Though GBS colonization is asymptomatic and, in general, does not cause problems, it can sometimes cause serious illness for the mother and the baby during gestation and after delivery. GBS infections in the mother can cause chorioamnionitis (intra-amniotic infection or severe infection of the placental tissues) infrequently, and postpartum infections (after birth). GBS urinary tract infections may induce labour and cause premature delivery (preterm birth) and miscarriage.

GBS is found in the gastrointestinal and genitourinary tract of humans. In different studies, GBS vaginal colonization rate ranges from 4 to 36%, with most studies reporting rates over 20%. These variations in the reported prevalence of asymptomatic (presenting no symptoms of disease) colonization could be related to the different detection methods used, and differences in populations studied.

Though GBS is an asymptomatic colonizer of the gastrointestinal human tract in up to 30% of otherwise healthy adults, including pregnant women,

this opportunistic harmless bacterium can, in some circumstances, cause severe invasive infections.

The following is a list of common signs and symptoms found with neonatal meningitis.

- Fever

- poor appetite

- anterior fontanelle bulging

- seizure

- jitteriness

- dyspnea

- irritability

- anorexia

- vomiting

- diarrhea

- abdominal distention (increase in abdominal size)

- neck rigidity

- cyanosis

- jaundice

- and sunset eyes (downward gaze of the eyes)

- abnormal body temperature (hypo-or hyperthermia)

- change of activity (lethargy or irritability)

Unfortunately these symptoms are unspecific and may point to many different conditions.

Laboratory features that are characteristic of neonatal bacterial meningitis include:

- Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF) by culture and/or visualization by Gram stain

- Increased CSF white blood cell (WBC) count (typically >1000 WBC/mL, but may be lower, especially with gram-positive organisms) with a predominance of neutrophils

- Elevated CSF protein concentration (>150 mg/dL in preterm (premature birth) and >100 mg/dL in term (on time) infants)

- Decreased CSF glucose concentration (<20 mg/dL [1.1 mmol/L] in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on time) infants)

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.

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.

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.

A vertically transmitted infection can be called a perinatal infection if it is transmitted in the perinatal period, which is the period starting at a gestational age of between 22 and 28 weeks (with regional variations in the definition) and ending seven completed days after birth.

The term congenital infection can be used if the vertically transmitted infection persists after childbirth.

An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 20 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens. EIDs are caused by newly identified species or strains (e.g. Severe acute respiratory syndrome, HIV/AIDS) that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile fever) or to an area undergoing ecologic transformation (e.g. Lyme disease), or be "reemerging" infections, like drug resistant tuberculosis. Nosocomial (hospital-acquired) infections, such as methicillin-resistant Staphylococcus aureus are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics. Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics. Many emerging diseases are zoonotic - an animal reservoir incubates the organism, with only occasional transmission into human populations.

The symptoms are like those associated with many other febrile diseases, but with emphasis on muscular pain and night sweats. The duration of the disease can vary from a few weeks to many months or even years.

In the first stage of the disease, sepsis occurs and leads to the classic triad of undulant fevers, sweating (often with characteristic foul moldy smell sometimes likened to wet hay), and migratory arthralgia and myalgia (joint and muscle pain). Blood tests characteristically reveal a low number of white blood cells and red blood cells, show some elevation of liver enzymes such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and demonstrate positive Bengal Rose and Huddleston reactions. Gastrointestinal symptoms occur in 70% of cases and include nausea, vomiting, decreased appetite, unintentional weight loss, abdominal pain, constipation, diarrhea, an enlarged liver, liver inflammation, liver abscess, and an enlarged spleen.

This complex is, at least in Portugal, Israel, and Jordan, known as Malta fever. During episodes of Malta fever, melitococcemia (presence of brucellae in blood) can usually be demonstrated by means of blood culture in tryptose medium or Albini medium. If untreated, the disease can give origin to focalizations or become chronic. The focalizations of brucellosis occur usually in bones and joints and spondylodiscitis of the lumbar spine accompanied by sacroiliitis is very characteristic of this disease. Orchitis is also common in men.

Diagnosis of brucellosis relies on:

1. Demonstration of the agent: blood cultures in tryptose broth, bone marrow cultures. The growth of brucellae is extremely slow (they can take up to two months to grow) and the culture poses a risk to laboratory personnel due to high infectivity of brucellae.

