Opportunistic Infections

OPPORTUNISTIC INFECTIONSAND LABORATORY DIAGNOSIS

AUGUSTINE BARNABA (MC/MLT/06/02)LIMBIKANI CHAPONDA (MC/MLT/06/04)EDSON MUMBA (MC/MLT/06/33)

WHAT IS AN OPPORTUNISTIC INFECTION?

Infection with an organism that is common, but rarely causes illness in person with strong immune system.

Because these organisms are commonly found in the environment but do not cause illness in healthy people, they are not contagious. They do not pose a risk to HIV negative people.

OPPORTUNISTIC INFECTIONS

Vulnerability to opportunistic infections varies depending on the extent of the immune system damage.

An opportunistic infection may affect different organ systems with different levels of severity, depending on the extent of immune system damage.

NATURAL PROGRESSION OF HIV DISEASE

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OPPORTUNISTIC INFECTION PREVENTION

Primary Prophylaxis giving medication to prevent an opportunistic infection

from occurring

Secondary Prophylaxis (Maintenance therapy) giving medication after an opportunistic infection is

treated to prevent it from recurring.

COTRIMOXAZOLE PROPHYLAXIS

Can prevent:

Pneumocystis carinii pneumonia Cerebral toxoplasmosis Malaria Parasitic diarrheas Disease caused by non-typhoid salmonella Disease caused by streptococcus pneumoniae

OI PROPHYLAXIS: PATIENT EDUCATION

Maintain good personal and food preparation hygiene. Drink bottled or boiled water. Eat only well cooked meat, fish, poultry. Wash fruits and vegetables well. Do not eat raw eggs. Do not handle turtles, chicks, ducklings, or cat feces.

PATHOPHYSIOLOGY

Impaired T-cell immunity and CD4+ T-cell depletion in HIV disease are the key elements in the pathophysiology of most OIs

An impairment in the host defence mechanisms and higher levels of plasma HIV RNA have been associated with increased rates of mucocutaneous candidiasis and colonisation with Candida

PATHOPHYSIOLOGY CONT…

HIV infection is an independent risk factor for acquisition of TB and rapid progression to disease. Defects of cellular immunity and macrophage function have been demonstrated in HIV-infected persons with TB.

Colonisation of the intestinal tract with mycobacterium avium complex (MAC) is believed to be the primary route of MAC infection in patients with AIDS, and precedes the appearance of bacteraemia and disseminated disease by several months


In patients with AIDS, progressive loss of cell-mediated immunity permits CMV re-activation and replication to begin and results in tissue necrosis in association with non-specific inflammation.

Increasing evidence suggests that lung damage occurring during Pneumocystis jiroveci pneumonia (PCP) is a result of the type and extent of the host inflammatory response to P jiroveci rather than a result of direct damage by the organism.


Cellular immunity, mediated by T cells, macrophages, and activity of cytokines and interferon-alpha, is necessary for maintaining quiescence of chronic T gondii infection.

In cryptococcal infection the microbes polysaccharide capsule is thought to be the primary virulence factor that elicits a local inflammatory response and the increased production of prostaglandins and several cytokines, particularly interferon-gamma.

LAB. DIAGNOSIS

CD4+ CELL COUNT TB can occur throughout the course of HIV disease but

the risk increases as the CD4+ count decreases. P jiroveci pneumonia (PCP) and candidiasis are more

likely when the CD4+ count is below 200 cells/µL. Toxoplasmosis occurs when the CD4+ count is below

100 cells/µL. CMV and mycobacterium avium complex (MAC) are

encountered with CD4+ count below 50 cells/µL. RESULTS: Variable

LAB. DIAGNOSIS CONT..

SPUTUM STAIN AND CULTURE Three sputum specimens obtained on 3 consecutive

days should be examined for AFB and cultured for mycobacteria.

Toluidine Blue O (TBO) staining has an acceptable sensitivity and very high specificity in expectorated sputum samples for PCP.

