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Friday, August 17, 2012

IS THERE PROOF THAT HIV-POSITIVE PERSONS CONSISTENTLY DEVELOP ILLNESSES THAT ARE RARE OR NEVER OCCUR IN HIV NEGATIVE PERSONS?


IS THERE PROOF THAT HIV-POSITIVE PERSONS CONSISTENTLY DEVELOP ILLNESSES THAT ARE RARE OR NEVER OCCUR IN HIV NEGATIVE PERSONS?
By Mohammed Al-Bayati
Sept. 2001

I am presenting here a brief description of the HIV-hypothesis and a list of AIDS- defining diseases as defined by the USA Centers for Disease Control and Prevention (CDC) and the scientists at the National Institute of Health (NIH)] to see if all of these illnesses really existed prior to making HIV the cause of AIDS by the CDC in 1984 or whether some of these diseases are rare or never occur in HIV negative persons.
Pathology of AIDS as described by the CDC
The HIV-hypothesis states that HIV causes AIDS by killing the CD4+ T cells directly or indirectly, and after long incubation times (about 10 years), the number of these cells will reach very low levels which lead to severe immune deficiency. Patients with CD4+ T cells < 200/µL usually suffer from opportunistic infections and certain forms of cancer such as Kaposi’s sarcoma and lymphoma. The USA Centers for Disease Control and Prevention (CDC) called the following opportunistic diseases and cancers AIDS-defining diseases when associated with low CD4+ T cells count (<500 /µL of blood) [1,2]
The CDC’s list of AIDS-defining diseases:
A) Viral, bacterial, fungal, and yeast infections:
  1. Candididiasis, oropharyngeal (thrush), bronchi, trachea, lungs, and vulvovaginal
  2. Listeriosis
  3. Toxoplasmosis of brain
  4. Histoplasmosis infection
  5. Isosporiasis
  6. Mycobacterium tuberculosis
  7. Pneumocystis carinii pneumonia
  8. Herpes zoster
  9. Cytomegalovirus.
  10. Bacillary angiomatosis
  11. Cryptococcosis
  12. Cryptosporidiosis
  13. Isosporiasis
  14. Salmonella septicemia, recurrent
  15. Pneumonia, recurrent
B) Idiopathic and inflammatory conditions:
  1. Diarrhea lasting more than one month
  2. Wasting disease
  3. Idiopathic thrombocytopenic purpura
  4. Peripheral neuropathy
  5. Encephalopathy
  6. Progressive multifocal leukoencephalopathy
  7. Pelvic inflammatory disease, particularly if complicated by tuboovarian abscess.
  8. Hairy leukoplakia, oral
C) Cancer
  1. Cervical dysplasia and carcinoma in situ
  2. Cervical cancer invasive
  3. Kaposi’s sarcoma
  4. Lymphoma, Burkitt’s (or equivalent term)
  5. Lymphoma, primary, of brain
My evaluation of the medical literature revealed that the list of opportunistic infections presented above are also described in patients receiving organ transplants and patients with chronic illnesses who are treated chronically with high doses of corticosteroids and other immunosuppressive agents and in people suffering from malnutrition. These illnesses have been reported prior and after the appearance of AIDS epidemic in the USA in 1981 in HIV-negative and HIV-positive individuals. In addition, some of the illnesses on the CDC’s list such as pelvic inflammatory disease, cervical dysplsia, and cervical cancer have been reported in women with normal immune system [1,2]. Below are the descriptions of seven of these illnesses that are called AIDS-defining diseases by the CDC and the pathology of malnutrition in relation to the immune system to illustrate my points. The epidemiology and the pathology of other diseases on the CDC list are described in Al-Bayati’s book [1] and Fauci et al.’s book [2].