2. Demonstration of antibodies against the agent either with the classic Huddleson, Wright, and/or Bengal Rose reactions, either with ELISA or the 2-mercaptoethanol assay for IgM antibodies associated with chronic disease

3. Histologic evidence of granulomatous hepatitis on hepatic biopsy

4. Radiologic alterations in infected vertebrae: the Pedro Pons sign (preferential erosion of the anterosuperior corner of lumbar vertebrae) and marked osteophytosis are suspicious of brucellic spondylitis.

The consequences of "Brucella" infection are highly variable and may include arthritis, spondylitis, thrombocytopenia, meningitis, uveitis, optic neuritis, endocarditis, and various neurological disorders collectively known as neurobrucellosis.

Rash which has a characteristic appearance, spreading pattern, and desquamating process

"Strawberry tongue"

- The tongue starts out by having a white coating on it while the papillae of the tongue are swollen and reddened. The protrusion of the red papillae through the white coating gives the tongue a "white strawberry" appearance.

- Then a few days later (following the desquamating process, or the shedding of the tissue which created the white coating) the whiteness disappears while the red and enlarged papillae give it the "red strawberry" appearance.

- Note that this involvement of the tongue is a part of the rash which is characteristic of scarlet fever.

Pastia's lines

- Lines of petechiae which appear as pink/red areas located in arm pits and elbow pits

Vomiting and abdominal pain

The features of scarlet fever can differ depending on the age and race of the person. Children less than 5 years old can have atypical presentations. Children less than 3 years old can present with nasal congestion and a lower grade fever. Infants can potentially only present with increased irritability and decreased appetite.

Children who have darker skin can have a different presentation in that the redness of the skin involved in the rash and the ring of paleness around the mouth can be less obvious. Suspicion based on accompanying symptoms and diagnostic studies are important in these cases.

Anaerobes can be isolated from most types of upper respiratory tract and head and neck and infection and are especially common in chronic ones. These include tonsillar, peritonsillar and retropharyngeal abscesses, chronic otitis media, sinusitis and mastoiditis, eye ocular) infections, all deep neck space infections, parotitis, sialadenitis, thyroiditis, odontogenic infections, and postsurgical and nonsurgical head and neck wounds and abscesses., The predominant organisms are of oropharyngeal flora origin and include AGNB, "Fusobacterium" and Peptostreptococcus spp.

Anaerobes involve almost all dental infections. These include dental abscesses, endodontal pulpitis and periodontal (gingivitis and periodontitis) infections, and perimandibular space infection. Pulpitis can lead to abscess formation and eventually spread to the mandible and other neck spaces. In addition to strict anaerobic bacteria, microaerophilic streptococci and "Streptococcus salivarius" can also be present.

"Fusobacterium" spp. and anaerobic spirochetes are often the cause of acute necrotizing ulcerative gingivitis (or Vincent's angina) which is a distinct form of ulcerative gingivitis.

Deep neck infections that develop as a consequence of oral, dental and pharyngeal infections are generally polymicrobial in nature. These include extension of retropharyngeal cellulitis or abscess, mediastinitis following esophagus perforation, and dental or periodontal abscess.

Brucellosis is a highly contagious zoonosis caused by ingestion of unpasteurized milk or undercooked meat from infected animals, or close contact with their secretions.

"Brucella" species are small, gram-negative, nonmotile, nonspore-forming, rod-shaped (coccobacilli) bacteria. They function as facultative intracellular parasites, causing chronic disease, which usually persists for life. Four species infect humans: "B. abortus", "B. canis", "B. melitensis", and "B. suis". "B. abortus" is less virulent than "B. melitensis" and is primarily a disease of cattle. "B. canis" affects dogs. "B. melitensis" is the most virulent and invasive species; it usually infects goats and occasionally sheep. "B. suis" is of intermediate virulence and chiefly infects pigs. Symptoms include profuse sweating and joint and muscle pain. Brucellosis has been recognized in animals and humans since the 20th century.

Anaerobes are able to cause all types of intracranial infections. These often cause subdural empyema, and brain abscess, and rarely cause epidural abscess and meningitis. The origin of brain abscess is generally an adjacent chronic ear, mastoid, or sinus infection oropharynx, teeth or lungs. Mastoid and ear or infections generally progress to the temporal lobe or cerebellum, while facial sinusitis commonly causes frontal lobe abscess. Hematogenous spread of the infection into the CNS often occurs after oropharyngeal, dental, or pulmonary infection. Infrequently bacteremia originating of another location or endocarditis can also cause intracranial infection.