RESULTS: Acid-fast bacilli (AFB) stain and mycobacterial culture

are positive in TB and MAC TBO staining is positive in PCP


Blood cultures Two blood cultures are usually sufficient for the

detection of disseminated MAC. One blood culture identifies 91% of patients with MAC bacteraemia, while a second blood culture increases the identification rate to 98%. However, up to 6 weeks of culture may be required, which limits the clinical utility.

Up to 75% of patients with HIV-associated cryptococcal meningitis have positive blood cultures. Blood cultures may be helpful if disseminated disease is suspected in the absence of meningitis.

RESULTS: May be positive in MAC and cryptococcus infection


CMV cultures Blood, other body fluids or tissue specimens; the test can be

done using conventional tube cell culture or shell vial assay. RESULTS presence or absence of cytopathic effects CMV serology The test is done using ELISA. The utility of CMV serology is

modest since invasive disease is more commonly due to re-activation than to primary infection

RESULTS: CMV-IgM titre is indicative of acute infection; CMV-IgG

titre suggests past infection


TOXOPLASMA GONDII SEROLOGY Presence of anti-T gondii IgM antibodies does not

necessarily indicate a recently acquired infection as they can remain elevated for more than 1 year. Recent T gondii infection is likely when serial specimens obtained at least 3 weeks apart and tested in parallel reveal at least a 4-fold increase in IgG titres.

RESULTS: Presence of anti-T gondii IgM and IgG suggest recent

and past infection, respectively


FULL BLOOD COUNT Anaemia is common in HIV-infected patients with

opportunistic infections. In disseminated MAC, the anaemia is an important negative predictor for survival, is usually profound, and is often accompanied by leukopenia and thrombocytopenia.

RESULTS Anaemia often accompanied by leukopenia and

thrombocytopenia


CRYPTOCOCCAL POLYSACCHARIDE ANTIGEN Very specific; sensitivity is greater than 90%. High

initial CSF titres (≥1:1024) are a marker of poor prognosis and correspond to a high organism burden. CSF antigen titres fall with successful treatment.

RESULTS From serum or CSF; titre above 1:4


LIVER FUNCTION TESTS Alkaline phosphatase is elevated in HIV-infected

patients with MAC or CMV hepatobiliary disease. In CMV hepatitis, it is usually accompanied by elevation of AST and ALT.

RESULTS: Elevated


LACTATE DEHYROGENASE Elevated in MAC, and frequently elevated in PCP.

Serial determinations of LDH during successful treatment for PCP show a gradual decline of LDH. Thus it may serve as a prognostic indicator in PCP.

However, elevated LDH should be interpreted with caution, because it is also elevated in patients with various other lung diseases, such as pulmonary TB and other bacterial pneumonias

RESULTS: Elevated

THE OPPORTUNISTIC INFECTIONS INCLUDE:

Fungal infections Pneumocystis jiroveci pneumonia (PCP) Candidiasis Cryptococcosis

Bacterial infections Tuberculosis Mycobacterium avium complex (MAC) infections

Parasitic infections Toxoplasmosis Cryptosporidiosis Isospridiam

Viral infections Herpes simplex virus infection (HSV) Cytomegalovirus virus CMV Varicella Zoster Virus

FUNGAL INFECTIONS

P JIROVECI PNEUMONIA

Pneumocystis microbes are classified in the fungus kingdom on the basis of DNA analysis but also share biologic characteristics with protozoa.

The organism that infects humans and causes PCP is now named Pneumocystis jiroveci.

HIV-infected patients with PCP have a similar presentation to non-HIV immunosuppressed patients, but the median duration of their symptoms before diagnosis is much longer (28 v 5 days, respectively)

Clinical features of PCP among HIV-infected children are similar to those in adults (i.e., fever, tachypnea, dyspnea, and cough).

LAB. DIAGNOSIS

Serum Lactic dehydrogenase (LDH) is ↑ but serial determinations of LDH during successful treatment for PCP show a gradual decline of LDH.