Tuberculosis (TB)
Tuberculosis (TB) is caused by Mycobacterium tuberculosis and is one of the diseases listed by the CDC as an AIDS-defining disease[1,2]. This disease has been known for more than one thousand years. It occurs most commonly in people suffering from malnutrition, cancer, diseases of the immune system, people treated chronically with immunosuppressive agents, and in illicit drug users. There is overwhelming published information demonstrating that HIV has nothing to do with TB. The best medical evidence to prove these points is presented by Fauci et al. [2].
Briefly, Fauci et al. reported that "TB is one of the oldest diseases known to effect humanity. This has been proved by the findings of tuberculous spinal disease in Egyptian mummies. During the industrial revolution and the period of related urbanization in the seventeenth and eighteenth centuries, tuberculosis became a problem of epidemic proportions in Europe, causing at least 20 percent of all deaths in England and Wales in 1650. In the eastern part of the United States, the annual mortality rate from tuberculosis in the early nineteenth century was approximately 400 per 100,000 population". They also stated that "approximately 3.8 million new cases of tuberculosis, 90 percent of them from developing countries, were reported to the World Health Organization in the early 1990s. However, because of a low level of case detection and poor reporting in many national programs, reported cases represent only a fraction of the total. It is estimated that 8.8 million cases of tuberculosis occurred worldwide in 1995, 95 percent of them in developing countries of Asia (5.5 million), Africa (1.5 million), the Middle East (747,000). It is also estimated that nearly 3 million deaths from tuberculosis occurred in 1995 and 98 percent of them in developing countries"[2]. Sheik et al. examined 183 cases of lymphadenopathy involving various sites in Indian children and they found that 49.2% proven to be of tubercular origin [3].
Fauci et al. also stated that "the risk of developing TB after being infected depends largely on endogenous factors, such as the individual’s innate susceptibility to diseases and level of function of cell-mediated immunity. Clinical illness directly following infection is classified as primary tuberculosis and is common among children up to 4 years of age. This form is often severe and disseminated. Dormant bacilli, however, may persist for years before being reactivated to produce secondary tuberculosis, which is often infectious. Overall, it is estimated that about 10% of infected persons will eventually develop active tuberculosis. Conditions known to increase the risk of active tuberculosis among persons infected with tubercle bacilli include silicosis; lymphoma, leukemia and other malignant neoplasm; hemophilia; chronic renal failure and hemodialysis; insulin- dependent diabetes mellitus; immunosuppressive treatment; and conditions associated with malnutrition"[2].
Furthermore, the risk factors in drug users of getting pneumonia and TB were also explained by Fauci et al. as follows: "Community-acquired bacterial pneumonia was commonly described among drug users. The putative risk factors in drug users included pulmonary aspiration resulting from intermittent overdose, deleterious effects of opiates on lung defenses and cough reflex, hypoventilation due to respiratory depression and smoking. The other important pulmonary infection described in drug injectors is tuberculosis. Infections due to M. tuberculosis were well documented in drug users before the AIDS epidemic, accounting for greater morbidity and mortality in this population than in the non-drug-using population. Although some authors attributed this greater impact to poverty, poor housing, and the social and demographic factors associated with both drug use and tuberculosis, others found an elevated risk of tuberculosis among drug users even after attempting to control for these other factors. There is also evidence that tuberculous meningitis and focal tuberculomas of the brain may be more common among drug users than other patients with tuberculosis, with or without HIV infections. Finally, ocular infections have been well described in drug injectors" [2].
In addition, the standard treatment for TB in patients with AIDS are glucocorticoids and isoniazid. The side effects of isoniazid are hepatitis, peripheral neuritis and optic neuritis. Peripheral neuropathy is considered one of the AIDS-defining disease by the CDC and the treatment for peripheral neuropathy is glucocorticoids [1,2,4,5,6]. The doses of glucocorticoid that are given to a patients with AIDS can cause AIDS in a healthy person [1,2,4,5,6].