Meningitis due to anaerobic bacteria is infrequent and may follow respiratory tract infection or complicate a cerebrospinal fluid shunt. Nerological shunt infections are often caused by skin bacteria such as "Propionibacterium acnes", or in instances of ventriculoperitoneal shunts that perforate the gut, by anaerobes of enteric origin (i.e. "Bacteroides fragilis")."Clostridium perfringens" can cause of brain abscesses and meningitis following intracranial surgery or head trauma.

The anaerobes often isolated from brain abscesses complicating respiratory and dental infections are anaerobic Gram-negative bacilli (AGNB, including Prevotella, "Porphyromonas", Bacteroides), "Fusobacterium" and Peptostreptococcus spp. Microaerophilic and other streptococci are also often isolated. Actinomyces are rarely isolated.

At the stage of encephalitis, antimicrobial therapy and utilization of measures to lower the increase in the intracranial pressure can prevent the formation of an intracranial abscess However, after an abscess has emerged, surgical removal or drainage may be necessary, along with an extended course of antimicrobial therapy (4–8 weeks). Some advocate complete drainage of intracranial abscess, while others use repeated aspirations of the abscess., Repeated aspirations of an abscess are preferable in those with multiple abscesses or when the abscess is located in a predominate brain site. Administration of antimicrobials in a high-dose for an extended period of time can offer an alternative treatment strategy in this type of patients and may substitute for surgical evacuation of an abscess.

Because of the poor penetration of many antimicrobial agents through the blood–brain barrier, there are few agents available for the treatment of intracranial infections. The antimicrobials with good intracranial penetration are metronidazole, chloramphenicol, penicillins, and meropenem. Optimally, the selection of antimicrobial is done according to the recovered isolates and their antimicrobial susceptibilities. A substantial improvement in patients' survival rate has occurred after the introduction of computed tomography (CT) and other scans and utilization of metronidazole therapy.

Additional problems may occur in the early stage of the illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature, and rapid breathing. Very low blood pressure may occur at an early stage, especially but not exclusively in meningococcal meningitis; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, the excessive activation of blood clotting, may obstruct blood flow to organs and paradoxically increase the bleeding risk. Gangrene of limbs can occur in meningococcal disease. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often fatal.

The brain tissue may swell, pressure inside the skull may increase and the swollen brain may herniate through the skull base. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing. The inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus). Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (in 30% of cases) and do not necessarily indicate an underlying cause. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication indicate a poorer long-term outcome.

Inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and which control, among other functions, eye movement, facial muscles, and hearing. Visual symptoms and hearing loss may persist after an episode of meningitis. Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area of the brain.

In adults, the most common symptom of meningitis is a severe headache, occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (the inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of bacterial meningitis cases. If none of the three signs are present, acute meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell. The fontanelle (the soft spot on the top of a baby's head) can bulge in infants aged up to 6 months. Other features that distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.

Nuchal rigidity occurs in 70% of bacterial meningitis in adults. Other signs include the presence of positive Kernig's sign or Brudziński sign. Kernig's sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's sign and Brudzinski's sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely.

Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.

Meningitis caused by the bacterium "Neisseria meningitidis" (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash, which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues on the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.

Symptoms may include fever and headache, but the distinguishing characteristic of this disease is attacks of severe pain in the lower chest, often on one side. The slightest movement of the rib cage causes a sharp increase of pain, which makes it very difficult to breathe, and an attack is therefore quite a frightening experience, although it generally passes off before any actual harm occurs. The attacks are unpredictable and strike "out of the blue" with a feeling like an iron grip around the rib cage. The colloquial names for the disease, such as 'The Devil's grip' (see also "other names" below) reflect this symptom.

Inoculation of throat washings taken from people with pleurodynia into the brains of newborn mice revealed that enteroviruses in the Coxsackie B virus group were likely to be the cause of pleurodynia, and those findings were supported by subsequent studies of IgM antibody responses measured in serum from people with pleurodynia. Other viruses in the enterovirus family, including echovirus and Coxsackie A virus, are infrequently associated with pleurodynia.

Hemolytic disease of the newborn (anti-RhE) is caused by the anti-RhE antibody of the Rh blood group system. The anti-RhE antibody can be naturally occurring, or arise following immune sensitization after a blood transfusion or pregnancy.

The anti-RhE antibody is quite common especially in the Rh genotype CDe/CDe; It usually only causes a mild hemolytic disease, but can cause a severe condition in the newborn. It can occur with other antibodies, usually the anti-Rhc antibody, which can also cause a severe hemolytic disease.

One study done by Moran et al., found that titers are not reliable for anti-E. Their most severe case of hemolytic disease of the newborn occurred with titers 1:2. Moran states that it would be unwise routinely to dismiss anti-E as being of little clinical consequence.

