Cyclosporiasis is an infection with the protozoan Cyclospora cayetanensis, a pathogen transmitted by feces or feces-contaminated fresh produce and water. Outbreaks have been reported due to contaminated raspberries. It is not spread from person to person. It can be a cause of diarrhea for travelers.

When an oocyst of Cyclospora cayetanensis enters the small intestine and invades the mucosa it incubates for about one week. After incubation the person begins to experience severe watery diarrhea, bloating, fever, stomach cramps, and muscle aches.

Oocysts can be present due to using contaminated water or human feces as fertilizer. This infection primarily affects humans and other primates.

Diagnosis can be difficult due to the lack of recognizable oocysts in the feces. Using tests like PCR-based DNA tests and acid-fast staining can help with identification. The infection is often treated with Co-trimoxazole, because traditional anti-protozoan drugs are not sufficient. To prevent transmission through food, cook food and try to avoid drinking stream water while outdoors.

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Cutaneous larva migrans (“CLM”) is a skin disease in humans, caused by the larvae of various nematode parasites, the most common of which is Ancylostoma braziliense.

Sometimes referred to as “creeping eruption” or “ground itch”, in some parts of the Southern USA this condition is also referred to as “sandworms,” as the larvae like to live in sandy soil.

These parasites are found in dog and cat feces and although they are able to infect the deeper tissues of these animals (through to the lungs and then the intestinal tract), in humans they are only able to penetrate the outer layers of the skin and thus create the typical wormlike burrows visible underneath the skin. The parasites apparently lack the collagenase enzymes required to penetrate through the basement membrane deeper into the skin.

The infection causes a red, intense itching eruption. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop.

CLM can be treated in a number of different ways:

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Cushing’s syndrome (also called hyperadrenocorticism or hypercorticism) is an endocrine disorder caused by high levels of cortisol in the blood. This hypercortisolism can be caused by intake of glucocorticoids, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH).[1] Cushing’s disease refers to one specific cause, namely an adenoma in the pituitary gland that produces large amounts of ACTH which in turn elevates cortisol.

Cushing’s syndrome is not confined to humans and is also a relatively common condition in domestic dogs and horses. It was described by American Dr. Harvey Cushing in 1932.[2]

There are several possible causes of Cushing’s syndrome. The most common is exogenous administration of glucocorticoids prescribed by physicians to treat other diseases (called iatrogenic Cushing’s). This can be an effect of steroid treatment of a variety of disorders such as asthma and rheumatoid arthritis, or in immunosuppression after an organ transplant. Administration of synthetic ACTH is also possible, but ACTH is less often prescribed due to cost and lesser utility.

Endogenous Cushing syndrome (also known as Cushing’s Disease) results from some derangement of the body’s own system of secreting cortisol. Normally, ACTH is released from the pituitary gland when necessary to stimulate the release of cortisol from the adrenal glands. In pituitary Cushing’s, a benign pituitary adenoma secretes ACTH. This is also known as Cushing’s disease and is responsible for 65% of endogenous Cushing’s. In adrenal Cushing’s, excess cortisol is produced by adrenal gland tumors, hyperplastic adrenal glands, or adrenal glands with nodular adrenal hyperplasia. Finally, tumors outside the normal pituitary-adrenal system can produce ACTH that affects the adrenal glands. This final etiology is called ectopic or paraneoplastic Cushing’s and is seen in diseases like small cell lung cancer.

Cushing’s syndrome can also be sub-classified according to whether or not the excess cortisol is dependent on increased ACTH. ACTH-dependent Cushing’s is driven by increased ACTH and includes exogenous ACTH administration as well as pituitary and ectopic Cushing’s. ACTH-independent Cushing’s shows increased cortisol, but the ACTH is not elevated but rather decreased due to negative feedback. It can be caused by exogenous administration of glucocorticoids or by adrenal adenoma, carcinoma, or nodular hyperplasia.