PCR Toluidine blue stains the cyst wall blue or lavender

Gomori's methenamine-silver stains the cyst wall brown or black

Giemsa or Wright's Stain, stains the trophozoites and intracystic sporozoites pale blue with a punctate red nucleus

Po2 >30 mm/Hg

CRYPTOCOCCUS INFECTION

Usually presents as a sub-acute meningitis or meningoencephalitis with fever, malaise and headache.

However, disseminated disease can occur, with or without concurrent meningitis.

In such cases, pulmonary involvement or skin lesions may be present.

LAB. DIAGNOSIS

CSF findings include: a mildly elevated protein, normal or slightly low glucose, a few lymphocytes and numerous organisms. India ink examination on the CSF should be performed. The cryptococcal antigen in the CSF is almost always

positive in patients with meningitis or meningoencephalitis.

Evaluation of cryptococcal antigen in the serum should also be considered.

Blood cultures: HIV-associated cryptococcal meningitis have positive blood

cultures for Cryptococcus neoformans.

Candidiasis

Candida albicans is the most common cause of mucosal and esophageal candidiasis.

The condition is often associated with low CD4+ cell count (<100/μl), high viral load, and neutropenia (<500/μL)

Patients may present with oral, oesophageal or vaginal infection.

Candidiasis cont..

Manifestations include pseudo-membranous candidiasis (oral thrush) with altered taste sensation and/or difficulty swallowing liquids and solids;

odynophagia or dysphagia in oesophageal disease,

In vaginal disease, erythema with adherent white discharge, marked itching, and swelling of labia

LAB.DIAGNOSIS

A scraping for microscopic examination for yeast forms, using a 10% potassium hydroxide (KOH) preparation, may show characteristic findings, including pseudo-hyphae and budding yeast.

Cultures are usually not necessary unless the lesions fail to resolve on antifungal treatment.

TAKE HOME MESSAGE

Opportunistic infections do not cause illness in healthy people and are not contagious.

Primary Prophylaxis prevents the first episode of an opportunistic infection.

Adherence to prophylactic medications is very important, especially to INH.

Good personal hygiene and careful food preparation can reduce (but not eliminate) risk for some opportunistic infections.

BACTERIAL INFECTIONS

TUBERCULOSIS (TB)

TB is an infectious disease that affects mainly the lungs (Pulmonary TB or PTB) but can also attack any part of the body such as kidney, spine and brain (Extra-pulmonary TB or EPTB).

The most common transmission is human to human although incidences of animal to human through unpasteurized cow’s milk.

THE CAUSE OF TB

Mycobacterium tuberculosis

Mycobacterium bovis

TB TRANSMISSION

Person to person

Via

Airborne transmission

In

Confined environment

RISK FACTORS FOR INFECTION

Exposure to TB bacilli Duration of exposure to a person with PTB Intensity of exposure

Note: Untreated AFB smear positive cases are the most

infectious. Development of the disease depends on individual

susceptibility; HIV increases the risk of getting TB disease

EPIDEMIOLOGY

1/3 of world’s population is infected with TB (WHO 2008 report).

In 2007,there were 9.27million new cases of TB (139 per 100,000 population) worldwide.

95% of TB cases and 98% of TB deaths are in the developing countries.

75% of TB cases in developing countries are in (15-50 years).

14.8% (1.37 million) of the 9.27 million were HIV positive In 2005 Swaziland had highest incidence of TB with1262

cases per 100,000.

PATHOPHYSIOLOGY

Infection with TB requires inhalation of droplet nuclei. Following deposition in the alveoli, M. tuberculosis is

engulfed by alveolar macrophages, but survives and multiplies within the macrophages.

Proliferating bacilli kill macrophages and are released; this event produces a response from the immune system.

Exposure may lead to clearance of M. tuberculosis, persistent latent infection or progression to primary disease.

PATHOPHYSIOLOGY CONT..

Active TB typically occurs through a process of re-activation.

Approximately 10% of individuals with latent infection will progress to active disease over their lifetime.

The risk is greatest within the 2 years following initial acquisition of M. tuberculosis.