Hemolytic disease of the newborn (anti-Rhc) can range from a mild to a severe disease. It is the third most common cause of severe HDN. Rh disease is the most common and hemolytic disease of the newborn (anti-Kell) is the second most common cause of severe HDN.

It occurs more commonly in women who are Rh D negative.

Cutaneous group B streptococcal infection may result in orbital cellulitis or facial erysipelas in neonates.

Glanders (from Middle English ' or Old French ', both meaning glands; , ; also known as "equinia", "farcy", and "malleus") is an infectious disease that occurs primarily in horses, mules, and donkeys. It can be contracted by other animals, such as dogs, cats, goats and humans. It is caused by infection with the bacterium "Burkholderia mallei", usually by ingestion of contaminated feed or water. Signs of glanders include the formation of nodular lesions in the lungs and ulceration of the mucous membranes in the upper respiratory tract. The acute form results in coughing, fever, and the release of an infectious nasal discharge, followed by septicaemia and death within days. In the chronic form, nasal and subcutaneous nodules develop, eventually ulcerating. Death can occur within months, while survivors act as carriers.

Glanders is endemic in Africa, Asia, the Middle East, and Central and South America. It has been eradicated from North America, Australia, and most of Europe through surveillance and destruction of affected animals, and import restrictions.

"B. mallei" is able to infect humans, so is classed as a zoonotic agent. Transmission occurs by direct contact with infected animals and entry is through skin abrasions, nasal and oral mucosal surfaces, or by inhalation.

The mallein test is a sensitive and specific clinical test for glanders. Mallein (ATCvet code: ), a protein fraction of the glanders organism ("B. mallei"), is injected intradermopalpebrally or given by eye drop. In infected animals, the eyelid swells markedly in 1 to 2 days.

Glanders has not been reported in the United States since 1945, except in 2000 when an American lab researcher suffered from accidental exposure. It is a notifiable disease in the UK, although it has not been reported there since 1928.

The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:

- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A

- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS

- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms

- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe

- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance

- Breakdown of public health; e.g. the current situation in Zimbabwe

- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas

- War and famine

- Bioterrorism; e.g. 2001 Anthrax attacks

- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases

The symptoms of CVID vary between people affected. Its main features are hypogammaglobulinemia and recurrent infections. Hypogammaglobulinemia manifests as a significant decrease in the levels of IgG antibodies, usually alongside IgA antibodies; IgM antibody levels are also decreased in about half of people. Infections are a direct result of the low antibody levels in the circulation, which do not adequately protect them against pathogens. The microorganisms that most frequently cause infections in CVID are bacteria Haemophilus influenzae, Streptococcus pneumoniae and Staphylococcus aureus. Pathogens less often isolated from people include Neisseria meningitidis, Pseudomonas aeruginosa and Giardia lamblia. Infections mostly affect the respiratory tract (nose, sinuses, bronchi, lungs) and the ears; they can also occur at other sites, such as the eyes, skin and gastrointestinal tract. These infections respond to antibiotics but can recur upon discontinuation of antibiotics. Bronchiectasis can develop when severe, recurrent pulmonary infections are left untreated.

In addition to infections, people with CVID can develop complications. These include:

- autoimmune manifestations, e.g. pernicious anemia, autoimmune haemolytic anemia (AHA), idiopathic thrombocytopenic purpura (ITP), psoriasis, vitiligo, rheumatoid arthritis, primary hypothyroidism, atrophic gastritis. Autoimmunity is the main type of complication in people with CVID, appearing in some form in up to 50% of individuals;

- malignancies, particularly Non-Hodgkin's lymphoma and gastric carcinoma;

- enteropathy, which manifests with a blunting of intestinal villi and inflammation, and is usually accompanied by symptoms such as abdominal cramps, diarrhea, constipation and, in some cases, malabsorption and weight loss. Symptoms of CVID enteropathy are similar to those of celiac disease, but don't respond to a gluten-free diet. Infectious causes must be excluded before a diagnosis of enteropathy can be made, as people with CVID are more susceptible to intestinal infections, e.g. by Giardia lamblia;

- lymphocytic infiltration of tissues, which can cause enlargement of lymph nodes (lymphadenopathy), of the spleen (splenomegaly) and of the liver (hepatomegaly), as well as the formation of granulomas. In the lung this is known as Granulomatous–lymphocytic interstitial lung disease.

Anxiety and depression can occur as a result of dealing with the other symptoms.

People generally complain of severe fatigue.