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==Historical prespective==
{{Spontaneous bacterial peritonitis}}
{{CMG}} ; {{AE}}{{SCh}}


==Overview==
B. Lagenbeck in 1839 in Germany was the first to demonstrate that a yeast-like fungus existed in the human oral infection "thrush." He also found that a fungus was able to cause thrush.<ref name="pmid18509848">{{cite journal |vauthors=Barnett JA |title=A history of research on yeasts 12: medical yeasts part 1, Candida albicans |journal=Yeast |volume=25 |issue=6 |pages=385–417 |year=2008 |pmid=18509848 |doi=10.1002/yea.1595 |url=}}</ref>


The genera ''Candida'', species ''albicans'' was described by botanist Christine Marie Berkhout. She described the fungus in her doctoral thesis, at the University of Utrecht in 1923. Over the years the classification of the genera and species has evolved. Obsolete names for this genus include ''Mycotorula'' and ''Torulopsis''. The species has also been known in the past as ''Monilia albicans'' and ''Oidium albicans''. The current classification is ''nomen conservandum'', which means the name is authorized for use by the [http://www.bgbm.org/iapt/nomenclature/code/SaintLouis/0000St.Luistitle.htm International Botanical Congress (IBC)].


==Natural history==
The full current taxonomic classification is available at ''[[Candida albicans]]''.
*SBP is treatable with antibiotics but early diagnosis and intiation of empiric antibiotics is the most important factor for survival.
*In a study performed in 2006, Each hour of delay of administration of empiric antibiotics was associated with increased mortality by 7.6% while administration of antibiotics at the first hour of hypotension increased overall survival to 79%.(3)


==Complications==
The genus ''Candida'' includes about 150 different species. However, only a few of those are known to cause human infections. ''C. albicans'' is the most significant pathogenic (=disease-causing) species. Other ''Candida'' species causing diseases in humans include ''C. tropicalis'', ''C. glabrata'', ''C. krusei'', ''C. parapsilosis'', ''C. dubliniensis'', and ''C. lusitaniae''.
The physician should have a high index of suspicion to diagnose SBP early and start empiric antibiotic therapy. The earlier the stage of diagnosis, the better the survival.
===Hypotension, hypothermia and shock:===
*With the progression of infection, septicaemia ensues with its classic symptoms and signs. Septicaemia and shock are associated with very bad prognosis.
===Altered mental status:===
*Hepatic decompensation in association with the progression of infection make altered mental status more likely to happen. Ammonia levels can be within normal limits or slightly elevated as hepatic decompensation is not the only element leading to the altered mental status.
===Paralytic ileus:===
*Peritoneal inflammation can be complicated with paralytiv=c ileus. Paralytic ileus is a very poor prognostic sign with increased mortality rate.
===Diarrhea:===
*Diarrhea is common due to associated intestinal bacterial overgrowth.(4)


==Prognosis==


*Mortality of SBP remains high. 1-year mortality rate is 30-90 (1), probably due to the advanced liver disease present in the first place.
==Classification:<ref name="urlCandidiasis | Types of Diseses | Fungal Diseases | CDC">{{cite web |url=https://www.cdc.gov/fungal/diseases/candidiasis/ |title=Candidiasis &#124; Types of Diseses &#124; Fungal Diseases &#124; CDC |format= |work= |accessdate=}}</ref>==
*Early admission and prophylactic cephalosporins might have a role in decreasing mortality rate.(2)
Candidiasis can be classified according to the site of infection into:


{| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; background: #f9f9f9; border: 1px #aaa solid; border-collapse: collapse;
===Localoized mucocutaneous:===
! colspan="2" style="background: #4479BA; text-align: center;" | {{fontcolor|#FFF| '''Disease'''}}
! colspan="1" style="background: #4479BA; text-align: center;" | Prominent clinical findings
!Lab tests
!Tratment
|-
| rowspan="3" |'''[[Primary peritonitis]]'''
|'''[[Primary peritonitis|Spontaneous bacterial peritonitis]]'''
|
* Absence of GI [[perforation]], most closely associated with [[cirrhosis]] and advanced liver disease.
* Presents with abrupt onset of [[fever]], [[abdominal pain]], [[distension]], and [[rebound tenderness]].
|
* Most have clinical and biochemical manifestations of advanced [[cirrhosis]] or [[nephrosis]] like [[leukocytosis]],[[hypoalbuminemia]],
* a prolonged [[prothrombin]] time. SAAG >1.1 g/dL, ↑s.lactic acid level, or a ↓ascitic fluid pH (< 7.31) supports the diagnosis. Gram staining reveals bacteria in only 25% of cases.
* Diagnosed by analysis of the ascitic fluid which reveals [[WBC]] > 500/ML, and [[PMN]] >250cells/ml.
* Culture of ascitic fluid inoculated immediately into [[blood culture]] media at the bedside usually reveals a single [[enteric]] organism, most commonly ''[[Escherichia coli]]'', ''[[Klebsiella]]'', or [[streptococci]].
|
* Once diagnosed,it is treated with [[Ceftriaxone]].
|-
|'''[[Tuberculous peritonitis]]'''
|
* Seen in 0.5% of new cases of [[tuberculosis]] particularly in young women in endemic areas as a primary infection.
* Presents with [[abdominal pain]] and [[distension]], [[fever]], [[night sweats]], [[weight loss]], and altered bowel habits.
|
* [[Ascites]] is present in about half of cases. Abdominal mass may be felt in a third of cases. The peritoneal fluid is characterized by a [[protein]] concentration > 3 g/dL with < 1.1 g/dL SAAG and [[lymphocyte]] predominance of [[WBC]].
* Definitive diagnosis in 80% of cases is by culture. Most patients presenting acutely are diagnosed only by [[laparotomy]].
|
* Combination antituberculosis chemotherapy is preferred in chronic cases.
|-
|'''Continuous Ambulatory Peritoneal Dialysis''' ('''CAPD peritonitis)'''
|
* Peritonitis is one of the major complications of [[peritoneal dialysis]] & 72.6% occurred within the first six months of peritoneal dialysis.
* Historically, [[coagulase-negative staphylococci]] were the most common cause of peritonitis in CAPD, presumably due to touch contamination or infection via the pericatheter route.
*
* Treatment for [[peritoneal dialysis]]-associated peritonitis consists of antimicrobial therapy, in some cases catheter removal is also warranted.
* Additional therapies for relapsing or recurrent peritonitis may include fibrinolytic agents and peritoneal lavage. Most episodes of peritoneal dialysis-associated peritonitis resolve with outpatient antibiotic treatment.
|
* Majority of peritonitis cases are caused by bacteria(50%-due to [[Gram-positive bacteria|gram positive]] organisms, 15% to [[gram negative]] organisms,20% were culture negative.2% of cases are caused by fungi, mostly [[Candida]] species. Polymicrobial infection in 4%.Exit-site infection was present in 13% and a peritoneal fluid leak in 3 % and M.tuberculosis 0.1%.
|
* Initial empiric antibiotic coverage for peritoneal dialysis-associated peritonitis consists of coverage for [[gram-positive]] organisms (by [[vancomycin]] or a first-generation [[cephalosporin]]) and [[gram-negative]] organisms (by a third-generation [[cephalosporin]] or an [[aminoglycoside]]). Subsequently, the regimen should be adjusted based on culture and sensitivity data. Cure rates are approximately 75%.
|-
| rowspan="2" |'''[[Acute bacterial secondary peritonitis|Secondary peritonitis]]'''
|'''[[Acute bacterial secondary peritonitis]]'''
|
* Occurs after perforating, penetrating, inflammatory, infectious, or [[ischemic]] injuries of the GI or GU tracts. Most often follows disruption of a hollow viscus→chemical peritonitis→bacterial peritonitis(polymicrobial, includes [[aerobic]] [[gram negative]] {[[E coli]], [[Klebsiella]], [[Enterobacter]], [[Proteus mirabilis]]} and gram positive { [[Enterococcus]], [[Streptococcus]]} and [[anaerobes]] {[[Bacteroides]], [[clostridia]]}).
* Presents with [[abdominal pain]], [[tenderness]], [[guarding]] or rigidity, [[distension]], free peritoneal air, and diminished [[bowel sounds]]. Signs that reflect irritation of the parietal peritoneum resulting [[ileus]]. Systemic findings include [[fever]], [[chills]] or [[rigors]], [[tachycardia]], [[sweating]], [[tachypnea]], [[restlessness]], [[dehydration]], [[oliguria]], [[disorientation]], and, ultimately, refractory [[shock]].
|
|