Pneumocystis carnii pneumonia (PCP)
PCP is one of the opportunistic infection classified by the CDC as an AIDS-defining disease. My review of the medical literature shows that this disease exist prior to HIV and has nothing to do with it . It occurs as a result of the use of local and/or systemic immunosuppressive agents, malnutrition, and other diseases that effects the immune system [1]. The predisposing factors for PCP were described by Fauci et al. [2]. Briefly, they stated that Pneumo-cystis carinii is an opportunistic pathogen whose natural habitat is the lung. The organism is an important cause of pneumonia in the compromised host. P. carinii pneumonia occurs in premature and malnourished infants; children with primary immunodeficiency diseases; and patients receiving immunosuppressive therapy (particularly glucocorticoids) for cancer, organ transplantation, and other disorders. Symptoms often began after the glucocorticoid dose has been tapered.
Jones et al. reviewed the medical records of 15,558 homosexual men and 4475 drug users. They found that 6.8% and 8.3% of homosexuals and drug users had PCP, respectively[7]. Sepkowitz et al. conduced a twelve-year retrospective review from a tertiary-care cancer center that included 134 HIV-negative cancer patients. Corticosteroids were found to be a significant risk factor for PCP in 116 (87%) of these patients. The median maximum corticosteroid dose was 80 mg prednisone and the median length of time receiving corticosteroids was 3 months [8]. In addition, Caiaffa et al. examined the risk factors for the first episode of bacterial pneumonia among 40 HIV-seropositive injection drug users (IDUs) and found that the most distinctive behavioral characteristic among these patients associated with an increased odds of bacterial pneumonia was the practice of smoking drugs other than cigarettes (marijuana, cocaine, crack). The association of smoking illicit drugs with bacterial pneumonia was independent of the level of immunosuppression, age, and cigarette smoking. Habitual marijuana smoking is also associated with chronic respiratory symptoms but causes functional impairment with chronic respiratory symptoms predominantly in large airways[9].
Recurrent pneumonia
Recurrent pneumonia caused by Streptococcus pneumoniae and Haemophilus influenzae is considered an AIDS-defining disease by the CDC. It has been very well documented that this disease can occur in any individual (HIV-positive or HIV-negative) if the conditions are favorable such as smoking, crowded environments such as gay bars, use of drugs, malnutrition, use of steroids. etc. These facts have been known for more than 100 years prior to the appearance of AIDS in America [1,2].
Fauci et al. [2] stated that "Streptococcus pneumoniae was recognized as a major cause of pneumonia in the 1880s and has been central focus of study to modern understanding of humoral immunity. S. pneumoniae colonizes the nasopharynx and can be isolated from 5 to 10 percent of healthy adults and from 20 to 40 percent from healthy children. Pneumococci spread from one individual to another as a result of extensive close contact; transmission may be enhanced by poor ventilation. Day-care centers have been a site of spread of penicillin-resistant stains. Epidemics among adults are associated by with crowded living conditions-e.g., in military barracks, prisons, and shelters for the homeless. The incidence of pneumoccocal bacteremia is relatively high among infants up to 2 years of age and low among teenagers and young adults; rates increase steadily beginning at around age 55. The incidence of pneumococcal bacteremia among adults exhibits a distinct midwinter peak and a striking dip in summer. The predisposing factors for Streptococcus infection are glucocorticoid treatment, defective antibody formation, malnutrition, alcoholism, infancy and aging, cigarette smoking. Etc"[2].