Symptoms include rapid weight gain, particularly of the trunk and face with sparing of the limbs (central obesity). A common sign is the growth of fat pads along the collar bone and on the back of the neck (buffalo hump) (known as a lipodystrophy) and a round face often referred to as a “moon face”. Other symptoms include excess sweating, telangiectasia (dilation of capillaries), thinning of the skin (which causes easy bruising and dryness, particularly the hands) and other mucous membranes, purple or red striae (the weight gain in Cushing’s stretches the skin, which is thin and weakened, causing it to hemorrhage) on the trunk, buttocks, arms, legs or breasts, proximal muscle weakness (hips, shoulders), and hirsutism (facial male-pattern hair growth). The excess cortisol may also affect other endocrine systems and cause, for example, insomnia, reduced libido, impotence, amenorrhoea and infertility. Patients frequently suffer various psychological disturbances, ranging from euphoria to psychosis. Depression and anxiety are also common.[3]

Cushing’s syndrome may present with striking and distressing skin changes including hyperhidrosis, dryness, fragility of the skin, facial acne, susceptibility to superficial dermatophyte and pityrosporon infections, a plethora over the cheeks, anterior neck, and V of the chest, and the characteristic purplish, atrophic striae on the abdomen.[4]:500

NOTE: Cortisol increases may be contributed to abdominoplasty, or gastric by-pass surgery.

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Crohn’s disease (also known as granulomatous colitis and regional enteritis) is an inflammatory disease of the digestive system which may affect any part of the gastrointestinal tract from mouth to anus. As a result, the symptoms of Crohn’s disease can vary significantly among afflicted individuals. The main gastrointestinal symptoms are abdominal pain, diarrhea (which may be visibly bloody), vomiting, or weight loss. [1][2][3] Crohn’s disease can also cause complications outside of the gastrointestinal tract such as skin rashes, arthritis, and inflammation of the eye.[1]

The precise cause of Crohn’s disease is not known. The disease occurs when the immune system attacks the gastrointestinal tract and for this reason, Crohn’s disease is considered an autoimmune disease. This autoimmune activity produces inflammation in the gastrointestinal tract, and therefore Crohn’s disease is classified as an inflammatory bowel disease. Research in 2007 has suggested that intestinal bacteria are theorized to drive immune activation. [4][5][6]

Like many other autoimmune diseases, Crohn’s disease is believed to be genetically linked. The highest risk occurs in individuals with siblings who have the disease. Males and females are equally affected. Smokers are three times more likely to develop Crohn’s disease.[7] Crohn’s disease affects between 400,000 and 600,000 people in North America.[8] Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000.[9] Crohn’s disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.[1][10] Unlike the other major types of inflammatory bowel disease, there is no known drug based or surgical cure for Crohn’s disease.[11] Treatment options are restricted to controlling symptoms, putting and keeping the disease in remission and preventing relapse.

The disease was independently described in 1904 by Polish surgeon Antoni Lesniowski and in 1932 by American gastroenterologist Burrill Bernard Crohn, for whom the disease was named. Crohn, along with two colleagues, described a series of patients with inflammation of the terminal ileum, the area most commonly affected by the illness.[12] For this reason, the disease has also been called regional ileitis[12] or regional enteritis.

Crohn’s disease is generally classified as an autoimmune disease. It invariably affects the gastrointestinal tract, and most gastroenterologists categorize the presenting disease by the affected areas. Ileocolic Crohn’s disease, which affects both the ileum (the last part of the small intestine that connects to the large intestine) and the large intestine, accounts for fifty percent of cases. Crohn’s ileitis, affecting the ileum only, accounts for thirty percent of cases, and Crohn’s colitis, affecting the large intestine, accounts for the remaining twenty percent of cases and may be particularly difficult to distinguish from ulcerative colitis. The disease can attack any part of the digestive tract, from mouth to anus. However, individuals affected by the disease rarely fall outside these three classifications, being affected in other parts of the gastrointestinal tract such as the stomach and esophagus.[1] Crohn’s disease may also be categorized by the behavior of disease as it progresses. This was formalized in the Vienna classification of Crohn’s disease.[13] There are three categories of disease presentation in Crohn’s disease: stricturing, penetrating, and inflammatory. Stricturing disease causes narrowing of the bowel which may lead to bowel obstruction or changes in the caliber of the feces. Penetrating disease creates abnormal passageways (fistulae) between the bowel and other structures such as the skin. Inflammatory disease (or non-stricturing, non-penetrating disease) causes inflammation without causing strictures or fistulae.[13][14]

Many people with Crohn’s disease have symptoms for years prior to the diagnosis.[15] The usual onset is between 15 and 30 years of age but can occur at any age.[16] Because of the ‘patchy’ nature of the gastrointestinal disease and the depth of tissue involvement, initial symptoms can be more vague than with ulcerative colitis. People with Crohn’s disease will go through periods of flare-ups and remission.