* [[Peritoneal lavage]], [[Laparoscopy]] are the treatment of choice.
|-
|'''[[Biliary peritonitis]]'''
|
* Most often seen in cases of rupture of pathological [[gallbladder]] or [[bile duct]] or [[cholangitic abscess]] or secondary to obstruction of  the biliary tract.
* Seen in alcoholic patients with [[ascites]].
|
|
|-
| colspan="2" |'''[[Tertiary peritonitis]]'''
|
* Persistence or recurrence of [[Infection|intraabdominal infection]] following apparently adequate therapy of [[Peritonitis|primary or secondary peritonitis]].
* [[Enterococcus]], [[Candida]], [[Staphylococcus epidermidis]], and [[Enterobacter]] being the most common organisms.
* Characterized by lack of response to appropriate surgical and [[antibiotic therapy]] due to disturbance in the hosts [[immune response]].
* Associated with [[Mortality|high mortality]] due to multi organ dysfunction. It presents in a similar way as other [[peritonitis]] but is recognized as an adverse outcome with poor prognosis.
|
|
|-
| colspan="2" |'''[[Familial Mediterranean fever (periodic peritonitis, familial paroxysmal polyserositis)]]'''
|
* Rare genetic condition which affects individuals of Mediterranean genetic background.
* Etiology is unclear.
* Presents with recurrent bouts of [[abdominal pain]] and [[tenderness]] along with [[pleuritic]] or [[joint pain]]. [[Fever]] and [[leukocytosis]] are common.
* [[Colchicine]] prevents but does not treat acute attacks.
|
|
|-
| colspan="2" |'''[[Granulomatous peritonitis]]'''
|
* A rare condition caused by disposable surgical fabrics or food particles from a [[perforated ulcer]], eliciting a vigorous [[granulomatous]] ([[delayed hypersensitivity]]) response in some patients 2-6 weeks after [[laparotomy]].
* Presents with [[abdominal pain]], [[fever]], [[nausea and vomiting]], [[ileus]], and systemic complaints, mild and diffuse [[abdominal tenderness]].
* Diagnosed by the demonstration of diagnostic Maltese cross pattern of starch particles.
* The disease is self-liniting.
* Treated with [[corticosteroids]] or [[Anti inflammatory medications|anti-inflammatory agents]].
|
|
|-
| colspan="2" |'''[[Sclerosing encapsulating peritonitis]]'''
|
* Seen in conditions associated with long term [[peritoneal dialysis]], shunts like VP & PV, history of abdominal surgeries, [[liver transplantation]].
* Symptoms include [[nausea]], [[abdominal pain]], [[diarrhea]], [[anorexia]], bloody [[ascites]].
|
|
|-
| colspan="2" |'''[[Intraperitoneal abscesses]]'''
|
* Most common etiologies being Gastrointestinal perforations, postoperative complications, and penetrating injuries.
* Signs and symptoms depend on the location of the abscess within the peritoneal cavity and the extent of involvement of the surrounding structures.
* Diagnosis is suspected in any patient with a predisposing condition. In a third of cases it occurs as a sequela of generalized peritonitis.
* The pathogenic organisms are similar to those responsible for peritonitis, but [[anaerobic]] organisms occupy an important role.
* Diagnosed best by [[CT-scans|CT]] scan of the abdomen.
* The mortality rate of serious intra-abdominal abscesses is about 30%.
* Treatment consists of prompt and complete [[CT]] or US guided drainage of the [[abscess]], control of the primary cause, and adjunctive use of effective antibiotics. Open drainage is reserved for abscesses for which percutaneous drainage is inappropriate or unsuccessful.
|
|
|-
| colspan="2" |'''[[Peritoneal mesothelioma]]'''
|
* Arises from the [[mesothelium]] lining the [[peritoneal cavity]].
* Its incidence is approximately 300-500 new cases being diagnosed in the United States each year.  As with [[pleural mesothelioma]], there is an association with an asbestos exposure.
* Most commonly affects men at the age of 50-69 years. Patients most often present with [[abdominal pain]] and later increased abdominal girth and ascites along with [[anorexia]], [[weight loss]] and [[abdominal pain]].
* [[Computed tomography|CT]] with intravenous contrast typically demonstrates the thickening of the peritoneum. [[Laparoscopy]] with tissue biopsy or CT guided tissue biopsy with immunohistochemical staining for [[calretinin]], [[cytokeratin]] 5/6, [[mesothelin]], and Wilms tumor 1 antigen remain the gold standard for diagnosis.
* Mean time from diagnosis to death is less than 1 year without treatment. 
* At [[laparotomy]] the goal is [[cytoreduction]] with [[excision]]. Debulking surgery and intraperitoneal [[chemotherapy]] improves survival in some cases.
|
|
|-
| colspan="2" |'''[[peritoneal carcinomatosis]]'''
|
* Associated with a history of [[ovarian]] or GI tract malignancy.
* Symptoms include [[ascites]], [[abdominal pain]], [[nausea]], [[vomiting]].
|
|
|}