Candidiasis
Candidiasis of the vagina can occur even in normal women, women treated with antibiotics, and in diabetic patients [1,2]. Fauci et al. stated that candidiasis is often preceded by increased colonization of the mouth, vagina, and stool with Candida due to broad-spectrum antibiotic therapy and additional local and systemic factors favor infection. Oropharyngeal thrush particularly occurs in neonates and in patients with diabetes mellitus. Vulvo-vaginal candidiasis is especially common in the third trimester of pregnancy. Candida from the perineum can enter the urinary tract via an indwelling bladder catheter. Cutaneous candidiasis most often involves macerated skin, such as that in the diapered area of infants, under pendulous breasts, or on hands constantly in water or covered by occlusive gloves. Intravenous drug abuse or third-degree burns can also provide a skin portal for Candida that can lead to deep candidiasis. Once Candida has passed the integmentary barrier, hematogenous seeding is particularly evident in the retina, kidney, spleen, and liver in very low birth weight babies ( neonates) and in patients suffering from neutropenia or use glucocorticoid therapy that markedly decrease host defense[2]. Belcomethasone dipropionate (glucocorticoid aerosol) is used to treat asthma and chronic respiratory infection in drug users, homosexuals, and heterosexuals. Localized infections with Candida albicans or Aspergillus niger have occurred in the mouth and pharynx and occasionally in the larynx. Positive culture for oralCandida may be present in up to 75% of patients. Glucocorticoid aerosols also have systemic side effects[1,4].
Histoplasmosis
This disease caused by a fungus found in the soil and effects healthy children and adults and immunocomprised hosts. It has been reported prior to the discovery of HIV. Its inclusion as an AIDS-defining disease by the CDC is a big puzzle to me and probably to any person who reads the description provided by Fauci et al. stated below [2].
Fauci et al. reported that "Histoplasmosis is a disease cause by Histoplasma capsulatum (fungus). Infection has been encountered in many areas of the world but is much more frequent in certain areas. Endemicity is probably contingent on the availability of proper conditions in nature for growth of the fungus. H. capsulatum prefers moist surface soil, particularly soil enriched by droppings of certain birds and bats. It is an opportunistic disease endemic to the Mississippi and Ohio River valleys, Puerto Rico, the Dominican Republic, and South America. Many case clusters have occurred 5 to 18 days after the exposure of groups of people to dust, while cleaning dirt-floored chicken coops, bulldozing, or cave exploring. Skin-test-reactivity in many endemic areas indicates that 80 percent or more of residents over age 16 have been exposed. Microconidia, or small spores, of H. capsulatum are small enough to reach the alveoli upon inhalation and begin to bud there. With time, an intense granulomatous reaction occurs. Caseation necrosis or calcification may mimic tuberculosis. Chronic pulmonary infection favors otherwise healthy males over the age of 40. A history of cigarette use is elicited from nearly all patients with chronic progressive pulmonary histoplasmosis. An acute, rapidly fatal course is most likely to be encountered among young children and immunosuppressed patients, including those with AIDS. The symptoms of acute infection include fever, emaciation, hepatosplenomegaly, lymphadenopathy, jaundice, anemia, leukopenia and thrombocytopenia. Chronic but equally lethal disseminated infection is more common among previously healthy adults"[2].
In addition, thrombocytopenia is one of the symptoms of acute histoplasmosis. Recall that this is also an AIDS-defining disease and the standard treatment for thrombocytopenia is glucocorticoids and immunosuppressive agents as described by Fauci et al. [2].
Cervical Cancer and Pelvic Inflammatory Disease (PID)
Diseases of the reproductive system are very common and were known prior to the AIDS era. They have no relation or any connection to HIV. They have been caused by sexually transmitted and nonsexually transmitted infectious agents and may be other factors and their occurrence is dependent on many physiological and environmental factors. They occur in women with or without immune deficiency. Adding these diseases to the list of AIDS-defining diseases is not supported by any scientific facts and it also made the picture of AIDS more complicated and horrifying.
A) Pelvic Inflammatory Disease (PID):
The CDC considered PID, particularly if complicated by tuboovarian abscess as an AIDS-defining disease with no medical justification. This disease is caused by very common infectious agents and drug use. Gonococcal infection and other sexually and nonsexual transmitted bacterial, viral, fungal infections, parasitic infections cause PID in immunocompromised women and in women with normal immune systems. The CDC in Atlanta estimates that at least 12 million U.S. residents acquire a sexually transmitted disease (STD) per year. Some authorities estimated that at least half of all Americans acquire a sexually transmitted infection by age 35. Fauci et al. stated that "about 850,000 cases of PID occurred per year during the mid 1970s and this period is prior to the AIDS epidemic [2].