A number of conditions can alter this risk, particularly HIV infection, in which the annual risk of developing active TB is 8% to 10%.

Immunocompromised conditions and treatment with immunosuppressing medicines, including systemic corticosteroids also contribute to re-activation.


Successful containment of TB is dependent on the cellular immune system, mediated primarily through T-helper cells (TH1 response).

T cells and macrophages form a granuloma with a centre that contains necrotic material (caseous centre), M. tuberculosis and peripheral granulation tissue consisting primarily of macrophages and lymphocytes; the granuloma serves to prevent further growth and spread of M. tuberculosis.

These individuals are non-infectious and have latent TB infection; the majority of these patients will have a normal CXR and be tuberculin skin test (TST) -positive.

PATHOGENESIS

Active TB typically occurs through a process of re-activation.

Approximately 10% of individuals with latent infection will progress to active disease over their lifetime.

The risk is greatest within the 2 years following initial acquisition of M. tuberculosis.

A number of conditions can alter this risk, particularly HIV infection, in which the annual risk of developing active TB is 8% to 10%.

Immunocompromised conditions and treatment with immunosuppressing medicines, including systemic corticosteroids and TNF-alpha antagonists, also contribute to re-activation.

PATHOGENESIS CONT..

Pulmonary TB Occurs when the primary infection does not heal completely and

there is continued multiplication of organisms in the lung several months or years later due to poor health, malnutrition and defective immune responses.

An inflammatory reaction leads to a liquefied destruction of the lung tissue with caseation (a cheese like mass).

Erosion through the wall of a bronchus leads to the discharge of the liquefied tissue and the formation of a cavity.

Bacilli multiply in the wall of the cavity and can be found in the sputum (‘open’ infectious stage).

PATHOGENESIS CONT..

Tuberculous Meningitis Tubercle bacilli reach the meninges in the blood. Occurs more frequently in non-immune infants and young

children as a complication of primary tuberculosis. Condition is often fatal unless treated an early stage.

Miliary tuberculosis Occurs if the site of primary infection ruptures through a blood

vessel and bacilli are disseminated throughout the body. Many small granulomata are formed which on a chest X-ray look

like millet seeds (hence name miliary TB). Pts are often acutely ill with fever. The liver, spleen and lymph

glands may be enlarged .

PATHOGENESIS CONT…

Renal and Urogenital TB Tubercle bacilli reach the kidneys and genital tract by way of the

blood circulation usually some years following primary infection. Renal infection is often suspected when repeated urine specimens

are found to contain pus cells but no organisms isolated by routine culture.

There may be frequency in passing urine, haematuria and usually a recurring fever.

Note Tuberculosis of the genital tract (epididymitis in males,

endometrial tuberculosis in females) can cause infertility and pelvic inflammatory disease.

PATHOGENESIS CONT….

Bone and Joint TB/Spinal TB A commonly infected site is the spine which may lead to collapse

of vertebrae and the formation of a ‘cold’ abscess in the groin. TB starts in an intervertebral disc and spreads along the and

longitudinal ligaments before involving adjacent vertebral bodies

NOTE Diagnosis of PTB in children is more difficult because there is

rarely a cough with sputum production. A diagnosis is usually made from a positive tuberculin reaction

and X-ray. There is weight loss and failure to thrive.

REMEMBER

The diagnosis of TB can be overlooked, as it may present with signs and symptoms (such as fevers, weight loss and malaise) that may be attributed to HIV itself

The clinical manifestations of pulmonary TB may be different depending on the level of immunosuppression in HIV-infected persons

A high index of suspicion must be maintained when evaluating an HIV-infected patient with symptoms suggestive of TB, as chest x-rays may appear normal in 7% to 14% of cases

Depending on the involved site, TB may present with shortness of breath, cough, lymphadenopathy, headache, meningism, abdominal pain, dysuria or abscess formation.

