV, there is a risk that after birth the infant may have CMV-related complications, the most common of which are associated with hearing loss, visual impairment, or diminished mental and motor capabilities. On the other hand, healthy infants and children who acquire CMV after birth have few, if any, symptoms or complications. However, preterm born infants infected with CMV after birth (especially via breastmilk). This can lead to cognitive and motor impairments later in life.

Congenital cytomegalovirus infection can be an important cause of intraventricular hemorrhage and neonatal encephalopathy.

Before puberty, the disease typically only produces flu-like symptoms, if any at all. When found, symptoms tend to be similar to those of common throat infections (mild pharyngitis, with or without tonsillitis).

In adolescence and young adulthood, the disease presents with a characteristic triad:

- Fever – usually lasting 14 days; often mild

- Sore throat – usually severe for 3–5 days, before resolving in the next 7–10 days.

- Swollen glands – mobile; usually located around the back of the neck (posterior cervical lymph nodes) and sometimes throughout the body.

Another major symptom is feeling tired. Headaches are common, and abdominal pains with nausea or vomiting sometimes also occur. Symptoms most often disappear after about 2–4 weeks. However, fatigue and a general feeling of being unwell (malaise) may sometimes last for months. Fatigue lasts more than one month in an estimated 28% of cases. Mild fever, swollen neck glands and body aches may also persist beyond 4 weeks. Most people are able to resume their usual activities within 2–3 months.

The most prominent sign of the disease is often the pharyngitis, which is frequently accompanied by enlarged tonsils with pus—an exudate similar to that seen in cases of strep throat. In about 50% of cases, small reddish-purple spots called petechiae can be seen on the roof of the mouth. Palatal enanthem can also occur, but is relatively uncommon.

Spleen enlargement is common in the second and third weeks, although this may not be apparent on physical examination. Rarely the spleen may rupture. There may also be some enlargement of the liver. Jaundice occurs only occasionally.

A small minority of people spontaneously present a rash, usually on the arms or trunk, which can be macular (morbilliform) or papular. Almost all people given amoxicillin or ampicillin eventually develop a generalized, itchy maculopapular rash, which however does not imply that the person will have adverse reactions to penicillins again in the future. Occasional cases of erythema nodosum and erythema multiforme have been reported.

The diagnosis of CMV colitis is based on serology, CMV antigen testing and colonscopy with biopsy.

Clinical suspicion should be aroused in the setting of immunocompromised patient but it is much rarer in immunocompetent patient.

Although it is known that CMV colitis is almost always caused by reactivation of latent CMV infection in immunocompromised patients, new infection of CMV or reinfection of different strain of CMV can cause colitis in immunocompetent hosts.

Because asymptomatic CMV viremia and viruria is common and about 1/3 of symptomatic CMV infection is caused by reinfection of different strain of CMV, the diagnosis of CMV colitis needs more direct causality. It is practically achieved by colonoscopy or sigmoidoscopy tissue sampling and pathological evidence of CMV infection under microscope. Positive CMV IgG doesn't necessarily mean that it is reactivation of latent infection because of the possibility of reinfection of different strain.

Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.

The most common clinical sign is subcutaneous edema of the limbs and hemorrhages on mucous membranes. Other clinical signs include depression, anorexia, fever, elevated heart and respiratory rate, reluctance to move, drainage from lymph nodes, exudation of serum from the skin, colic, epistaxis and weight loss. Rarely, horses may also develop disseminated intravascular coagulation (DIC), leading to infarction of various organs, or chronic myositis and muscle atrophy.