Rubin and Farber reported that inflammation of the cervix is exceedingly common and is related to its constant exposure to the bacterial flora in the vagina. Acute and chronic cervicitis result from infection with many microorganisms, particularly the endogenous vaginal aerobes and anaerobes, Streptococcus, Staphylococcus, and EnterococcusNeisseria gonorrhoeae, and Herpes simplex type 2. Some agents are sexually transmitted, whereas others may be introduced by foreign bodies, such as residual fragments of tampons. Excluding N. gonorrhoeaeStreptococcus andStaphylococcus are usually encountered after parturition[10].
In addition, Fauci et al. presented a list of pathogenic agents on page 813 of their book [2] that cause pelvic inflammatory diseases in women and HIV is not among them. They stated that acute PID is almost exclusively a diseases of active women. Important risk factors include a history of salpingitis, a recent history of vaginal douching, and the use of an IUD, particularly the Dalkon shield. Factors cited as possibly contributing to intracanalicular upward spread of gonococci and chlamydiae from the endocervix to endosalpnix include estrogen dominated cervical mucus, attachment to sperm that migrate upward into the tube, use of an IUD, vaginal douching, and menstruation. The onset of symptoms of N. gonorrhoeae-associated and C. trachomatis-associated PID often occurs during or soon after the menstrual period.
Furthermore, the effects of alcohol and illicit drugs on the function of the reproductive system in females are very extensive. Fauci et al. reported that the repeated ingestion of high doses of ethanol by women can result in amenorrhea, decrease in ovarian size, absence of corpora lutea with associated infertility and spontaneous abortions. Women who abuse cocaine have reported major derangement in menstrual cycle function, including galactorrhea, amenorrhea, and infertility. Chronic cocaine abuse may cause persistent hyperprolactinemia as a consequence of cocaine-induced disorders of dopaminergic regulation of prolactin secretion by the pituitary. Cocaine abuse, particularly the smoking of crack by pregnant women, has been implicated in causing an increased risk of congenital malformations and of perinatal cardiovascular diseases in the mother [2]. The only relation between HIV and PID is that they both may be acquired by sexual transmission. Otherwise, PID is an individual entity, not a result of HIV [1].
B) Cervical Dysplasia and Cancer
The CDC also included cervical dysplasia and cervical cancer as AIDS indicator diseases in women. These diseases have nothing to do with HIV. These illnesses have been reported in women with normal immune function and women having immune depression [2,10]. Fauci et al. stated that "Carcinoma of the cervix was once the most common cause of cancer death in women, but over the past 30 years, the mortality rate has decreased by 50 percent. In 1996, there were approximately 15,700 new cases of invasive cervix cancer, and more than 50,000 cases of carcinoma in situ. The disease remains the major gynecologic cancer in underdeveloped countries. It is more common in lower socioeconomic groups, women with early initial sexual activity, multiple sexual partners, and in smokers. Many of these factors suggest a venereal transmission. It appears that the human papillomia viruses (HPV) has an important etiologic role. Uncomplicated HPV lower genital tract infection and condylomatous atypia of the cervix can progress to cervical intraepithelial neoplasia (CIN). This lesion precedes invasive cervical carcinoma and is classified as low-grade squamous intraepithelial lesion (SIL), high grade SIL, and carcinoma in situ. Carcinoma in situ demonstrates cytologic evidence of neoplasma without invasion through the basement membrane, can persist unchanged for 10 to 30 years, but eventually progresses to invasive carcinoma" [2].