LABORATORY DIAGNOSIS

Acid-fast bacilli (AFB) stain: Ziel-Neelsen or Auramine-phenol 3 sputum specimens should be obtained on 3 consecutive days,

examined for AFB. Specimens obtained through bronchoscopy with bronchoalveolar

lavage and trans-bronchial biopsy may be useful in the evaluation of an abnormal chest x-ray when sputum smears are negative.

In extra-pulmonary TB, specimens from other sites should be also examined for AFB.

Culture Lowenstein Jensen egg medium. Molecular tests: nucleic acid amplification (NAA); PCR Can detect nucleic acid sequences unique to organisms in the

Mycobacterium tuberculosis complex, allowing for a rapid diagnosis.

LABORATORY DIAGNOSIS CONT..

Tuberculin Skin Test Tuberculin is a purified protein derived from tubercle bacilli. Also

known as PPD (purified protein derivative). Following infection with M. tuberculosis, a person develops

hypersensitivity to tuberculin. Tuberculin injected into the skin of an infected person produces a

delayed local reaction after 24-48 hours. This reaction is quantified by measuring the diameter of skin

induration (thickening) at the site of the reaction.

Note The test does not measure immunity. By it itself, it does not

indicate the presence or extent of TB disease; it only indicates infection with M. tuberculosis.

ACID FAST PRINCIPLE

Primary stain penetrates cell wall. Intense decolorization does not release primary stain

from the cell wall of AFB. Color of AFB based on primary stain. Counter stain provides contrasting background

SMEAR PREPARATION AND STAINING

STAINING CHARACTERISTICS

oMycobacteria are called Acid Fast Bacilli (AFB) due to their microscopic appearance after decolorizing.

oOrganisms appear red on a blue background

MALAWI DIAGNOSIS SET UP

Reference Laboratory CHSU Microscopy (ZN and Auramine-phenol) Culture (Lowenstein Jensen egg-medium)

Central Hospitals Microscopy (ZN and Auramine-phenol) Tuberculin Skin test (PPD)

District Hospitals Microscopy (ZN /Auramine-phenol)

Health Centre Microscopy (ZN)

MALAWI DIAGNOSIS SET UP CONT..

Culture is done only at the Reference Lab To manage treatment failures and patients that have

relapsed. To monitor multi-drug resistance To identify M. tuberculosis variants and strains e.g.

M. bovis.

MYCOBACTERIUM AVIUM COMPLEX Mycobacterium avium complex refers to multiple

related species of non-tuberculous mycobacteria (e.g., M. avium, M. intracellulare, M. paratuberculosis)

Typically occurs in AIDS patients who have CD4+ counts below 50 cells/µL

Clinical presentation may include symptoms and signs (e.g., persistent fever, night sweats, fatigue, weight loss and anorexia).

More unusual presentations include palatal and gingival ulceration,septic arthritis and osteomyelitis, endophthalmitis, pericarditis and GI bleeding.

LAB. DIAGNOSIS

FBC may show anaemia (often severe) and leukopenia. Abnormal LFTs, including elevated alkaline

phosphatase and LDH, and low albumin. Bacteraemia: blood cultures should be drawn from all

patients. The most sensitive method for the detection of mycobacteraemia is by a lysis-centrifugation blood culture system.Biopsy of bone marrow (or colon in colitis) with culture from tissue obtained may be useful, although blood cultures are more sensitive.

In patients with CD4+ count of 50 cells/microlitre or greater, a history of fever for more than 30 days, a haematocrit below 30% or a serum albumin level below 30 g/L (<3.0 g/dL) are sensitive predictors of MAC bacteraemia.

VIRAL OI

Opportunistic Infections

62

Clinical Latency

At CD4 cell counts over 500 cells/uL many complications overlap with conditions found in uninfected populations (bacterial pneumonia, tuberculosis, minor skin conditions), but they may be more frequent.

At CD4 counts between 200 and 500 cells/uL other conditions and opportunistic infections may begin to appear (Kaposi’s sarcoma, oral candidiasis, herpes zoster, etc.).

