Zinc deficiency  is defined either as insufficient zinc to meet the needs of the body, or as a serum zinc level below the normal range. However, since a decrease in the serum concentration is only detectable after long-term or severe depletion, serum zinc is not a reliable biomarker for zinc status. Common symptoms include increased rates of diarrhea. Zinc deficiency affects the skin and gastrointestinal tract; brain and central nervous system, immune, skeletal, and reproductive systems. Zinc deficiency in humans is caused by reduced dietary intake, inadequate absorption, increased loss, or increased body system use. The most common cause is reduced dietary intake. In the U.S., the Recommended Dietary Allowance (RDA) is 8 mg/day for women and 11 mg/day for men.The highest concentration of dietary zinc is found in oysters, meat, beans, and nuts. Increasing the amount of zinc in the soil and thus in crops and animals is an effective preventive measure. Zinc deficiency may affect up to 2 billion people worldwide. Signs and symptoms
Skin, nails and hair
Zinc deficiency may manifest as acne, eczema, xerosis (dry, scaling skin), seborrheic dermatitis, or alopecia (thin and sparse hair). It may also impair or possibly prevent wound healing. Mouth
Zinc deficiency can manifest as non-specific oral ulceration, stomatitis, or white tongue coating. Rarely it can cause angular cheilitis (sores at the corners of the mouth). Vision, smell and taste
Severe zinc deficiency may disturb the sense of smell and taste.
Rats can develop the infection, and help spread the infection to other fleas that bite them, and help multiply the number of infected fleas that can then infect humans. Less often, endemic typhus is caused by Rickettsia felis and transmitted by fleas carried by cats or opossums. In the United States of America, murine typhus is found most commonly in southern California, Texas and Hawaii. In some studies, up to 13% of children were found to have serological evidence of infection. Diagnosis
As of 2014, early diagnosis continued to be based on clinical suspicion, and treatment of the disease is indicated even before laboratory results confirm its presence. Because of the lag between the onset of infection and the appearance of antibodies in a blood test, serologic tests are merely confirmatory and retrospective. Weil-Felix agglutination reactions are not sensitive to the disease. Indirect fluorescence antibody assays  that are specific to R. typhi antigens are the recommended route for detection and diagnosis: diagnostic titers are present in half of all cases within the first week of infection and in nearly all cases by day-15. The sharing of antigens by rickettsiae means routine serologic evaluation will not distinguish between murine typhus and epidemic typhus. Bacterial cultures are rarely performed because although they are highly accurate for diagnosis, the biohazard risk of generating them is often considered too high. Treatment
The disease can be fatal if left untreated, but endemic typhus is highly treatable with antibiotics.