It has been also reported in a standard pathology text book that, fifty years ago, cervical cancer was the leading cause of cancer death in American women [10]. With the introduction and widespread application of cytologic screening, the incidence of invasive cervical cancer has been halved and the mortality rate has dramatically decreased. The Papanicolaou smear detects premalignant diseases long before invasion has occurred. Even one smear during a women’s lifetime (which is clearly inadequate), reduces the risk of invasive cancer 10-fold. Cervical cancer remains an important cause of cancer mortality in the United States. With improved surveillance, there has been a marked increase in the incidence of its precursor lesions, cervical intraepithelial neoplasia (CIN), also known as cervical dysplasia and carcinoma in situ. Squamous cell carcinoma is by far the most common type of cervical cancer. Despite its declining frequency in the United States, it still has an incidence of 13,000 new cases annually (15 new cases annually per 100,000 women). By contrast, In Central and South America, parts of Asia, and Africa, squamous cell cancer of the cervix remains a major cause of cancer death. In some high-risk areas, its incidence is 100 new cases annually per 100,000 women [10].
Malnutrition and AIDS
It has been stated that the finding of atrophy of lymphoid tissue in people suffering from malnutrition was observed as early as 1925. For example, Jackson’s review on this topic in 1925 noted that many investigators had found a pronounced tendency of atrophy of lymphoid tissue in all conditions of malnutrition. Thymus weight was exquisitely sensitive to malnutrition and was earlier designated as the "barometer of nutrition [11].
I have found an extensive literature describing the impact of malnutrition on the function and the structure of the immune system in people in Africa. This information clearly demonstrates that AIDS in Africa is caused by starvation and not by HIV. The functions of the immune system, especially the cellular immunity, are impaired in malnutrition cases. The severity of the impairment is dependent on the degree of malnutrition in both human and animals. Table 1 contains a brief description of studies, including 345 malnourished children and two experimental models that show the impact of food deprivation on the size of the thymus and the lymphoid organs [1]. For example, the size of the thymus of 42 malnourished children was reduced by 90% as compared with a case-match normal controls. In a second study involving 110 malnourished children, the thymic area was found to be 20% of the size in healthy children. In addition, Table 2 contains a brief description of the result of studies that included 493 malnourished children who showed impairment in the function of the immune system; especially the cellular immunity[1].
The reduction in the thymus and the lymphoid tissue size and the reduction in the function of the immune system of malnourished children and animals were reversed after proper feeding as shown in Table 3. For example, the size of the thymus increased from 20% of normal in a malnourished child to 107% of normal following 9 weeks of proper feeding. The reversal of the reduction in CD4+T cell count in HIV+ pregnant women following proper feeding was also reported by Fawzi et al. [12]. Briefly, the influence of diet on T cells counts in peripheral blood in 1,075 HIV-infected pregnant women who had poor nutritional status were studied. The CD4+ T cell counts of the women who received multivitamin increased from 424/µL to 596/µL during six months of proper feeding [1,12 ].
The incidence of starvation, parasitic diseases, septicemia, and low birth weight are very high in Africa and other developing countries [1,2]. Table 4 contains a brief description of eleven studies that include the prevalence of malnutrition and diseases in 1,425 infants and 5,834 children surveyed in nine countries. For example, the mortality among 299 severely malnourished children in Zambia was 25.8%. Pneumonia and diarrhea were the major causes of death. In India, 49% of 183 cases of lymphoadenopathy in children were found to be due to tuberculosis [1].
High prevalence of malnutrition and disease in Africa and other developing countries is also reported by Fauci et al. who stated that, "insufficient consumption of protein and energy causes loss of both body mass and adipose tissue, although one or the other loss may predominate in a given individual. Protein energy malnutrition (PEM) occurs primarily under two circumstances: in developing nations it may be present in endemic form, and under famine conditions the prevalence may approach 25 percent. In children of developing nations two syndromes of PEM have been distinguished:(1) maramus, manifested by stunted growth, loss of adipose tissue, generalized wasting of protein mass; and (2) kwashiorkor, manifested by growth failure, edema, and hypoalbuminemia, fatty liver, and preservation of subcutaneous. Mixed forms are common in both children and adults" [2]
Fauci et al. also stated that "the magnitude of malnutrition problem worldwide is immense [2]. In 1983 the World Health Organization estimated that 300 million children had growth retardation secondary to malnutrition. Gastrointestinal infections frequently precipitate clinical PEM because of the associated diarrhea, associated anorexia, vomiting, increased metabolic needs, and decreased intestinal absorption. Parasitic infections play a major role in many parts of the world. Cell-mediated immunity is impaired as indicated by all standard tests. Common infections and opportunistic infections can lead to increased morbidity and mortality. Pneumonia is common. All wounds and incisions heal more slowly in PEM. Wound dehiscence is common. Nearly every aspect of reproduction is impaired in the woman with PEM, including implantation, fetal growth, lactation, and parturition. The infants are stunted in size and may have cognitive impairment if they survive"[2].