Herpes Simplex infection

Caused by two closely related viruses, identified as type 1 and type 2. They cause a wide variety of primary and recurrent mucocutaneous infections.

Following a 1 0 infection, the virus maintains a latent state, and recurrent disease is caused by reactivation of the latent viral infection.

Primary genital herpes is the most common cause of genital ulceration. The typical incubation period is 3 to 14 days after sexual exposure. The primary lesion begins as a small group of painful, pruritic vesicles, which break down to form ulcerating, pustular lesions in 2 to 4 days..

HSV cont…

By the time the patient sees a physician, the lesions are usually in the ulcerative phase. Painful, enlarged inguinal lymph nodes are common. New lesions will continue to form during the first week of the primary illness in about 75% of patients

About 2/3 of patients will have systemic symptoms including fever and headache. Fewer than 10 % of patients will develop aseptic meningitis or urinary retention. The duration of the illness may total 14 to 21 days..

In the immunocompromised patient, herpetic infections may be associated with progressive mucocutaneous ulcerations of the face, mouth, or anogenital regions. Lesions may coalesce, forming large, superficial ulcers that last for weeks or months.

Herpes Simplex

HSV cont…

Herpes Simplex Lesions begin as painful, pruritic grouped vesicles Vesicles break down to form an ulcer Lesions are located in the anogenital areaCutaneous anthrax Ulcer is painless Lesion is located on exposed parts of the body Ulcer and eschar are surrounded by characteristic non-

pitting edema

Cytomegalovirus (CMV)

Member of the herpes virus family

(EBV, varicella-zoster, herpes simplex) Worldwide seroprevalence 30-100% Found in body fluids

Blood, saliva, urine, breast milk Most people are infected with CMV at some point in

life

Types of CMV Infection

Primary infection

(asymptomatic to mononucleosis like syndrome in immune competent individuals)

Latent infection

(presence of viral genome in mononuclear leukocytes, endothelial cells, and organs in the absence of active replication of infectious virus)

Reactivation during a period of immunosuppression 20 to drugs or intercurrent infection (eg, HIV).

Reinfection

(new strain of CMV)

CMV continue..

is usually an asymptomatic infection. Clinically significant CMV disease frequently develops in patients immunocompromised by HIV, solid-organ transplantation, and bone-marrow transplantation.

congenital transmission from a mother with acute infection during pregnancy is a significant cause of neurological abnormalities and deafness in newborns

CMV diseases

CMV retinitis is a common opportunistic infection in late-stage AIDS, typically with CD4+ lymphocyte counts of less than 50 cells/µL. Typically, patients exhibit a progressive decrease in visual acuity, which may progress to blindness if untreated.

Gastritis and Colitis-CMV may infect the gastrointestinal tract from the oral cavity through the colon. The typical manifestation of disease is ulcerative lesions.

CMV disease cont..

Pneumonia -Adults manifesting CMV infection as a mononucleosis syndrome may occasionally have

pneumonia. Hepatitis

Detection of CMV Infection

Immune status: serology (IgG) Active infection (viremia)

Histology Viral culture Shell vial culture Antigenemia assay CMV PCR (qualitative/quantitative)

Varicella- zoster virus (VZV)

commonly causes chicken-pox in children and both shingles and postherpetic neuralgia in adults.

10 infection results in chickenpox (varicella), which may rarely result in complications including encephalitis or pneumonia.

VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia. In about 10-20% of cases, VZV reactivates later in life producing a disease known as herpes zoster or shingles. Serious complications of shingles include postherpetic neuralgia, zoster multiplex, myelitis, or herpes ophthalmicus.

Pathogenesis

Replication of the virus occurs in the respiratory and viremia follows.

Virus is taken up by endothelial cells where it undergoes replication.

Immumne sytem is overwhelmed and during 2nd viremia chills and fever becomes evident.

Virus lodges in capillary endothelial cells of the skin and then spread to the epithelial cells followed by rash development and vesicle formation confine in facial, lumbar and thoracic areas.

Pathogenesis contin..