*Oropharyngeal candidiasis
*Esophageal candidiasis
*Candida vulvovaginitis
*Chronic mucocutaneous candidiasis.


* [[Peritonitis]]: Presents with [[abdominal pain]] and [[guarding which]] is seldom seen in spontaneous bacterial peritonitis.
====Invasive Candidiasis:====
* [[Pyelonephritis]] : Pain in the [[costovertebral angle]].
More serious and usually presenting in an immunocompromised host.
* [[Appendicitis]]: Presents with a typical history of radiation of [[pain]] from [[umbilicus]] to [[McBurney's point]] compared to diffuse pain in [[spontaneous bacterial peritonitis]].


*Candidaemia
*Candida endophthalmitis
*Candida endocarditis
*Candida osteoarticular disease


==Pathophysiology:==
Candida is a normal commensal of skin and mucous membranes. A competent immune system and an intact regenerating healthy skin prevent the virulence of Candida.


The main virulence factors that mediate the infection: (2)
#Secreting '''molecules that mediate adherence''' into host cells
#Production of '''hydrolases''' which has a lytic effect on tissues and facilitate the invasion by the bacteria.
#'''Polymorphism:''' Candida has the ability to grow either as pseudohyphae (elongated elipsoid form) or in a yeast form (rounded to oval budding form. While the role of #polymorphism is not clearly understood in the virulence of Candida, it’s noted that species capable of producing the most severe form of the disease has this ability.
#'''Biofilm production:''' which means the ability to form a thick layer of the organism on the mucosal surfaces or even on catheters and  dentures.


Patients was candida vulvovaginitis were found to have decreased levels of mannose binding lectins (MBL) . Further investigations revealed that 2 genetic mutations in genes responsible for MBL and IL4 production increase the host susceotibility of getting recurrent candidal vulvovaginitis.(3)


==Risk factors:==
Any condition that compromises cell mediated immunity, worsens the general status of the patient or provide a favorable medium for candida to form biofilms  put the patient at increased risk for having candidiasis.(4)
===Conditions that compromises cell mediated immunity:===
*T cell deficiencies as in DiGeorge syndrome, Wiscot-Aldrich syndrome and ataxia-telengictasia.
*Bone marrow transplant
*Leukaemias
*Corticosteroids use or immunosuppresive drugs.
===Conditions that worsens the general condition:===
*Malignancies
*Recent chemotherapy
*Trauma
*Recent surgery
*Prolonged hospitalization
*Broad spectrum antibiotics
*Renal failure
*Haemodialysis (especially if prolonged)
===Dentures that provide a favorable media for forming biofilms:===
*Prolonged central venous catheters insertion
*Prolonged foley’s catheter insertion
*Prolonged mechanical ventilation
==Clinical manifaestations:==
Oropharyngeal candidiasis:(5), (6)
Many cases are asymptomatic (mild disease or poor general condition)
Dysphagia or odynphagia
Difficulty tasting food
feeling of mouth fullness and discomfort
Candida esophagitis:(7)
Candida esophagitis usually comes late in the course of AIDS (or any immunodeficiency) (8), so patient has the symptoms and signs of the underlying disease.
Odynophagia
Weight loss due to decreased food intake.
Candida vulvovaginitis:
Symptoms of [[vulvovaginitis]] caused by [[Candida]] [[species]] are indistinguishable and include the following:<ref name="pmid97946642">{{cite journal| author=Eckert LO, Hawes SE, Stevens CE, Koutsky LA, Eschenbach DA, Holmes KK| title=Vulvovaginal candidiasis: clinical manifestations, risk factors, management algorithm. | journal=Obstet Gynecol | year= 1998 | volume= 92 | issue= 5 | pages= 757-65 | pmid=9794664 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9794664  }}</ref><ref name="pmid16990387">{{cite journal |vauthors=Eckert LO |title=Clinical practice. Acute vulvovaginitis |journal=N. Engl. J. Med. |volume=355 |issue=12 |pages=1244–52 |year=2006 |pmid=16990387 |doi=10.1056/NEJMcp053720 |url=}}</ref><ref name="pmid9500475">{{cite journal |vauthors=Sobel JD, Faro S, Force RW, Foxman B, Ledger WJ, Nyirjesy PR, Reed BD, Summers PR |title=Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations |journal=Am. J. Obstet. Gynecol. |volume=178 |issue=2 |pages=203–11 |year=1998 |pmid=9500475 |doi= |url=}}</ref>
*[[Pruritus]] is the most significant symptom
*Change in the amount and the color of [[vaginal discharge]]: It is characterized by a thick, white "cottage cheese-like" vaginal discharge
*Pain on urination ([[dysuria]])
*Pain on sexual intercourse (dyspareunia)
*[[Vulvovaginal]] soreness
*Symptoms aggravate a week before the menses.
Chronic mucocutaneous candidiasis (CMCC): (9)
CMCC is a syndrome characterized by chronic or recurrent superficial candida infection in the skin and mucous membranes in association with endocrinal and autoimmune deficiencies. (10)
Characterized by inability of T cells to react to candidal antigens.
Presents with:
Recurrent or chronic candidal infections.
Infection is usually superficial though invasive candidiasis is encountered especially in new born.(11)
Enocrinopathies as hypoparathyroidism and adrenal insufficiency may accompany chronic candidiasis.
Invasive candidiasis:
Candidaemia: (12)
mimics the presentation of sepsis:
*[[Fever]]: in patient who is known immunodeficient, fevers are usually high and spiking.
*A [[capillary leak syndrome]] can develop with severe [[swelling]], [[edema]], and third spacing of fluids.
*General [[symptoms]] can include flu like symptoms as well as shaking chills or [[rigors]].(13)
*If the [[respiratory system]] is the primary source for sepsis then [[sore throat]], productive [[cough]], and [[pleuritic chest pain]] may be present.
Candida osteoarticular disease:
invasion of bones usually presents after weks to months after candidaemia.
Fever is not present in all patients
Loss of function, pain and tenderness are the main presenting symptoms.
Candida endophthalmitis:
Candida endophthalmitis presents in severly immunocompromised patients but most common risk factor is IV drug abuse.
Fever: is not present consistently in all patients except associated candiaemia is present.
Red eye.
Floaters and decreased visual acuity: but markedly decreased vision is not present till very late in the course of the disease.
Eye pain