Sibanda and Stanczuk reviewed all lymph node histopathology reports of lymph node biopsy submitted to the Histopathology unit in Harare, Zimbabwe in the period of January 1988 to June 1990. The commonest diseases in the 2,194 lymph node specimens submitted were: non specific hyperplasia (33%), tuberculous lymphadenitis (27%); metastases (12%), Kaposi’s sarcoma (9%); and lymphomas (7%). Kaposi’s sarcoma involving the lymph nodes was reported in 176 (9%) of the lymph nodes [13]. In children, the prevalence was higher in children under 5 years than in 6-15 year bracket. Approximately two thirds (65%) of all patients with KS were aged between 20 and 40 years [13].
Table 1. Pathology of the lymphoid tissues in malnourished children and experimental animals[1]
Study TypePopulation SizeDescription of findings in a population of 345 children and two experimental animal models
Autopsy of Malnur. Children118The results of autopsy of malnourished children showed:
1) Both thymus and peripheral lymphoid tissues are reduced in bulk in states of protein-calorie malnutrition (PCM), this reduction being disproportionately greater than the loss of body weight.
2) Severe thymic atrophy was presented in 70% of marasmus cases and 85% of Kwashiorkor cases. 59.3% of the children had marasmic and Kwashiorkor symptoms [14].
 60The results of autopsy showed:
1) Acute involution and severe chronic atrophy of the thymus.
2) Atrophy of lymph nodes with depletion of lymphocytes.
3) Atrophy of spleen with depletion of lymphocytes[15].
Clinical Test110The mean standardized thymic area (STA) in severely malnourished children was found to be 20% of the size in health Children[16].
 57All severely malnourished children (n=42) had a severe involution of the thymus gland (average surface area = 48 mm2). The average size in healthy children is 446 mm2[17].
Animal Studies: Mice Severely Marasmic mice had extreme atrophy of the thymus, lymph nodes, spleen and severe lymphocytopenia[1].
Animal Studies: Rats Growing The status of the thymus of growing rats fed for 45 days after weaning on a low-quality dietary protein (7.5% maize) was compared to that in an age-matched control group receiving a diet containing casein at the same concentration. Thymus weight, cell number, and the absolute number of T cells were significantly lower in experimental group than in the control group[18].

Table 2. Depression of immune system functions in malnourished children [1]
Study TypePopulation SizeDescription of findings in a population of 493 children
T cells blood number & calorie functions on in22The production of migration inhibitory factor (MIF) from lymphocytes of children with moderate protein malnutrition (PCM) was found to be highly impaired vitro stimulation with Candida albicans antigen[19].
 33The blood T cells counts and the lymphocyte response to PHA were found significantly depressed in 14 children suffering from kwashiorkor and 8 children with marasmus[20].
 39The lymphocyte transformation rates in response to PHA stimulation were found to be significantly lower in 30 children with PCM than 9 healthy control[21].
 69Significant reduction in the absolute number and percentage of T-lymphocytes in the blood of malnourished children were observed[22].
blood60Sixty children with malnutrition were investigated.
1) CD3+ T, CD4+ T, and CD8+ T cells in peripheral blood of mild malnutrition children were significantly decreased in contrast to normal control.
2) The reductive degree of CD8+ T and CD4+ T cells correlated with severity of malnutrition.