Vesicles fall off become crusted and fall off within 1wk ( chicken pox)

During vesicle development, virus is transported to cranial nerves and dorsal root ganglion by movement along the sensory nerve.

During immunosupresion, latent virus in posterior root or cranial sensory nerve ganglion is reactivated.

Virus moves down to the skin and produce lesions Lesions heal 3-4wks and subsides

Pathogenesis cont

Posthepatic neuralgia frequently occurs in adults >60yrs old. (Due to scarring of in the ganglia and afferent portions of the sensory nerves.

Zoster develops early in the course of disease in immunocompromised patients.

PARASITIC OI

Toxoplasmosis

Etiological agent-T gondii Acquired by both immunocompetent and

immunocompromised individuals. Human get infected by ingestion of infected warm

blooded animals or ingestion of contaminated food with cat feces.

Trophozoites 1st invade the intestinal mucosa and may invade any organ where they develop into tissue cysts

Cysts remain dormant in immunocomptent person but are reactivated when immune system is impaired

Toxoplasmosis cont…

10 site of infection is the brain followed by lungs.

In pregnant woman T. gondii infection may result to congenital toxoplasmosis.

Congenital toxoplasmosis may lead to: Mental retardation Chorioretinitis Cerebral calcifition


Seropositivity for anti-toxoplasma IgG antibodies makes the diagnosis more likely; however, absence of these antibodies does not exclude it

CSF shows mild mononuclear pleocytosis and elevated protein. Giemsa staining can show tachyzoites. DNA amplification can be useful in detecting T gondii in the CSF.

Cryptosporidiosis

A highly infectious intestinal parasite found most commonly among farm and domesticated animals. It is transmitted through contaminated food and water.

Results in watery diarrhea which resolves < 1 months but becomes unreletented in immunocompromised. Other symptoms include; weight loss, abdominal cramps, nausea, vomiting, fever, and headache.

In immunocompromised patients fluid loss may reach up to 3 to 6 liters per day.

LABORATORY DIAGNOSISLABORATORY DIAGNOSIS

acid-fast stain is traditionally used to most reliably and specifically detect the presence of cryptosporidial oocysts .

Immunologically, anti-cryptosporidial IgM, IgG, and IgA can be detected by ELISA or by the antibody immunofluorescence assay (IFA).

genetic methods of detecting C. parvum PCR (Polymerase Chain Reaction) or other DNA-based detection methods.

acid-fast stain

Isospra belli

Infection with I. belli begins when the mature oocyst is ingested in water or food.

In the immunocompetent, infection is generally asymptomatic or a self-limiting gastro-enteritis.

Infection in immunocompromised individuals ranges from a self-limiting enteritis to severe diarrhoeal illness resembling that of cryptosporidiosis.


Oocytes can be demonstrated in faeces after formal ether concentration where they appear as translucent, oval structures measuring 20-33m by 10-19m.

oocysts can be seen in a faecal smear stained by a modified Ziehl-Neelsen method , where they stain a granular red colour against a green background, or by phenol-auramine. Oocyte stained by MZN

REFERENCES:

www.aids-etc.org www.aidsinfo.nih.gov CDC. Guidelines for the prevention of opportunistic

infections in persons infected with human immunodeficiency virus: a summary. MMWR 1995;44(No. RR-8).

CDC. Guidelines for the prevention of opportunistic infections in persons infected with human immunodeficiency virus. MMWR 1997;46(No. RR-12).

CDC. Guidelines for the prevention of opportunistic infections in persons infected with human immunodeficiency virus. MMWR 1999;48(No. RR-10).

REFERENCES CONT..

CDC. Guidelines for the prevention of opportunistic infections among HIV-infected persons–- recommendations of the U.S. Public Health Service and the Infectious Disease Society of America. MMWR 2002;51(No. RR-8).

TB/HIV A clinical Manual 2nd ED WHO Monica Cheesebrough Part II Basic Medical Microbiology Robert boy F.Boyd 5th ED

pages 411- 417, 515 - 517

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