==References==
==References==
{{reflist|2}}
[[Category:Gastroenterology]]
[[Category:Emergency medicine]]
[[Category:Infectious disease]]

Latest revision as of 20:41, 2 May 2017

Historical prespective

B. Lagenbeck in 1839 in Germany was the first to demonstrate that a yeast-like fungus existed in the human oral infection "thrush." He also found that a fungus was able to cause thrush.[1]

The genera Candida, species albicans was described by botanist Christine Marie Berkhout. She described the fungus in her doctoral thesis, at the University of Utrecht in 1923. Over the years the classification of the genera and species has evolved. Obsolete names for this genus include Mycotorula and Torulopsis. The species has also been known in the past as Monilia albicans and Oidium albicans. The current classification is nomen conservandum, which means the name is authorized for use by the International Botanical Congress (IBC).

The full current taxonomic classification is available at Candida albicans.

The genus Candida includes about 150 different species. However, only a few of those are known to cause human infections. C. albicans is the most significant pathogenic (=disease-causing) species. Other Candida species causing diseases in humans include C. tropicalis, C. glabrata, C. krusei, C. parapsilosis, C. dubliniensis, and C. lusitaniae.


Classification:[2]

Candidiasis can be classified according to the site of infection into:

Localoized mucocutaneous:

  • Oropharyngeal candidiasis
  • Esophageal candidiasis
  • Candida vulvovaginitis
  • Chronic mucocutaneous candidiasis.

Invasive Candidiasis:

More serious and usually presenting in an immunocompromised host.

  • Candidaemia
  • Candida endophthalmitis
  • Candida endocarditis
  • Candida osteoarticular disease

Pathophysiology:

Candida is a normal commensal of skin and mucous membranes. A competent immune system and an intact regenerating healthy skin prevent the virulence of Candida.

The main virulence factors that mediate the infection: (2)

  1. Secreting molecules that mediate adherence into host cells
  2. Production of hydrolases which has a lytic effect on tissues and facilitate the invasion by the bacteria.
  3. Polymorphism: Candida has the ability to grow either as pseudohyphae (elongated elipsoid form) or in a yeast form (rounded to oval budding form. While the role of #polymorphism is not clearly understood in the virulence of Candida, it’s noted that species capable of producing the most severe form of the disease has this ability.
  4. Biofilm production: which means the ability to form a thick layer of the organism on the mucosal surfaces or even on catheters and dentures.