Abdominal pain may be the initial symptom of Crohn’s disease. The pain is commonly cramp-like and is not relieved by defecation.[citation needed] It is often accompanied by diarrhea, which may or may not be bloody, though diarrhea is not uncommon especially in those who have had surgery. People who have had surgery or multiple surgeries often end up with short bowel syndrome of the gastrointestinal tract. The nature of the diarrhea in Crohn’s disease depends on the part of the small intestine or colon that is involved. Ileitis typically results in large-volume watery feces. Colitis may result in a smaller volume of feces of higher frequency. Fecal consistency may range from solid to watery. In severe cases, an individual may have more than 20 bowel movements per day and may need to awaken at night to defecate.[1][10][17][18] Visible bleeding in the feces is less common in Crohn’s disease than in ulcerative colitis, but may be seen in the setting of Crohn’s colitis.[1] Bloody bowel movements are typically intermittent, and may be bright or dark red in colour. In the setting of severe Crohn’s colitis, bleeding may be copious.[10] Flatulence and bloating may also add to the intestinal discomfort.[10]

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Cri du chat syndrome (French for cry or call of the cat referring to the specific mew-like cry of affected children), also known as cri-du-chat syndrome, chromosome 5p deletion syndrome, 5p minus syndrome or Lejeune’s syndrome, is a rare genetic disorder due to a missing part of chromosome 5. It was first described by Jérôme Lejeune in 1963.[1] The condition affects an estimated 1 in 20,000 to 50,000 live births. The disorder is found in people of all ethnic backgrounds and is more common in females by a 4:3 ratio.[2]

The syndrome gets its name from the characteristic of the cry of infants born with the disorder. The infant sounds just like a meowing kitten, due to problems with the larynx and nervous system. This cry identifies the syndrome. About 1/3 of children lose the cry by age 2. Other symptoms of cri du chat syndrome may include:

In addition, common findings include hypotonia, microcephaly, growth retardation, a round face with full cheeks, hypertelorism, epicanthal folds, down-slanting palpebral fissures, strabismus, flat nasal bridge, down-turned mouth, micrognathia, low-set ears, short fingers, single palmar creases, and cardiac defects (eg, ventricular septal defect [VSD], atrial septal defect [ASD], patent ductus arteriosus [PDA], tetralogy of Fallot). People with Cri du chat are fertile and can reproduce.

Less frequently encountered findings include cleft lip and palate, preauricular tags and fistulas, thymic dysplasia, gut malrotation, megacolon, inguinal hernia, dislocated hips, cryptorchidism, hypospadias, rare renal malformations (eg, horseshoe kidneys, renal ectopia or agenesis, hydronephrosis), clinodactyly of the fifth fingers, talipes equinovarus, pes planus, syndactyly of the second and third fingers and toes, oligosyndactyly, and hyperextensible joints.

Late childhood and adolescence findings include severe mental retardation, microcephaly, coarsening of facial features, prominent supraorbital ridges, deep-set eyes, hypoplastic nasal bridge, severe malocclusion, and scoliosis.

Affected females reach puberty, develop secondary sex characteristics, and menstruate at the usual time. The genital tract is usually normal in females except for a report of a bicornuate uterus.

In males, testes are often small, but spermatogenesis is thought to be normal.

Dermatoglyphics: Transverse flexion creases, distal axial triradius, increased whorls and arches on digits, single line on the palm of the hand (simian crease).

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Craniosynostosis,[1] is a medical condition in which some or all of the sutures in the skull of an infant or child close too early,[2] causing problems with normal brain and skull growth. It can result in craniostenosis, which is the skull deformity caused by the premature closure of the cranial sutures. Also intracranial pressure can be increased.

In humans, the adult skull is normally made up of 28 bones. The flat bones making up the cranial vault are joined together by sutures: rigid articulations permitting very little movement.

At birth, the human skull is made up of 45 separate bony elements. As growth occurs, many of these bony elements gradually fuse together into solid bone (for example, the frontal bones).

The bones of the roof of the skull are initially separated by regions of dense connective tissue. At birth these regions are fibrous and moveable, necessary for birth and later growth. Larger regions of connective tissue, called fontanelles, occur where certain bony elements meet. As growth and ossification progress, the connective tissue of the fontanelles is invaded and replaced by bone. The posterior fontanelle usually closes by eight weeks, but the anterior fontanelle can remain up to eighteen months.

When one or more sutures fuse prematurely, skull growth can be restricted perpendicular to the suture. If multiple sutures fuse while the brain is still increasing in size, intracranial pressure can increase.

Primary craniosynostosis is believed to be a result of primary defect in the mesenchymal layer ossification in the cranial bones. Secondary craniosynostosis is a result of primary failure of brain growth.