3) CD8+ T, CD4+ T and CD4+ T/CD8+ T ratio of moderate and severe malnutrition with infection were much lower than those without infection[23].
T and B cells10090% of the children were severely malnourished.
1) Significant reduction in the absolute lymphocytes count.
2) Significant reduction in T cells count.
3) Reduction in skin reaction to Dinitrochlorobenzene[24].
B cell Function & Humoral Immunity170The severely malnourished children showed the following abnormalities compared to normal healthy group.
1) Significantly higher serum levels IgA1 and IgA2.
2) Reduction in C3 level and an increase in C4 level[25].

Table 3. Recovery of the lymphoid organs and immune system functions of malnourished children and experimental animals after feeding [1]
Study TypePopulation SizeDescription of findings in a population of 150 children and in one experimental model
Feeding & Thymus size110The thymus size were measured weakly for 9 weeks in 110 malnourished children, mean age of 16.9 months.
The results show that:
1) The mean standardized thymic are (STA) at week zero was 70 mm2 (20% of normal), normal STA=350 mm2.
2) The average STA for these children at 5, 7, and 9 weeks of proper feedings were 63% , 83% , and 107% of normal respectively[16].
 40The lymphocyte function of 30 black children with PCM as assessed by the delayed hypersensitivity reaction and morphology of lymphocyte transformation was found to be impaired. Serum cortisol level was elevated. The function of lymphocyte and cortisol level returned to normal after 30 days of feeding[23].
Experimental model: Mice Low protein diets initiated at weaning in Balb/c mice caused a rapid and profound reduction in thymus weight and cellularity. Thymus weight fell to less than that of an involuted thymus of adult mice and remained depressed for as long as diets were fed. Thymus growth was reinitiated promptly when high protein diets were fed to deprived animals. Thymus regeneration appeared to be due to both a resident population of stem cells[26].

Table 4. List of selected studies describing the prevalence of malnutrition and infectious diseases in children in Africa and other developing nations[1]
Parameters StudiedCountryResults of studies in a population of 1425 infants and 5834 children
Birth weightsNigeria18.7% of 1041 pregnant women delivered low birth weight babies <2.5 kg[27].
 Kenya11% of 123 pregnant women delivered low birth weight babies[28].
Nutritional Status & health in ChildrenTrinidad & Tobago49.5% of 1620 children evaluated were suffering from some degree of malnutrition and 12.5% were considered as moderately or severely malnourished[29].
 Uganda21.5% of 261 infants and toddles examined were found in poor health (3.8% suffering from kwashiorkor and 5.7 with marasmus).
Infections rate: 23% diarrhea, 32% malaria[30]
 NigeriaPrevalence of malnutrition was determined in 204 children (3-5y): was 60.8% for stunting, 7.4% for wasting, and for 27.5% underweight[31].
 CongoThe health status of 2429 children were evaluated. Prevalence was 27.5% for stunting & 5.5% for Wasting = 5.5%[32].
GoiterLesotho Highlands17.5% of 10-14 years old children had goiter (Children from 395 households were evaluated)[33].
SepticemiaNigeriaThe incidence of septicemia was 9.6% of medical admissions and the overall mortality rate = 28.3%[34].
TuberculosisIndia49% of 183 cases of lympadenopathy in children was found to be tuberculosis[3].
Parasitic infectionNigeria704 children (5-19 years) were evaluated. Infection rates: 32.4% hookworm; 22.9% ascariasis; 17% hematuria (schistomiasis)[35].
Mortality RateZambiaThe mortality rate among 299 severely malnourished children was 25.8%. Pneumonia and diarrhea were the major causes of death[36].


Mohammed A. Al-Bayati, PhD, DABT, DABVT.
Toxi-Health International
Dixon, CA 95620
http://www.toxi-health.com
Email:maalbayati@toxi-health.com
Phone: (707) 678-4484
Fax: (707) 678-8505

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