Patients was candida vulvovaginitis were found to have decreased levels of mannose binding lectins (MBL) . Further investigations revealed that 2 genetic mutations in genes responsible for MBL and IL4 production increase the host susceotibility of getting recurrent candidal vulvovaginitis.(3)

Risk factors:

Any condition that compromises cell mediated immunity, worsens the general status of the patient or provide a favorable medium for candida to form biofilms put the patient at increased risk for having candidiasis.(4)

Conditions that compromises cell mediated immunity:

  • T cell deficiencies as in DiGeorge syndrome, Wiscot-Aldrich syndrome and ataxia-telengictasia.
  • Bone marrow transplant
  • Leukaemias
  • Corticosteroids use or immunosuppresive drugs.

Conditions that worsens the general condition:

  • Malignancies
  • Recent chemotherapy
  • Trauma
  • Recent surgery
  • Prolonged hospitalization
  • Broad spectrum antibiotics
  • Renal failure
  • Haemodialysis (especially if prolonged)

Dentures that provide a favorable media for forming biofilms:

  • Prolonged central venous catheters insertion
  • Prolonged foley’s catheter insertion
  • Prolonged mechanical ventilation

Clinical manifaestations:

Oropharyngeal candidiasis:(5), (6)

Many cases are asymptomatic (mild disease or poor general condition) Dysphagia or odynphagia Difficulty tasting food feeling of mouth fullness and discomfort

Candida esophagitis:(7)

Candida esophagitis usually comes late in the course of AIDS (or any immunodeficiency) (8), so patient has the symptoms and signs of the underlying disease. Odynophagia Weight loss due to decreased food intake.

Candida vulvovaginitis:

Symptoms of vulvovaginitis caused by Candida species are indistinguishable and include the following:[3][4][5]

  • Pruritus is the most significant symptom
  • Change in the amount and the color of vaginal discharge: It is characterized by a thick, white "cottage cheese-like" vaginal discharge
  • Pain on urination (dysuria)
  • Pain on sexual intercourse (dyspareunia)
  • Vulvovaginal soreness
  • Symptoms aggravate a week before the menses.

Chronic mucocutaneous candidiasis (CMCC): (9)

CMCC is a syndrome characterized by chronic or recurrent superficial candida infection in the skin and mucous membranes in association with endocrinal and autoimmune deficiencies. (10) Characterized by inability of T cells to react to candidal antigens. Presents with: Recurrent or chronic candidal infections. Infection is usually superficial though invasive candidiasis is encountered especially in new born.(11) Enocrinopathies as hypoparathyroidism and adrenal insufficiency may accompany chronic candidiasis.

Invasive candidiasis:

Candidaemia: (12) mimics the presentation of sepsis:

Candida osteoarticular disease: invasion of bones usually presents after weks to months after candidaemia. Fever is not present in all patients Loss of function, pain and tenderness are the main presenting symptoms.

Candida endophthalmitis: Candida endophthalmitis presents in severly immunocompromised patients but most common risk factor is IV drug abuse.

Fever: is not present consistently in all patients except associated candiaemia is present. Red eye. Floaters and decreased visual acuity: but markedly decreased vision is not present till very late in the course of the disease. Eye pain

References

  1. ↑ Barnett JA (2008). "A history of research on yeasts 12: medical yeasts part 1, Candida albicans". Yeast. 25 (6): 385–417. doi:10.1002/yea.1595. PMID 18509848.
  2. ↑ "Candidiasis | Types of Diseses | Fungal Diseases | CDC".
  3. ↑ Eckert LO, Hawes SE, Stevens CE, Koutsky LA, Eschenbach DA, Holmes KK (1998). "Vulvovaginal candidiasis: clinical manifestations, risk factors, management algorithm". Obstet Gynecol. 92 (5): 757–65. PMID 9794664.
  4. ↑ Eckert LO (2006). "Clinical practice. Acute vulvovaginitis". N. Engl. J. Med. 355 (12): 1244–52. doi:10.1056/NEJMcp053720. PMID 16990387.
  5. ↑ Sobel JD, Faro S, Force RW, Foxman B, Ledger WJ, Nyirjesy PR, Reed BD, Summers PR (1998). "Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations". Am. J. Obstet. Gynecol. 178 (2): 203–11. PMID 9500475.
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