Physicians diagnose craniosynostosis through physical examination, plain x-rays, and CT scans. [3]

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The pubic or crab louse (Pthirus or Phthirus pubis) is a parasitic insect which spends its entire life on human hair and feeds exclusively on blood. Humans are the only known host of this parasite. Humans can also be infested with body lice (Pediculus humanus humanus) and with head lice (Pediculus humanus capitis).

Pubic lice usually infect a new host only by close contact between individuals, usually through sexual intercourse. Parent to child infestations are more likely to occur through routes of shared towels, clothing, beds or closets. Adults are more frequently infested than children.

A pubic louse infestation is usually diagnosed by carefully examining pubic hair for nits, nymphs and adults. Lice and nits could be removed either with forceps or by cutting the infested hair with scissors (with the exception of the eye area). A magnifying glass or a stereo-microscope can be used for the exact identification. If lice are detected in one family member, the entire family needs to be checked and only those who are infested with living lice should be treated.

Although any part of the body may be colonized, crab lice favour the hairs of the genital (Fig. 1) and peri-anal region. Especially in male patients, pubic lice and eggs can also be found in hair on the abdomen (Fig. 2) and under the armpits as well as on the beard and mustache, while in children they are usually found in eye-lashes (Fig. 3). Infestation with pubic lice is called Phthiriasis or Pediculosis pubis, while infestation of eye-lashes with pubic lice is called Phthiriasis palpebrarum [1]. The main symptom is itching, usually in the pubic hair area. It results from hypersensitivity to louse saliva, and it becomes strong enough two or more weeks following initial infestation. In the majority of infestations a characteristic grey-blue or slate colouration appears (maculae caeruleae) at the feeding site, which may last for days and is also characteristic for the infestation. Pubic lice are primarily spread through sweat and body contact or sexual contact. Therefore, all partners with whom the patient has had sexual contact within the previous 30 days should be evaluated and treated, and sexual contact should be avoided until all partners have successfully completed treatment and are thought to be cured. Because of the strong association between the presence of pubic lice and classic sexually transmitted diseases (STD), patients diagnosed with pubic lice should undergo evaluation for other STDs. Infection in a young child or teenager may indicate sexual abuse.[2][3]

Crab lice can be treated with Permethrin 1% cream rinse and pyrethrins. They can be used for this purpose and are the drugs of choice for pregnant or lactating women. These agents should be applied to the affected areas and washed off after 10 minutes. Shaving off or grooming any hair in the affected areas with a fine-toothed comb is necessary to ensure full removal of the dead lice and nits, though it does not suffice as treatment on its own. Resistance of pubic lice to pyrethroids must be, if at all, very rare. A second treatment after 10 days is recommended. Pubic lice on the eyelashes can be treated with a permethrin formulation by applying the solution to the infested hair with an applicator. It is dangerous to remove lice or eggs in the eyelashes by plucking or cutting the hairs.

Lindane shampoo (1%), a pediculocide, is approved by the U.S. Food and Drug Administration (FDA) as safe and effective when used as directed for the second-line treatment of pubic lice (crabs). While serious side effects have been reported, they are considered to be rare and have almost always resulted from misuse of medication, such as excessive application and oral ingestion. To minimize this risk, Lindane medications are now dispensed in small single-use bottles. [4] [5] The Centers for Disease Control and Prevention (CDC) notes that lindane should not be used immediately after a bath or shower, and it should not be used by persons who have extensive dermatitis, women who are pregnant or lactating or children aged under two years. [6] The FDA similarly warns against use in patients with a history of uncontrolled seizures disorders and premature infants, and recommends cautious use in infants, children, the elderly, and individuals with other skin conditions (e.g., atopic dermatitis, psoriasis) and in those who weigh less than 110 lbs (50 kg).[4]

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Conjunctivitis (commonly called “Pink Eye” in North America, and “Madras eye” in India[1]) is an inflammation of the conjunctiva (the outermost layer of the eye and the inner surface of the eyelids), most commonly due to an allergic reaction or an infection (usually viral, but sometimes bacterial[2]).

Blepharoconjunctivitis is the combination of conjunctivitis with blepharitis (inflammation of the eyelids).

Keratoconjunctivitis is the combination of conjunctivitis and keratitis (corneal inflammation).

Episcleritis is an inflammatory condition that produces a similar appearance to conjunctivitis, but without discharge or tearing.

The viral and bacterial forms of conjunctivitis are contagious and were first discovered by Scottish doctors. It can be caused by coming in contact with another individual who is already infected.[3]

Redness (Hyperaemia), irritation (Chemosis) and watering (Epiphora) of the eyes are symptoms common to all forms of conjunctivitis.

Acute allergic conjunctivitis is typically itchy, sometimes distressingly so, and often involves some lid swelling. Chronic allergy often causes just itch or irritation.

Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, and/or a sore throat. Its symptoms include watery discharge and variable itch. The infection usually begins with one eye, but may spread easily to the other.

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Congenital cystic adenomatoid malformation (CCAM) is a congenital disorder similar to bronchopulmonary sequestration. In CCAM, usually an entire lobe of lung is replaced by a non-working cystic piece of abnormal lung tissue. This abnormal tissue will never function as normal lung tissue.

In most cases the outcome of a fetus with CCAM is very good. However in a rare few cases the cystic mass grows so large as to limit the growth of the surrounding lung and cause pressure against the heart. In these situations, the CCAM can be life-threatening for the fetus.

CCAMs are often identified during routine prenatal ultrasonography. Indentifying characteristics on the sonogram include: an echogenic (bright) mass appearing in the chest of the fetus, displacement of the heart from its normal position, a flat or everted (pushed downward) diaphragm, or the absence of visible lung tissue.

CCAMS are classified into three different types based largely on their gross appearance. Type I has large (>2 cm) multiloculated cysts. Type II has smaller uniform cysts. Type III is not grossly cystic, referred to as the “adenomatoid” type. Microscopically, the lesions are not true cysts, but communicate with the surrounding parenchyma.

In most cases, a fetus with CCAM is closely monitored during pregnancy and the CCAM is removed via surgery after birth. A few fetuses may develop fluid collections within the chest cavity and in those situations a Harrison catheter shunt can be used to drain the fluid into the amniotic fluid.

Very large cystic masses might pose a danger during birth because of the airway compression. In this situation, a special surgical type of delivery called the EXIT procedure may be used.

In rare extreme cases, where fetus’s heart is in danger, fetal surgery can be performed to remove the CCAM. If non-immune hydrops fetalis develop, there is a near universal mortality of the fetus. Fetal surgery can improve the survival percentage up to 50-60%.

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Congenital adrenal hyperplasia (CAH) refers to any of several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of cortisol from cholesterol by the adrenal glands (steroidogenesis). Most of these conditions involve excessive or deficient production of sex steroids and can alter development of primary or secondary sex characteristics in some affected infants, children, or adults. Only a small minority of people with CAH can be said to have an intersex condition, but this attracted American public attention in the late 1990s and many accounts of varying accuracy have appeared in the popular media. Approximately 95% of cases of CAH are due to 21-hydroxylase deficiency.

Examples of conditions caused by various forms of CAH:

Cortisol is an adrenal steroid hormone that is required for normal endocrine function. Production begins in the second month of fetal life. Poor cortisol production is a hallmark of most forms of CAH. Inefficient cortisol production results in rising levels of ACTH, which in turn induces overgrowth (hyperplasia) and overactivity of the steroid-producing cells of the adrenal cortex. The defects causing adrenal hyperplasia are congenital (i.e., present at birth).

Cortisol deficiency in CAH is usually partial, and not the most serious problem for an affected person. Synthesis of cortisol shares steps with synthesis of mineralocorticoids such as aldosterone, androgens such as testosterone, and estrogens such as estradiol. The resulting excessive or deficient production of these three classes of hormones produce the most important problems for people with CAH. Specific enzyme inefficiencies are associated with characteristic patterns of over- or underproduction of mineralocorticoids or sex steroids.

In all its forms, congenital adrenal hyperplasia due to 21-hydroxylase deficiency accounts for about 95% of diagnosed cases of CAH. Unless another specific enzyme is mentioned, “CAH” in nearly all contexts refers to 21-hydroxylase deficiency.

CAH due to deficiencies of enzymes other than 21-hydroxylase present many of the same management challenges as 21-hydroxylase deficiency, but some involve mineralocorticoid excess or sex steroid deficiency.

Further variability is introduced by the degree of enzyme inefficiency produced by the specific alleles each patient has. Some alleles result in more severe degrees of enzyme inefficiency. In general, severe degrees of inefficiency produce changes in the fetus and problems in prenatal or perinatal life. Milder degrees of inefficiency are usually associated with excessive or deficient sex hormone effects in childhood or adolescence, while the mildest form of CAH interferes with ovulation and fertility in adults.

Finally, specific problems may also differ with the genetic sex of the affected person. For example, the most common type of CAH, due to deficient 21-hydroxylase activity, can produce ambiguous genitalia in XX fetuses but not XY.

Treatment of all forms of CAH may include any of:

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